FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Bountali, A
   Tonge, DP
   Mourtada-Maarabouni, M
AF Bountali, Aikaterini
   Tonge, Daniel P.
   Mourtada-Maarabouni, Mirna
TI RNA sequencing reveals a key role for the long non-coding RNA MIAT in
   regulating neuroblastoma and glioblastoma cell fate
SO INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
LA English
DT Article
DE MIAT; RNA sequencing; Oxidative stress; Apoptosis; Neuroblastoma;
   Glioblastoma
ID INVASION; GLIOMA; PERSPECTIVES; MECHANISMS; EXPRESSION; MIGRATION;
   GENETICS; HYPOXIA; SP1
AB Myocardial Infarction Associated Transcript (MIAT) is a subnuclear lncRNA that interferes with alternative splicing and is associated with increased risk of various heart conditions and nervous system tumours. The current study aims to elucidate the role of MIAT in cell survival, apoptosis and migration in neuroblastoma and glioblastoma multiforme. To this end, MIAT was silenced by MIAT-specific siRNAs in neuroblastoma and glioblastoma cell lines, and RNA sequencing together with a series of functional assays were performed. The RNA sequencing has revealed that the expression of an outstanding number of genes is altered, including genes involved in cancer-related processes, such as cell growth and survival, apoptosis, reactive oxygen species (ROS) production and migration. Furthermore, the functional studies have confirmed the RNA sequencing leads, with our key findings suggesting that MEAT knockdown eliminates long-term survival and migration and increases basal apoptosis in neuroblastoma and glioblastoma cell lines. Taken together with the recent demonstration of the involvement of MIAT in glioblastoma, our observations suggest that MIAT could possess tumour-promoting properties, thereby acting as an oncogene, and has the potential to be used as a reliable biomarker for neuroblastoma and glioblastoma and be employed for prognostic, predictive and, potentially, therapeutic purposes for these cancers. (C) 2019 Elsevier B.V. All rights reserved.
C1 [Bountali, Aikaterini; Tonge, Daniel P.; Mourtada-Maarabouni, Mirna] Keele Univ, Fac Nat Sci, Sch Life Sci, Newcastle Under Lyme ST5 5BG, England.
C3 Keele University
RP Mourtada-Maarabouni, M (corresponding author), Keele Univ, Fac Nat Sci, Sch Life Sci, Newcastle Under Lyme ST5 5BG, England.
EM m.m.maarabouni@keele.ac.uk
OI /0000-0001-8324-1325; Tonge, Daniel/0000-0002-3499-2752
FU Faculty of Natural Sciences, Keele University
FX Aikaterini Bountali is supported by a studentship awarded by the Faculty
   of Natural Sciences, Keele University.
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NR 57
TC 33
Z9 35
U1 0
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0141-8130
EI 1879-0003
J9 INT J BIOL MACROMOL
JI Int. J. Biol. Macromol.
PD JUN 1
PY 2019
VL 130
BP 878
EP 891
DI 10.1016/j.ijbiomac.2019.03.005
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Applied; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA HV8SE
UT WOS:000466253000093
PM 30836187
DA 2025-04-10
ER

PT J
AU Qu, XH
   Wei, HD
   Zhai, Y
   Que, HP
   Chen, Q
   Tang, F
   Wu, Y
   Xing, GC
   Zhu, YP
   Liu, SJ
   Fan, M
   He, FC
AF Qu, XH
   Wei, HD
   Zhai, Y
   Que, HP
   Chen, Q
   Tang, F
   Wu, Y
   Xing, GC
   Zhu, YP
   Liu, SJ
   Fan, M
   He, FC
TI Identification, characterization, and functional study of the two novel
   human members of the semaphorin gene family
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSMEMBRANE SEMAPHORIN; LUNG-CANCER; PROTEIN; CELL; RECEPTORS;
   EXPRESSION; MIGRATION; CLONING; VERTEBRATES; COLLAPSIN
AB We cloned two novel human transmembrane semaphorins, (HSA)SEMA6C and (HSA)SEMA6D, that belong to the class VI subgroup of the semaphorin family. The genes for SEMA6C and SEMA6D are mapped on chromosome 1q12-21.1 and 15q21.1, respectively. Among the adult tissues, SEMA6C is expressed only in skeletal muscle, whereas SEMA6D is expressed abundantly in kidney, brain, and placenta and moderately in the heart and skeletal muscles. During murine development, neither SEMA6C nor SEMA6D was expressed in embryonic day 10.5 (E10.5) embryos, but both were highly expressed in the areas of the lateral ventricle, the striatum, the wall of the midbrain, the pons/midbrain junction, and the choroid plexus of E13 embryos. Were neurons, neither axons nor astrocytes, highly expressed both semaphorins. Three isoforms of SEMA6C and five isoforms of SEMA6D derived from alternative splicing were identified, and their expression was regulated in a tissue- and development-dependent manner. Deletion analysis indicated that a sema domain and a PSI domain are integrally necessary for correct post-translation modification and subcellular localization. The extracellular domain of SEMA6C inhibited axonal extension of nerve growth factor-differentiated PC12 cells and induced the growth cone collapse of chicken dorsal root ganglion, rat hippocampal neurons, and rat cortical neurons in a dose-responsive manner. SEMA6D acted like SEMA6C except it had no significant effect on the growth cones of rat cortical neurons.
C1 Chinese Natl Human Genome Ctr, Beijing Inst Radiat Med, Dept Genom & Proteom, Beijing 100850, Peoples R China.
   Beijing Inst Basic Med Sci, Dept Neurosci, Beijing 100850, Peoples R China.
C3 Academy of Military Medical Sciences - China; Academy of Military
   Medical Sciences - China; Institute of Basic Medical Sciences (IBMS)
RP He, FC (corresponding author), Chinese Natl Human Genome Ctr, Beijing Inst Radiat Med, Dept Genom & Proteom, 27 Taiping Rd, Beijing 100850, Peoples R China.
RI Qu, Xuanhui/J-6839-2014; He, FC/KGL-6713-2024
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NR 31
TC 61
Z9 77
U1 0
U2 13
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 20
PY 2002
VL 277
IS 38
BP 35574
EP 35585
DI 10.1074/jbc.M206451200
PG 12
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 595PB
UT WOS:000178117000117
PM 12110693
OA hybrid
DA 2025-04-10
ER

PT J
AU Gromadzinski, L
   Paukszto, L
   Lepiarczyk, E
   Skowronska, A
   Lipka, A
   Makowczenko, KG
   Lopienska-Biernat, E
   Jastrzebski, JP
   Holak, P
   Smolinski, M
   Majewska, M
AF Gromadzinski, Leszek
   Paukszto, Lukasz
   Lepiarczyk, Ewa
   Skowronska, Agnieszka
   Lipka, Aleksandra
   Makowczenko, Karol G.
   Lopienska-Biernat, Elzbieta
   Jastrzebski, Jan P.
   Holak, Piotr
   Smolinski, Michal
   Majewska, Marta
TI Pulmonary artery embolism: comprehensive transcriptomic analysis in
   understanding the pathogenic mechanisms of the disease
SO BMC GENOMICS
LA English
DT Article
DE Pulmonary embolism; RNA-seq; Molecular pathways; Endoplasmic reticulum
ID DEEP VENOUS THROMBOSIS; ENDOTHELIAL-CELLS; VEIN THROMBOSIS; COLLAGEN;
   PROTEIN; MODEL; THY-1; COAGULATION; RELEASE; PACKAGE
AB Background Pulmonary embolism (PE) is a severe disease that usually originates from deep vein thrombosis (DVT) of the lower extremities. This study set out to investigate the changes in the transcriptome of the pulmonary artery (PA) in the course of the PE in the porcine model. Methods The study was performed on 11 male pigs: a thrombus was formed in each right femoral vein in six animals, and then was released to induce PE, the remaining five animals served as a control group. In the experimental animals total RNA was isolated from the PA where the blood clot lodged, and in the control group, from the corresponding PA segments. High-throughput RNA sequencing was used to analyse the global changes in the transcriptome of PA with induced PE (PA-E). Results Applied multistep bioinformatics revealed 473 differentially expressed genes (DEGs): 198 upregulated and 275 downregulated. Functional Gene Ontology annotated 347 DEGs into 27 biological processes, 324 to the 11 cellular components and 346 to the 2 molecular functions categories. In the signaling pathway analysis, KEGG 'protein processing in endoplasmic reticulum' was identified for the mRNAs modulated during PE. The same KEGG pathway was also exposed by 8 differentially alternative splicing genes. Within single nucleotide variants, the 61 allele-specific expression variants were localised in the vicinity of the genes that belong to the cellular components of the 'endoplasmic reticulum'. The discovered allele-specific genes were also classified as signatures of the cardiovascular system. Conclusions The findings of this research provide the first thorough investigation of the changes in the gene expression profile of PA affected by an embolus. Evidence from this study suggests that the disturbed homeostasis in the biosynthesis of proteins in the endoplasmic reticulum plays a major role in the pathogenesis of PE.
C1 [Gromadzinski, Leszek] Univ Warmia & Mazury, Sch Med, Dept Cardiol & Internal Med, Coll Medicum, Warszawska Str 30, PL-10082 Olsztyn, Poland.
   [Paukszto, Lukasz] Univ Warmia & Mazury, Dept Bot & Nat Protect, Placlodzki 1, PL-10727 Olsztyn, Poland.
   [Lepiarczyk, Ewa; Skowronska, Agnieszka; Majewska, Marta] Univ Warmia & Mazury, Sch Med, Dept Human Physiol & Pathophysiol, Coll Medicum, Warszawska Str 30, PL-10082 Olsztyn, Poland.
   [Lipka, Aleksandra] Univ Warmia & Mazury, Sch Med, Dept Gynecol & Obstet, Coll Medicum, Zolnierska Str 18, PL-10561 Olsztyn, Poland.
   [Makowczenko, Karol G.] Univ Warmia & Mazury, Fac Biol & Biotechnol, Dept Anim Anat & Physiol, Oczapowskiego 1A, PL-10719 Olsztyn, Poland.
   [Lopienska-Biernat, Elzbieta] Univ Warmia & Mazury, Fac Biol & Biotechnol, Dept Biochem, Oczapowskiego Str 1A, PL-10719 Olsztyn, Poland.
   [Jastrzebski, Jan P.] Univ Warmia & Mazury, Fac Biol & Biotechnol, Dept Plant Physiol Genet & Biotechnol, Oczapowskiego Str 1A, PL-10719 Olsztyn, Poland.
   [Holak, Piotr] Univ Warmia & Mazury, Fac Vet Med, Dept Surg & Radiol Clin, Oczapowskiego Str 14, PL-10719 Olsztyn, Poland.
   [Smolinski, Michal] Univ Clin Hosp Olsztyn, Clin Cardiol & Internal Dis, Warszawska Str 30, PL-10082 Olsztyn, Poland.
C3 University of Warmia & Mazury; University of Warmia & Mazury; University
   of Warmia & Mazury; University of Warmia & Mazury; University of Warmia
   & Mazury; University of Warmia & Mazury; University of Warmia & Mazury;
   University of Warmia & Mazury
RP Majewska, M (corresponding author), Univ Warmia & Mazury, Sch Med, Dept Human Physiol & Pathophysiol, Coll Medicum, Warszawska Str 30, PL-10082 Olsztyn, Poland.
EM marta.majewska@uwm.edu.pl
RI Lipka, Aleksandra/AAM-1631-2020; Jastrzębski, Jan/D-6423-2014;
   Lepiarczyk, Ewa/I-7756-2019; Majewska, Marta/JNS-3323-2023;
   Łopieńska-Biernat, Elzbieta/AAN-6140-2020; Paukszto,
   Lukasz/AAV-8585-2021; Gromadziński, Leszek/JQV-3800-2023; Jastrzebski,
   Jan Pawel/C-3714-2015
OI Lipka, Aleksandra/0000-0003-0815-6635; Majewska,
   Marta/0000-0001-5856-6929; Lopienska-Biernat,
   Elzbieta/0000-0003-3265-5207; Makowczenko, Karol/0000-0003-3758-4452;
   Jastrzebski, Jan Pawel/0000-0001-8699-7742
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NR 96
TC 1
Z9 1
U1 0
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD JAN 9
PY 2023
VL 24
IS 1
AR 10
DI 10.1186/s12864-023-09110-0
PG 20
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 7T3PD
UT WOS:000911356000003
PM 36624378
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Heidari, Z
   Naeimzadeh, Y
   Fallahi, J
   Savardashtaki, A
   Razban, V
   Khajeh, S
AF Heidari, Zahra
   Naeimzadeh, Yasaman
   Fallahi, Jafar
   Savardashtaki, Amir
   Razban, Vahid
   Khajeh, Sahar
TI The Role of Tissue Factor In Signaling Pathways of Pathological
   Conditions and Angiogenesis
SO CURRENT MOLECULAR MEDICINE
LA English
DT Review
DE Tissue factor; pathological conditions; asthma; cardiovascular diseases;
   viral infection; cancer; angiogenesis
ID ENDOTHELIAL GROWTH-FACTOR; FACTOR CYTOPLASMIC DOMAIN; HYPOXIA-INDUCIBLE
   FACTOR-1-ALPHA; PROTEASE-ACTIVATED RECEPTORS; COAGULATION-FACTORS VIIA;
   FACTOR EXPRESSION; BLOOD-COAGULATION; HEMOSTATIC SYSTEM; LIVER FIBROSIS;
   CANCER CELLS
AB Tissue factor (TF) is an integral transmembrane protein associated with the extrinsic coagulation pathway. TF gene expression is regulated in response to inflammatory cytokines, bacterial lipopolysaccharides, and mechanical injuries. TF activity may be affected by phosphorylation of its cytoplasmic domain and alternative splicing. TF acts as the primary initiator of physiological hemostasis, which prevents local bleeding at the injury site. However, aberrant expression of TF, accompanied by the severity of diseases and infections under various pathological conditions, triggers multiple signaling pathways that support thrombosis, angiogenesis, inflammation, and metastasis. Protease-activated receptors (PARs) are central in the downstream signaling pathways of TF. In this study, we have reviewed the TF signaling pathways in different pathological conditions, such as wound injury, asthma, cardiovascular diseases (CVDs), viral infections, cancer and pathological angiogenesis. Angiogenic activities of TF are critical in the repair of wound injuries and aggressive behavior of tumors, which are mainly performed by the actions of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1 (HIF1-alpha). Pro-inflammatory effects of TF have been reported in asthma, CVDs and viral infections, including COVID-19, which result in tissue hypertrophy, inflammation, and thrombosis. TF-FVII induces angiogenesis via clotting-dependent and -independent mechanisms. Clotting-dependent angiogenesis is induced via the generation of thrombin and cross-linked fibrin network, which facilitate vessel infiltration and also act as a reservoir for endothelial cells (ECs) growth factors. Expression of TF in tumor cells and ECs triggers clotting-independent angiogenesis through induction of VEGF, urokinase-type plasminogen activator (uPAR), early growth response 1 (EGR1), IL8, and cysteine-rich angiogenic inducer 61 (Cyr61).
C1 [Heidari, Zahra; Naeimzadeh, Yasaman; Fallahi, Jafar; Razban, Vahid] Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Mol Med, Shiraz, Iran.
   [Savardashtaki, Amir] Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Med Biotechnol, Shiraz, Iran.
   [Savardashtaki, Amir] Shiraz Univ Med Sci, Infertil Res Ctr, Shiraz, Iran.
   [Khajeh, Sahar] Shiraz Univ Med Sci, Bone & Joint Dis Res Ctr, Shiraz, Iran.
C3 Shiraz University of Medical Science; Shiraz University of Medical
   Science; Shiraz University of Medical Science; Shiraz University of
   Medical Science
RP Razban, V (corresponding author), Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Mol Med, Shiraz, Iran.; Khajeh, S (corresponding author), Shiraz Univ Med Sci, Bone & Joint Dis Res Ctr, Shiraz, Iran.
EM razban_vahid@yahoo.com; saharkh7@gmail.com
RI Khajeh, Sahar/ABA-5098-2021; Fallahi, Jafar/ABG-3805-2021; heidari,
   zahra/AAO-8370-2021; Razban, Vahid/D-8334-2014; Savardashtaki,
   Amir/M-6041-2018
OI Naeimzadeh, Yasaman/0000-0003-3937-1426; Khajeh,
   Sahar/0000-0003-1614-2962; Razban, Vahid/0000-0002-8966-6081;
   Savardashtaki, Amir/0000-0003-1700-9426
FX Declared none.
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NR 228
TC 7
Z9 7
U1 3
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1566-5240
EI 1875-5666
J9 CURR MOL MED
JI Curr. Mol. Med.
PY 2024
VL 24
IS 9
BP 1135
EP 1151
DI 10.2174/0115665240258746230919165935
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA XR1U5
UT WOS:001263323000008
PM 37817529
DA 2025-04-10
ER

PT J
AU Greco, R
   Tassorelli, C
   Mangione, AS
   Levandis, G
   Certo, M
   Nappi, G
   Bagetta, G
   Blandini, F
   Amantea, D
AF Greco, Rosaria
   Tassorelli, Cristina
   Mangione, Antonina Stefania
   Levandis, Giovanna
   Certo, Michelangelo
   Nappi, Giuseppe
   Bagetta, Giacinto
   Blandini, Fabio
   Amantea, Diana
TI Neuroprotection by the PARP inhibitor PJ34 modulates cerebral and
   circulating RAGE levels in rats exposed to focal brain ischemia
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE Cerebral ischemia; Full-length RAGE; MCAo; PARP inhibition; sRAGE
ID GLYCATION END-PRODUCTS; C-REACTIVE PROTEIN; CORONARY-ARTERY-DISEASE;
   IN-VIVO MODELS; SOLUBLE RECEPTOR; POLY(ADP-RIBOSE) POLYMERASE; STROKE
   SUBTYPES; POSTISCHEMIC BRAIN; PLASMA BIOMARKERS; ATHEROSCLEROSIS
AB The receptor for advanced glycation end products (RAGE) has a potential role as a damage-sensing molecule; however, to date, its involvement in the pathophysiology of stroke and its modulation following neuroprotective treatment are not completely understood. We have previously demonstrated that expression of distinct RAGE isoforms, recognized by different antibodies, is differentially modulated in the brain of rats subjected to focal cerebral ischemia. Here, we focus on the full-length membrane-bound RAGE isoform, showing that its expression is significantly elevated in the striatum, whereas it is reduced in the cortex of rats subjected to transient middle cerebral artery occlusion (MCAo). Notably, the reduction of cortical levels of full-length RAGE detected 24 h after reperfusion is abolished by systemic administration of a neuroprotective dose of the poly(ADP-ribose) polymerase (PARP) inhibitor, N-(6-oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide (PJ34). More interestingly, a significant reduction of plasma soluble RAGE (sRAGE) occurs 24 h after reperfusion and this effect is reverted by a neuroprotective dose of PJ34. Soluble forms of RAGE, generated either by alternative splicing or by proteolysis of the full-length form, effectively bind advanced glycation end products, thereby competing with the cell surface full-length RAGE, thus providing a 'decoy' function that may counteract the adverse effects of receptor signaling in neurons and may possibly exert cytoprotective effects. Thus, our data confirm the important role of RAGE in ischemic cerebral damage and, more interestingly, suggest the potential use of sRAGE as a blood biomarker of stroke severity and of neuroprotective treatment efficacy. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Greco, Rosaria; Tassorelli, Cristina; Mangione, Antonina Stefania; Nappi, Giuseppe] C Mondino Natl Neurol Inst, Headache Sci Ctr, Lab Neurophysiol Integrat Autonom Syst, Pavia, Italy.
   [Tassorelli, Cristina] Univ Pavia, Dept Brain & Behav, I-27100 Pavia, Italy.
   [Levandis, Giovanna; Blandini, Fabio] C Mondino Natl Neurol Inst, Ctr Res Neurodegenerat Dis, Lab Funct Neurochem, Pavia, Italy.
   [Certo, Michelangelo; Bagetta, Giacinto; Amantea, Diana] Univ Calabria, Dept Pharm Hlth & Nutr Sci, I-87036 Arcavacata Di Rende, CS, Italy.
C3 IRCCS Fondazione Casimiro Mondino; University of Pavia; IRCCS Fondazione
   Casimiro Mondino; University of Calabria
RP Greco, R (corresponding author), Natl Neurol Inst C Mondino Fdn, Via Mondino 2, I-27100 Pavia, Italy.
EM rosaria.greco@mondino.it
RI Amantea, Diana/A-6231-2010; Tassorelli, Cristina/AAC-1483-2019; Nappi,
   Giuseppe/AAF-4962-2021; Bagetta, Giacinto/N-9716-2018; greco,
   rosaria/K-8828-2016; Blandini, Fabio/J-2658-2016; Bagetta,
   Giacinto/E-8402-2012; CERTO, MICHELANGELO/K-6784-2014
OI greco, rosaria/0000-0001-6577-0629; Blandini, Fabio/0000-0002-0178-1289;
   Bagetta, Giacinto/0000-0001-8540-6218; CERTO,
   MICHELANGELO/0000-0002-5568-3465; Nappi, Giuseppe/0000-0003-4274-5281;
   Amantea, Diana/0000-0002-7513-3495
FU Italian Ministry of Health
FX This study was supported by a grant from the Italian Ministry of Health
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NR 65
TC 18
Z9 18
U1 0
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD DEC 5
PY 2014
VL 744
BP 91
EP 97
DI 10.1016/j.ejphar.2014.10.006
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA AW0YB
UT WOS:000346016000012
PM 25446913
DA 2025-04-10
ER

PT J
AU Jiang, H
   Toscano, JF
   Schiraldi, M
   Song, SS
   Schlick, KH
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AF Jiang, Hao
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   Liou, Raymond
   Lyden, Patrick D.
   Pan, Jianwei
   Zhan, Renya
   Saver, Jeffrey L.
   Gonzalez, Nestor R.
TI Differential Expression of Vascular Endothelial Growth
   Factor-A165 Isoforms Between Intracranial Atherosclerosis and
   Moyamoya Disease
SO JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
LA English
DT Article
DE VEGF-A(165); isoforms; intracranial atherosclerosis; moyamoya disease
ID CORONARY COLLATERAL GROWTH; VEGF-A; ISCHEMIC-STROKE; CT ANGIOGRAPHY;
   ANGIOGENESIS
AB Background: Vascular endothelial growth factor-A(165) (VEGF-A(165)) has been identified as a combination of 2 alternative splice variants: proangiogenic VEGF-A(165 )a and anti-angiogenic VEGF-A(165)b. Intracranial atherosclerotic disease (ICAD) and moyamoya disease (MMD) are 2 main types of intracranial arterial steno-occlusive disorders with distinct capacities for collateral formation. Recent studies indicate that VEGF-A(165) regulates collateral growth in ischemia. Therefore, we investigated if there is a distinctive composition of VEGF-A(165) isoforms in ICAD and MMD. Methods: Sixty-six ICAD patients, 6 MMD patients, and 5 controls were enrolled in this prospective study. ICAD and MMD patients received intensive medical management upon enrollment. Surgery was offered to 9 ICAD patients who had recurrent ischemic events, 6 MMD patients, and 5 surgical controls without ICAD. VEGF-A(165)a and VEGF-A(165)b plasma levels were measured at baseline, within 1 week after patients having surgery, and at 1, 3, and 6 months after treatment. Results: A significantly higher baseline VEGF-A(165)a/b ratio was observed in MMD compared to ICAD (P = .016). The VEGF-A(165)a/b ratio increased significantly and rapidly after surgical treatment in ICAD (P = .026) more so than in MMD and surgical controls. In patients with ICAD receiving intensive medical management, there was also an elevation of the VEGF-A(165)a/b ratio, but at a slower rate, reaching the peak at 3 months after initiation of treatment (baseline versus 3 months VEGF-A(165)a/b ratio, P = .028). Conclusions: Our study shows an increased VEGF-A(165)a/b ratio in MMD compared to ICAD, and suggests that both intensive medical management and surgical revas-cularization elevate the VEGF-A(165)a/b ratio in ICAD patients.
C1 [Jiang, Hao; Toscano, Juan F.; Schiraldi, Michael; Gonzalez, Nestor R.] Cedars Sinai Med Ctr, Gonzalez Neurovasc Lab, Dept Neurosurg, Los Angeles, CA 90048 USA.
   [Jiang, Hao; Pan, Jianwei; Zhan, Renya] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Neurosurg, Hangzhou, Zhejiang, Peoples R China.
   [Song, Shlee S.; Schlick, Konrad H.; Dumitrascu, Oana M.; Lyden, Patrick D.; Gonzalez, Nestor R.] Cedars Sinai Med Ctr, Dept Neurol, Los Angeles, CA 90048 USA.
   [Liou, Raymond] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
   [Saver, Jeffrey L.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA.
C3 Cedars Sinai Medical Center; Zhejiang University; Cedars Sinai Medical
   Center; Stanford University; University of California System; University
   of California Los Angeles
RP Gonzalez, NR (corresponding author), Cedars Sinai Med Ctr, Dept Neurosurg Vasc & Endovasc Neurosurg, AHSP, 127 So San Vicente Blvd,6th Floor,Suite A6600, Los Angeles, CA 90048 USA.
EM Nestor.Gonzalez@cshs.org
RI Penchev, Plamen/GOH-1883-2022; Gonzalez, Nestor/AFH-8484-2022; Saver,
   Jeffrey/AFT-4279-2022; Schlick, Konrad/KEI-5265-2024
OI Pan, Jianwei/0000-0001-6353-1843; Gonzalez, Nestor/0000-0002-8277-6317
FU American Heart Association [14ISA20870000]; NIH [K23 NS079477-01A1];
   Science and Technology Department of Zhejiang Province [2015C34007]
FX This work was supported by grants from the American Heart Association
   (14ISA20870000), NIH (K23 NS079477-01A1), and the Science and Technology
   Department of Zhejiang Province (2015C34007) and by the philanthropic
   support of the Margo and Irwin Winkler Family.
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NR 36
TC 6
Z9 6
U1 1
U2 18
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1052-3057
EI 1532-8511
J9 J STROKE CEREBROVASC
JI J. Stroke Cerebrovasc. Dis.
PD FEB
PY 2019
VL 28
IS 2
BP 360
EP 368
DI 10.1016/j.jstrokecerebrovasdis.2018.10.004
PG 9
WC Neurosciences; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA HG0IX
UT WOS:000454628100021
PM 30392834
OA Green Submitted, Green Accepted
DA 2025-04-10
ER

PT J
AU Helfman, DM
   Berthier, C
   Grossman, J
   Leu, M
   Ehler, E
   Perriard, E
   Perriard, JC
AF Helfman, DM
   Berthier, C
   Grossman, J
   Leu, M
   Ehler, E
   Perriard, E
   Perriard, JC
TI Nonmuscle tropomyosin-4 requires coexpression with other low molecular
   weight isoforms for binding to thin filaments in cardiomyocytes
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE tropomyosin; neonatal cardiomyocyte; sarcomere; green fluorescent
   protein
ID FLUORESCENTLY LABELED ACTIN; ALPHA-TROPOMYOSIN; MONOCLONAL-ANTIBODIES;
   CULTURED-CELLS; PROTEIN; YEAST; GENE; MICROFILAMENTS; LOCALIZATION;
   EXPRESSION
AB Vertebrate tropomyosins (TMs) are expressed from four genes, and at least 18 distinct isoforms are generated via a complex pattern of alternative RNA splicing and alternative promoters. The functional significance of this isoform diversity is largely unknown and it remains to be determined whether specific isoforms are required for assembly and integration into distinct actin-containing structures. The ability of nonmuscle (TM-1, -2, -3, -4, -5(NM1), -5a or -5b) and striated muscle (skeletal muscle alpha-TM) isoforms to incorporate into actin filaments of neonatal rat cardiomyocytes (NRCs) was studied using expression plasmids containing TM-fusions with GFP (green fluorescent protein) as well as with VSV- or HA-epitope tags. All isoforms, except of fibroblast TM-4, were able to incorporate into the I-band of NRCs, When TM-4 was co-transfected with other low molecular weight (LMW) isoforms of TM (TM-5, TM-5a and TM-5b), it was able to incorporate into sarcomeres of NRCs. This result was not obtained when TM-4 was co-transfected with high molecular weight (HMW) TMs (TM-1, TM-2 or skeletal muscle alpha-TM). These data demonstrate that the ability of TM-4 to bind to actin filaments can be specifically influenced by its interaction with other LMW TM isoforms. In addition, cells that incorporated the muscle or nonmuscle GFP-TMs into their sarcomeres continued to beat and exhibited sarcomeric contraction. These studies provide the first in vivo demonstration of synergistic effects between TM isoforms for binding to actin filaments. These results have important implications in understanding actin filament dynamics in nonmuscle cell systems, especially during development and in transformed cells, where alterations in the ratio of different LMW isoforms might lead to changes in their interactions with actin filaments. Furthermore, these studies demonstrate that GFP-TM can be used to study thin-filament dynamics in muscle cells and actin filament dynamics in nonmuscle cells.
C1 Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
   Swiss Fed Inst Technol, Inst Cell Biol, CH-8093 Zurich, Switzerland.
C3 Cold Spring Harbor Laboratory; Swiss Federal Institutes of Technology
   Domain; ETH Zurich
RP Helfman, DM (corresponding author), Cold Spring Harbor Lab, POB 100, Cold Spring Harbor, NY 11724 USA.
EM helfman@cshi.org
RI berthier, christine/AAO-1247-2021; Helfman, David/C-2058-2011
OI BERTHIER, Christine/0000-0002-9608-643X; Ehler,
   Elisabeth/0000-0001-5646-5964
FU NCI NIH HHS [CA58607] Funding Source: Medline
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NR 43
TC 25
Z9 27
U1 0
U2 0
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS,
   ENGLAND CB4 4DL
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD FEB
PY 1999
VL 112
IS 3
BP 371
EP 380
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 168WB
UT WOS:000078715200011
PM 9885290
DA 2025-04-10
ER

PT J
AU Mondéjar-Parreño, G
   Cogolludo, A
   Perez-Vizcaino, F
AF Mondejar-Parreno, Gema
   Cogolludo, Angel
   Perez-Vizcaino, Francisco
TI Potassium (K<SUP>+</SUP>) channels in the pulmonary vasculature:
   Implications in pulmonary hypertension Physiological, pathophysiological
   and pharmacological regulation
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Potassium channels; Pulmonary hypertension; Smooth muscle; Endothelium;
   Proliferation; Pharmacology
ID SMOOTH-MUSCLE-CELLS; ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION;
   5-HYDROXYTRYPTAMINE TRANSPORTER GENE; ANGIOTENSIN-CONVERTING ENZYME;
   ARTERIAL-HYPERTENSION; ION CHANNELS; ATP CHANNELS; HYDROGEN-SULFIDE;
   CHRONIC HYPOXIA; DOWN-REGULATION
AB The large K+ channel functional diversity in the pulmonary vasculature results from the multitude of genes expressed encoding K+ channels, alternative RNA splicing, the post-transcriptional modifications, the presence of homomeric or heteromeric assemblies of the pore-forming alpha-subunits and the existence of accessory beta-subunits modulating the functional properties of the channel. K+ channels can also be regulated at multiple levels by different factors controlling channel activity, trafficking, recycling and degradation. The activity of these channels is the primary determinant of membrane potential (Em) in pulmonary artery smooth muscle cells (PASMC), providing an essential regulatory mechanism to dilate or contract pulmonary arteries (PA). K+ channels are also expressed in pulmonary artery endothelial cells (PAEC) where they control resting Em, Ca2+ entry and the production of different vasoactive factors. The activity of K+ channels is also important in regulating the population and phenotype of PASMC in the pulmonary vasculature, since they are involved in cell apoptosis, survival and proliferation. Notably, K+ channels play a major role in the development of pulmonary hypertension (PH). Impaired K+ channel activity in PH results from: 1) loss of function mutations, 2) downregulation of its expression, which involves transcription factors and microRNAs, or 3) decreased channel current as a result of increased vasoactive factors (e.g., hypoxia, 5-HT, endothelin-1 or thromboxane), exposure to drugs with channel-blocking properties, or by a reduction in factors that positively regulate K+ channel activity (e.g., NO and prostacyclin). Restoring K+ channel expression, its intracellular trafficking and the channel activity is an attractive therapeutic strategy in PH. (C) 2021 Elsevier Inc. All rights reserved.
C1 [Mondejar-Parreno, Gema; Cogolludo, Angel; Perez-Vizcaino, Francisco] Univ Complutense Madrid, Dept Pharmacol & Toxicol, Sch Med, Pza Ramon y Cajal S-N, Madrid 28040, Spain.
   [Mondejar-Parreno, Gema; Cogolludo, Angel; Perez-Vizcaino, Francisco] Inst Invest Sanitaria Gregorio Maranon IiSGM, Madrid, Spain.
   [Mondejar-Parreno, Gema; Cogolludo, Angel; Perez-Vizcaino, Francisco] Ciber Enfermedades Resp CIBERES, Madrid, Spain.
C3 Complutense University of Madrid; CIBER - Centro de Investigacion
   Biomedica en Red; CIBERES
RP Perez-Vizcaino, F (corresponding author), Univ Complutense Madrid, Dept Pharmacol & Toxicol, Sch Med, Pza Ramon y Cajal S-N, Madrid 28040, Spain.
RI Cogolludo, Angel/A-6129-2011; Perez-Vizcaino, Francisco/A-9735-2011
OI Perez-Vizcaino, Francisco/0000-0001-6309-7418
FU Ministerio de Economia y Competitividad [PID2019-107363RB-I00,
   SAF201677222R]; CardiovascularMedical Research and Education Fund;
   Comunidad de Madrid [B2017/BMD-3727]; Fundacion Contra la Hipertension
   Pulmonar; CIBERES/Fundacion Contra la Hipertension PulmonarEMPATHY
FX The research of the authors was funded by Ministerio de Economia y
   Competitividad grants (PID2019-107363RB-I00 to FP-V and SAF201677222R to
   FP-V and AC), the CardiovascularMedical Research and Education Fund
   (AC), Comunidad de Madrid (B2017/BMD-3727 to AC) and Fundacion Contra la
   Hipertension Pulmonar. GM-P is supported by a predoctoral
   CIBERES/Fundacion Contra la Hipertension PulmonarEMPATHY grant.
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NR 304
TC 26
Z9 28
U1 2
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
EI 1879-016X
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD SEP
PY 2021
VL 225
AR 107835
DI 10.1016/j.pharmthera.2021.107835
EA MAR 2021
PG 27
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TD7ML
UT WOS:000669506100015
PM 33744261
DA 2025-04-10
ER

PT J
AU Dai, L
   Zitnan, D
   Adams, ME
AF Dai, Li
   Zitnan, Dusan
   Adams, Michael E.
TI Strategic expression of ion transport peptide gene products in central
   and peripheral neurons of insects
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE ITP-like peptide; ITPL; ITP gene; RT-PCR; in situ hybridization;
   immunolabeling; neurosecretory cells; corpora cardiaca; Manduca sexta;
   Bombyx mori; Aedes aegypti
ID CRUSTACEAN CARDIOACTIVE PEPTIDE; HYPERGLYCEMIC-HORMONE FAMILY; PRAWN
   MARSUPENAEUS-JAPONICUS; MOLT-INHIBITING HORMONE; CRAB CARCINUS-MAENAS;
   MOTH MANDUCA-SEXTA; NEUROSECRETORY-CELLS; NERVOUS-SYSTEM; SHORE CRAB;
   ITP-L
AB Structurally related ion transport peptides (ITP) and crustacean hyperglycemic hormones (CHH) are increasingly implicated in diverse metabolic and developmental functions in arthropods. We identified a conserved ITP gene encoding two peptides by alternative splicing in Manduca sexta, Bombyx mori, and Aedes aegypti: A C-terminally amidated ITP and a C-terminally unblocked ITP-like peptide (ITPL), which share common N-terminal sequences but have divergent C-termini. In the moth M. sexta, these peptides are expressed in two, regionally distinct neuronal populations in the central and peripheral nervous systems (CNS, PNS). MasITP expression is confined to the brain in five pairs of lateral neurosecretory cells (type Ia(2)) projecting ipsilateral axons into the retrocerebral complex and three to five pairs of adjacent small neurons that arborize extensively within the brain. Expression of MasITPL is comparatively weak in the brain but strong in the ventral ganglia and the PNS, where MasITP is absent. MasITPL occurs in bilaterally paired neurons of all thoracic and abdominal ganglia. In the PNS, MasITPL is coexpressed with crustacean cardioactive peptide in type II link nerve neurons (L1) of abdominal segments 2-7, which project axons into neurohemal transverse nerves. During metamorphosis, additional expression of MasITPL is observed in two pairs of small lateral neurons in the brain and one pair of ventromedial neurons in each of AG2-6. A similar pattern of differential ITP and ITPL expression was observed in the CNS and PNS of B. mori and Schistocerca americana. These distinctive cellular expression patterns suggest that ITP and ITPL have evolved specialized physiological functions in arthropods.
C1 Univ Calif Riverside, Dept Entomol, Riverside, CA 92521 USA.
   Univ Calif Riverside, Dept Cell Biol & Neurosci, Riverside, CA 92521 USA.
   Slovak Acad Sci, Inst Zool, Bratislava, Slovakia.
C3 University of California System; University of California Riverside;
   University of California System; University of California Riverside;
   Slovak Academy of Sciences; Institute of Zoology, SAS
RP Adams, ME (corresponding author), Univ Calif Riverside, Dept Entomol, 2103 Biol Sci Bldg, Riverside, CA 92521 USA.
EM michael.adams@ucr.edu
RI Adams, Michael/ABF-6728-2020
FU NIGMS NIH HHS [GM67310] Funding Source: Medline
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NR 33
TC 36
Z9 39
U1 0
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD JAN 10
PY 2007
VL 500
IS 2
BP 353
EP 367
DI 10.1002/cne.21192
PG 15
WC Neurosciences; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Zoology
GA 115MB
UT WOS:000242737300011
PM 17111378
DA 2025-04-10
ER

PT J
AU Pinter, K
   Grignani, RT
   Czibik, G
   Farza, H
   Watkins, H
   Redwood, C
AF Pinter, Katalin
   Grignani, Robert T.
   Czibik, Gabor
   Farza, Hend
   Watkins, Hugh
   Redwood, Charles
TI Embryonic expression of AMPK γ subunits and the identification of a
   novel γ2 transcript variant in adult heart
SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
LA English
DT Article
DE AMP-activated protein kinase; PRKAG2 transcripts; Cardiomyopathy
ID ACTIVATED PROTEIN-KINASE; PARKINSON-WHITE-SYNDROME; SKELETAL-MUSCLE;
   HYPERTROPHIC CARDIOMYOPATHY; DISEASE; GLYCOGEN; PRKAG2; MUTATIONS;
   SUBFAMILY; ISOFORMS
AB AMP-activated protein kinase (AMPK), the key sensor and regulator of cellular energy status, is a heterotrimeric enzyme with multiple isoforms for each subunit (alpha 1/alpha 2; beta 1/beta 2; gamma 1/gamma 2/gamma 3). Mutations in PRKAG2, which encodes the gamma 2 regulatory subunit, cause a cardiomyopathy characterized by hypertrophy and conduction abnormalities. The two reported PRKAG2 transcript variants, gamma 2-short and gamma 2-long (encoding 328 and 569 amino acids respectively), are both widely expressed in adult tissues. We show that both gamma 2 variants are also expressed during cardiogenesis in mouse embryos; expression of the gamma 3 isoform was also detected unexpectedly at this stage. As neither gamma 2 transcript is cardiac specific nor differentially expressed during embryogenesis, it is paradoxical that the disease is largely restricted to the heart. However, a recently annotated gamma 2 transcript, termed gamma 2-3B as transcription starts at an alternative exon 3b, has been identified; it is spliced in-frame to exon 4 thus generating a protein of 443 residues in mouse with the first 32 residues being unique. It is increasingly expressed in the developing mouse heart and quantitative PCR analysis established that gamma 2-3B is the major PRKAG2 transcript (similar to 60%) in human heart. Antibody against the novel N-terminal sequence showed that gamma 2-3B is predominantly expressed in the heart where it is the most abundant gamma 2 protein. The abundance of gamma 2-3B and its tissue specificity indicate that gamma 2-3B may have non-redundant role in the heart and hence mediate the predominantly cardiac phenotype caused by PRKAG2 mutations. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Pinter, Katalin; Grignani, Robert T.; Czibik, Gabor; Farza, Hend; Watkins, Hugh; Redwood, Charles] Univ Oxford, Dept Cardiovasc Med, John Radcliffe Hosp, Oxford OX3 9DU, England.
C3 University of Oxford
RP Redwood, C (corresponding author), Univ Oxford, Dept Cardiovasc Med, John Radcliffe Hosp, W Wing Level 6, Oxford OX3 9DU, England.
EM credwood@well.ox.ac.uk
RI ; Czibik, Gabor/U-9295-2018
OI Grignani, Robert/0009-0002-4389-1053; Watkins, Hugh/0000-0002-5287-9016;
   Czibik, Gabor/0000-0002-4914-6794
FU British Heart Foundation; Wellcome Trust Functional Genomics Initiative;
   Agency for Science, Technology and Research, Singapore; School of
   Medicine, National University Singapore
FX This work was supported by the British Heart Foundation and the Wellcome
   Trust Functional Genomics Initiative. R. T. Grignani was sponsored by
   the MBBS-PhD Programme (Agency for Science, Technology and Research,
   Singapore and School of Medicine, National University Singapore).
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NR 31
TC 20
Z9 21
U1 0
U2 12
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2828
EI 1095-8584
J9 J MOL CELL CARDIOL
JI J. Mol. Cell. Cardiol.
PD SEP
PY 2012
VL 53
IS 3
BP 342
EP 349
DI 10.1016/j.yjmcc.2012.05.017
PG 8
WC Cardiac & Cardiovascular Systems; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Cell Biology
GA 993LO
UT WOS:000307861400007
PM 22683324
OA Green Published, hybrid
DA 2025-04-10
ER

PT J
AU Schrattenholz, A
   Soskic, V
AF Schrattenholz, Andre
   Soskic, Vukic
TI NMDA receptors are not alone: Dynamic regulation of NMDA receptor
   structure and function by neuregulins and transient cholesterol-rich
   membrane domains leads to disease-specific nuances of glutamate
   signalling
SO CURRENT TOPICS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE nMDA receptor; neuregulin; cholesterol; excitotoxicity;
   neurodegeneration; dihydropyrimidinase-related protein 2; PARP-1;
   mitochondrial apoptotic pathway
ID D-ASPARTATE RECEPTOR; DIHYDROPYRIMIDINASE-RELATED PROTEIN-2; NICOTINIC
   ACETYLCHOLINE-RECEPTORS; POSTSYNAPTIC DENSITY PROTEINS; LONG-TERM
   POTENTIATION; ISCHEMIC BRAIN-DAMAGE; SPINAL-DORSAL-HORN; NR2B SUBUNIT;
   MOLECULAR-MECHANISMS; MULTIPLE-SCLEROSIS
AB Glutamate receptors of the N-methyl-D-asparate (NMDA-) subtype are tetrameric allosteric and ligand-gated calcium channels. They are modulated by a variety of endogenous ligands and ions and play a pivotal role in memory-related signal transduction due to a voltage-dependent block by magnesium, which makes them Hebbian coincidence detectors. On the structural level NMDA receptors have an enormous flexibility due to seven genes (NR1, NR2A-D and NU3A-B), alternative splicing, RNA-editing and extensive posttranslational modifications, like phosphorylation and glycosylation. NMDA receptors are thought to be responsible for excitotoxicity and subsequent downstream events like neuroinflammation and apoptosis and thus have been implicated in many important human pathologies, ranging from amyotrophic lateral sclerosis, Alzheimer's and Parkinson' disease, depression, epilepsy, trauma and stroke to schizophrenia. This fundamental significance of NMDA receptor-related excitotoxicity is discussed in the context of the developing clinical success of Memantine, but moreover set into relation to various proteomic and genetic markers of said diseases. The very complex localisational and functional regulation of NMDA receptors appears to be dependent on neuregulins and receptor tyrosine kinases in cholesterol-rich membrane domains (lipid rafts), calcium-related mitochondrial feedback-loops and subsynaptic structural elements like PSD-95 (post-synaptic density protein of 95 W). The flexibility and multitude of interaction partners and possibilities of these highly dynamic molecular systems are discussed in terms of drug development strategies, in particular comparing high affinity and sub-type specific ligands to currently successful or promising therapies.
C1 ProteoSys AG, D-55129 Mainz, Germany.
C3 ProteoSys AG
RP Schrattenholz, A (corresponding author), ProteoSys AG, Carl Zeiss Str 51, D-55129 Mainz, Germany.
EM andre.schrattenholz@proteosys.com
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NR 246
TC 43
Z9 47
U1 0
U2 16
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0266
EI 1873-5294
J9 CURR TOP MED CHEM
JI Curr. Top. Med. Chem.
PY 2006
VL 6
IS 7
BP 663
EP 686
DI 10.2174/156802606776894519
PG 24
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 049SO
UT WOS:000238037200003
PM 16719808
DA 2025-04-10
ER

PT J
AU Miano, JM
AF Miano, JM
TI Serum response factor: toggling between disparate programs of gene
   expression
SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
LA English
DT Review
DE promoter; transgenic; evolution; genome; bioinformatics; smooth muscle;
   calponin; integrin; myosin; myocardin; SM22
ID SMOOTH-MUSCLE-CELLS; HEAVY-CHAIN GENE; PROTEIN-BINDING SITE; FIBROBLAST
   GROWTH FACTOR-2; ALPHA-ACTIN EXPRESSION; HUMAN ELASTIN PROMOTER;
   EMBRYONIC STEM-CELLS; IMMEDIATE-EARLY GENE; C-FOS ENHANCER; TRANSGENIC
   MICE
AB Serum response factor (SRF) is a widely expressed transcription factor involved in orchestrating disparate programs of gene expression linked to muscle differentiation and cellular growth. Vascular smooth muscle cell (SMC) differentiation, for example, is marked by the coordinate expression of several contractile and cytoskeletal genes regulated directly by SRF through one or more CArG-box elements in the immediate vicinity of transcription start sites. In vascular disease, this CArG-dependent program of SMC differentiation is compromised and numerous CArG-dependent early growth-response genes are activated. Thus, SRF must toggle between programs of SMC differentiation and growth depending on local environmental cues. Moreover, SRF must distinguish between a course of SMC differentiation and programs of cardiac and skeletal muscle differentiation. Several mechanisms exist to ensure context- and cell-specific programs of SRF-dependent gene expression. These include regulated expression, DNA binding, and alternative splicing of SRF, flanking sequences adjacent to and chromatin remodeling of CArG boxes. RhoA-mediated alterations in the cytoskeleton, and association of SRF with a variety of cell-restricted cofactors including the recently discovered myocardin coactivator. Although many SMC-differentiation genes require critical evolutionarily conserved CArG boxes for SMC-restricted promoter activity in cultured cells and transgenic mice, the expression of a growing number of similarly restricted genes appears to be independent of SRF. Thus, parallel circuits of gene transcription have evolved for the appropriate expression of all genes that define mammalian SMC lineages. The purpose of this review is to summarize the history and progress made in SRF research with emphasis on the role this transcription factor plays in facilitating a program of SMC-restricted gene expression. (C) 2003 Elsevier Science Ltd. All rights reserved.
C1 Univ Rochester, Med Ctr, Cardiovasc Res Ctr, Rochester, NY 14642 USA.
C3 University of Rochester
RP Miano, JM (corresponding author), Univ Rochester, Med Ctr, Cardiovasc Res Ctr, 601 Elmwood Ave, Rochester, NY 14642 USA.
EM j.m.miano@rochester.edu
RI Miano, Joseph/L-5634-2018
OI Miano, Joseph/0000-0001-7522-3207
FU NHLBI NIH HHS [HL-62572] Funding Source: Medline
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NR 185
TC 498
Z9 590
U1 0
U2 37
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2828
EI 1095-8584
J9 J MOL CELL CARDIOL
JI J. Mol. Cell. Cardiol.
PD JUN
PY 2003
VL 35
IS 6
BP 577
EP 593
DI 10.1016/S0022-2828(03)00110-X
PG 17
WC Cardiac & Cardiovascular Systems; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Cell Biology
GA 692QZ
UT WOS:000183672900003
PM 12788374
DA 2025-04-10
ER

PT J
AU Mohiddin, SA
   Lu, SJ
   Cardoso, JP
   Carroll, S
   Jha, S
   Horowits, R
   Fananapazir, L
AF Mohiddin, SA
   Lu, SJ
   Cardoso, JP
   Carroll, S
   Jha, S
   Horowits, R
   Fananapazir, L
TI Genomic organization, alternative splicing, and expression of human and
   mouse N-RAP, a nebulin-related LIM protein of striated muscle
SO CELL MOTILITY AND THE CYTOSKELETON
LA English
DT Article
ID CARDIAC MYOFIBRILLOGENESIS; LOCALIZATION; MYOFIBRILS; ANTIBODIES;
   SEQUENCE; ACTIN; TITIN; HEART
AB Linkage analysis identifies 10q24-26 as a disease locus for dilated cardiomyopathy (DCM), a region including the N-RAP gene. N-RAP is a nebulin-like LIM protein that may mediate force transmission and myofibril assembly in cardiomyocytes. We describe the sequence, genomic structure, and expression of human N-RAP, as well as an initial screen to determine whether N-RAP mutations cause cardiomyopathy. Human expressed sequence tag databases were searched with the published 3,528-bp mouse N-RAP open reading frame (ORF). Putative cDNA sequences were interrogated by direct sequencing from cardiac and skeletal muscle RNA. We identified two human N-RAP isoforms with ORFs of 5,085 bp (isoform C) and 5,190 bp (isoform S), encoding products of 193-197 kDa. Genomic database searches localize N-RAP to human chromosome 10q25.3 and match isoforms C and S to 41 and 42 exons. Only isoform C is detected in human cardiac RNA; in skeletal muscle, approximately 10% is isoform C and approximately 90% is isoform S. We investigated apparent differences between human N-RAP cDNA and mouse sequences. Two mouse N-RAP isoforms with ORFs of 5,079 and 5,184 bp were identified with similar to85% similarity to human isoforms; published mouse sequences include cloning artifacts truncating the ORF. Murine and human isoforms have similar gene structure, tissue specificity, and size. N-RAP is especially conserved within its nebulin-like and LIM domains. We expressed both N-RAP isoforms and the previously described truncated N-RAP in embryonic chick cardiomyocytes. All constructs targeted to myofibril precursors and the cell periphery, and inhibited myofibril assembly. Several human N-RAP polymorphisms were detected, but none were unique to cardiomyopathy patients. N-RAP is highly conserved and exclusively expressed in cardiac and skeletal muscle. Genetic abnormalities remain excellent candidate causes for cardiac and skeletal myopathies. (dagger)Published 2003 Wiley-Liss, Inc.
C1 NHLBI, NIH, Bethesda, MD 20892 USA.
   NIAMSD, NIH, Bethesda, MD 20892 USA.
   Boston Childrens Hosp, Boston, MA USA.
C3 National Institutes of Health (NIH) - USA; NIH National Heart Lung &
   Blood Institute (NHLBI); National Institutes of Health (NIH) - USA; NIH
   National Institute of Arthritis & Musculoskeletal & Skin Diseases
   (NIAMS); Harvard University; Boston Children's Hospital
RP NHLBI, NIH, Bldg 10,Room 7B15, Bethesda, MD 20892 USA.
EM mohiddis@nhlbi.nih.gov
OI Mohiddin, Saidi/0000-0002-1031-4084
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NR 23
TC 30
Z9 36
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0886-1544
J9 CELL MOTIL CYTOSKEL
JI Cell Motil. Cytoskeleton
PD JUL
PY 2003
VL 55
IS 3
BP 200
EP 212
DI 10.1002/cm.10123
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 696TL
UT WOS:000183903300005
PM 12789664
DA 2025-04-10
ER

PT J
AU Mazzuca, MQ
   Khalil, RA
AF Mazzuca, Marc Q.
   Khalil, Raouf A.
TI Vascular endothelin receptor type B: Structure, function and
   dysregulation in vascular disease
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Endothelium; Smooth muscle; Calcium; Blood pressure; Hypertension
ID SMOOTH-MUSCLE-CELLS; PULMONARY ARTERIAL-HYPERTENSION; HIGH-SALT DIET;
   HUMAN CORONARY-ARTERIES; RAT MESENTERIC-ARTERY; ETB-RECEPTOR;
   NITRIC-OXIDE; ET(B) RECEPTORS; DEFICIENT RATS; BLOOD-PRESSURE
AB Endothelin-1 (ET-1) is a major regulator of vascular function, acting via both endothelin receptor type A (ETAR) and type B (ETBR). Although the role of ETAR in vascular smooth muscle (VSM) contraction has been studied, little is known about ETBR. ETBR is a G-protein coupled receptor with a molecular mass of similar to 50 kDa and 442 amino acids arranged in seven transmembrane domains. Alternative splice variants of ETBR and heterodimerization and cross-talk with ETAR may affect the receptor function. ETBR has been identified in numerous blood vessels with substantial effects in the systemic, renal, pulmonary, coronary and cerebral circulation. ETBR in the endothelium mediates the release of relaxing factors such as nitric oxide, prostacyclin and endothelium-derived hyperpolarizing factor, and could also play a role in ET-1 clearance. ETBR in VSM mediates increases in [Ca2+](i), protein kinase C, mitogen-activated protein kinase and other pathways of VSM contraction and cell growth. ET-1/ETAR signaling has been associated with salt-sensitive hypertension (HTN) and pulmonary arterial hypertension (PAH), and ETAR antagonists have shown some benefits in these conditions. In search for other pathogenetic factors and more effective approaches, the role of alterations in endothelial ETBR and VSM ETBR in vascular dysfunction, and the potential benefits of modulators of ETBR in treatment of HTN and PAH are being examined. Combined ETAR/ETBR antagonists could be more efficacious in the management of conditions involving upregulation of ETA(R) and ETBR in VSM. Combined ETAR antagonist with ETBR agonist may need to be evaluated in conditions associated with decreased endothelial ETBR expression/activity. (C) 2012 Elsevier Inc. All rights reserved.
C1 Brigham & Womens Hosp, Div Vasc & Endovasc Surg, Vasc Surg Res Lab, Boston, MA 02115 USA.
   Harvard Univ, Sch Med, Boston, MA 02115 USA.
C3 Harvard University; Harvard University Medical Affiliates; Brigham &
   Women's Hospital; Harvard University; Harvard Medical School
RP Khalil, RA (corresponding author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Vasc Surg, 75 Francis St, Boston, MA 02115 USA.
EM raouf_khalil@hms.harvard.edu
FU National Heart, Lung, and Blood Institute [HL-65998, HL-98724]; Eunice
   Kennedy Shriver National Institute of Child Health and Human Development
   [HD-60702]
FX This work was supported by grants from National Heart, Lung, and Blood
   Institute (HL-65998 and HL-98724) and The Eunice Kennedy Shriver
   National Institute of Child Health and Human Development (HD-60702).
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NR 142
TC 121
Z9 142
U1 0
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD JUL 15
PY 2012
VL 84
IS 2
BP 147
EP 162
DI 10.1016/j.bcp.2012.03.020
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 953BY
UT WOS:000304843100002
PM 22484314
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Gohda, T
   Tanimoto, M
   Moon, JY
   Gotoh, H
   Aoki, T
   Matsumoto, M
   Shibata, T
   Ohsawa, I
   Funabiki, K
   Tomino, Y
AF Gohda, Tomohito
   Tanimoto, Mitsuo
   Moon, Ju-Young
   Gotoh, Hiromichi
   Aoki, Tatsuya
   Matsumoto, Masakazu
   Shibata, Terumi
   Ohsawa, Isao
   Funabiki, Kazuhiko
   Tomino, Yasuhiko
TI Increased serum endogenous secretory receptor for advanced glycation
   end-product (esRAGE) levels in type 2 diabetic patients with decreased
   renal function
SO DIABETES RESEARCH AND CLINICAL PRACTICE
LA English
DT Article
DE esRAGE; AGES; CML; diabetic nephropathy; hemodialysis
ID VASCULAR ENDOTHELIAL-CELLS; CORONARY-ARTERY-DISEASE; SOLUBLE RECEPTOR;
   PLASMA-LEVELS; RAGE; ATHEROSCLEROSIS; NEPHROPATHY; PROTEIN; ACTIVATION;
   SRAGE
AB Background: The binding of advanced glycation end-products (AGES) to their receptor for AGES (RAGE) may play an important role in the development of diabetic vascular complications. Recently, soluble RAGE (sRAGE) has been identified as an alternative splicing form of RAGE. Furthermore, administration of sRAGE improved atherosclerosis in type 2 diabetic mice.
   Objective: The objective of the present study is to investigate the role of endogenous secretory RAGE (esRAGE) as a biological marker for type 2 diabetic nephropathy, and also to determine whether serum esRAGE levels are associated with serum AGES [including N epsilon-(carboxymethyl) lysine-protein adducts (CML) and pentosidine] levels.
   Materials and methods: Serum esRAGE levels were examined in 107 type 2 diabetic patients including those on hemodialysis (HD). Diabetic patients were divided into three groups as follows: Group A [patients without nephropathy, i.e. normoalbuminuric stage (AER < 30 mu g/ mg creatinine)], Group B [patients with nephropathy (AER > 30 mu g/mg creatinine) but excluding HD patients], and Group C (HD patients).
   Results: Serum esRAGE and AGES (including CML and pentosidine) levels in Group C were significantly higher than in Group A or B. In single linear univariate correlation, serum esRAGE levels were correlated using body mass index (BMI), duration of diabetes, and serum creatinine, high-density lipoprotein (HDL)-cholesterol and AGES (including CML and pentosidine) levels. Furthermore, in stepwise multivariate regression analysis, the levels of serum creatinine and duration of diabetes were independently associated with serum esRAGE levels. Conclusion: Serum esRAGE levels are associated with the severity of renal dysfunction and duration of diabetes in type 2 diabetic patients. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Gohda, Tomohito; Tanimoto, Mitsuo; Moon, Ju-Young; Gotoh, Hiromichi; Aoki, Tatsuya; Matsumoto, Masakazu; Shibata, Terumi; Ohsawa, Isao; Funabiki, Kazuhiko; Tomino, Yasuhiko] Juntendo Univ, Sch Med, Div Nephrol, Dept Internal Med,Bunkyo Ku, Tokyo 1138421, Japan.
C3 Juntendo University
RP Tomino, Y (corresponding author), Juntendo Univ, Sch Med, Div Nephrol, Dept Internal Med,Bunkyo Ku, Hongo 2-1-1, Tokyo 1138421, Japan.
EM yasu@med.juntendo.ac.jp
RI GOHDA, TOMOHITO/Y-6867-2019
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NR 30
TC 42
Z9 46
U1 0
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0168-8227
EI 1872-8227
J9 DIABETES RES CLIN PR
JI Diabetes Res. Clin. Pract.
PD AUG
PY 2008
VL 81
IS 2
BP 196
EP 201
DI 10.1016/j.diabres.2008.04.013
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 349OE
UT WOS:000259289400011
PM 18550199
DA 2025-04-10
ER

PT J
AU Al-Saaidi, R
   Rasmussen, TB
   Palmfeldt, J
   Nissen, PH
   Beqqali, A
   Hansen, J
   Pinto, YM
   Boesen, T
   Mogensen, J
   Bross, P
AF Al-Saaidi, Rasha
   Rasmussen, Torsten B.
   Palmfeldt, Johan
   Nissen, Peter H.
   Beqqali, Abdelaziz
   Hansen, Jakob
   Pinto, Yigal M.
   Boesen, Thomas
   Mogensen, Jens
   Bross, Peter
TI The LMNA mutation p.Arg321Ter associated with dilated cardiomyopathy
   leads to reduced expression and a skewed ratio of lamin A and lamin C
   proteins
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Dilated cardiomyopathy; LMNA; Laminopathies; Premature termination codon
   mutation; Nonsense mediated mRNA decay; Haploinsufficiency
ID STRUCTURAL ORGANIZATION; CONDUCTION-SYSTEM; A/C MUTATIONS; GENE
AB Dilated cardiomyopathy (DCM) is a disease of the heart muscle characterized by cardiac chamber enlargement and reduced systolic function of the left ventricle. Mutations in the LMNA gene represent the most frequent known genetic cause of DCM associated with disease of the conduction systems. The LMNA gene generates two major transcripts encoding the nuclear lamina major components lamin A and lamin C by alternative splicing. Both haploinsuffiency and dominant negative effects have been proposed as disease mechanism for premature termination codon (PTC) mutations in LMNA. These mechanisms however are still not clearly established. In this study, we used a representative LMNA nonsense mutation, p.Arg321Ter, to shed light on the molecular disease mechanisms. Cultured fibroblasts from three DCM patients carrying this mutation were analyzed. Quantitative reverse transcriptase PCR and sequencing of these PCR products indicated that transcripts from the mutant allele were degraded by the nonsense-mediated mRNA decay (NMD) mechanism. The fact that no truncated mutant protein was detectable in western blot (WB) analysis strengthens the notion that the mutant transcript is efficiently degraded. Furthermore, WB analysis showed that the expression of lamin C protein was reduced by the expected approximately 50%. Clearly decreased lamin A and lamin C levels were also observed by immunofluorescence microscopy analysis. However, results from both WB and nano-liquid chromatography/mass spectrometry demonstrated that the levels of lamin A protein were more reduced suggesting an effect on expression of lamin A from the wild type allele. PCR analysis of the ratio of lamin A to lamin C transcripts showed unchanged relative amounts of lamin A transcript suggesting that the effect on the wild type allele was operative at the protein level. Immunofluorescence microscopy analysis showed no abnormal nuclear morphology of patient fibroblast cells. Based on these data, we propose that heterozygosity for the nonsense mutation causes NMD degradation of the mutant transcripts blocking expression of the truncated mutant protein and an additional trans effect on lamin A protein levels expressed from the wild type allele. We discuss the possibility that skewing of the lamin A to lamin C ratio may contribute to ensuing processes that destabilize cardiomyocytes and trigger cardiomyopathy (C) 2013 Elsevier Inc. All rights reserved.
C1 [Al-Saaidi, Rasha; Palmfeldt, Johan; Bross, Peter] Aarhus Univ, Res Unit Mol Med, DK-8200 Aarhus N, Denmark.
   [Al-Saaidi, Rasha; Palmfeldt, Johan; Bross, Peter] Aarhus Univ Hosp, DK-8200 Aarhus N, Denmark.
   [Rasmussen, Torsten B.] Aarhus Univ Hosp, Dept Cardiol, DK-8200 Aarhus N, Denmark.
   [Nissen, Peter H.] Aarhus Univ Hosp, Dept Clin Biochem, DK-8200 Aarhus N, Denmark.
   [Beqqali, Abdelaziz; Pinto, Yigal M.] Univ Amsterdam, Acad Med Ctr, Heart Failure Res Ctr, NL-1105 AZ Amsterdam, Netherlands.
   [Hansen, Jakob] Univ Aarhus, Bioanalyt Unit, Dept Forens Med, DK-8000 Aarhus C, Denmark.
   [Boesen, Thomas] Univ Aarhus, Dept Mol Biol & Genet, DK-8000 Aarhus C, Denmark.
   [Mogensen, Jens] Odense Univ Hosp, Dept Cardiol, DK-5000 Odense, Denmark.
C3 Aarhus University; Aarhus University; Aarhus University; Aarhus
   University; University of Amsterdam; Academic Medical Center Amsterdam;
   Aarhus University; Aarhus University; University of Southern Denmark;
   Odense University Hospital
RP Bross, P (corresponding author), Aarhus Univ, Res Unit Mol Med, Dept Clin Med, HLTH, Brendstrupgaardsvej 100, DK-8200 Aarhus N, Denmark.
EM peter.bross@ki.au.dk
RI Hansen, Jakob/W-1318-2017; Bross, Peter/B-7219-2013; Beqqali,
   Abdelaziz/F-8568-2013
OI Bross, Peter/0000-0001-9526-8525; Nissen, Peter H./0000-0002-8201-1306;
   Rasmussen, Torsten Bloch/0000-0003-1468-7248; Boesen,
   Thomas/0000-0002-5633-6844; Mogensen, Jens/0000-0002-8813-573X;
   Palmfeldt, Johan/0000-0001-5585-639X; Beqqali,
   Abdelaziz/0000-0003-1390-5821
FU Institute of Clinical Medicine; Aarhus University Hospital; John and
   Birthe Meyer Foundation; Lundbeck Foundation; Arvid Nielsson Foundation
FX The authors wish to thank Christian Knudsen, Margrethe Kjeldsen, Kirsten
   Kruse Olsen, and Kirsten Ha Id for their technical support. We wish also
   to thank all patients for providing skin biopsies. The study was
   supported by grants from the Institute of Clinical Medicine, Aarhus
   University Hospital, the John and Birthe Meyer Foundation, the Lundbeck
   Foundation and the Arvid Nielsson Foundation.
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NR 26
TC 23
Z9 25
U1 2
U2 8
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4827
EI 1090-2422
J9 EXP CELL RES
JI Exp. Cell Res.
PD NOV 15
PY 2013
VL 319
IS 19
BP 3010
EP 3019
DI 10.1016/j.yexcr.2013.08.024
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA 250LI
UT WOS:000326853900011
PM 24001739
DA 2025-04-10
ER

PT J
AU Balbi, C
   Milano, G
   Fertig, TE
   Lazzarini, E
   Bolis, S
   Taniyama, Y
   Sanada, F
   Di Silvestre, D
   Mauri, P
   Gherghiceanu, M
   Lüscher, TF
   Barile, L
   Vassalli, G
AF Balbi, Carolina
   Milano, Giuseppina
   Fertig, Tudor E.
   Lazzarini, Edoardo
   Bolis, Sara
   Taniyama, Yoshiaki
   Sanada, Fumihiro
   Di Silvestre, Dario
   Mauri, Pierluigi
   Gherghiceanu, Mihaela
   Luescher, Thomas F.
   Barile, Lucio
   Vassalli, Giuseppe
TI An exosomal-carried short periostin isoform induces cardiomyocyte
   proliferation
SO THERANOSTICS
LA English
DT Article
DE extracellular vesicles; exosomes; periostin; isoforms; cardiomyocyte;
   proliferation; Hippo pathway
ID PROTEIN; REGENERATION; ORIGIN; KINASE; CELLS
AB Although a small number of cardiomyocytes may reenter the cell cycle after injury, the adult mammalian heart is incapable of a robust cardiomyocyte proliferation. Periostin, a secreted extracellular matrix protein, has been implicated as a regulator of cardiomyocyte proliferation; however, this role remains controversial. Alternative splicing of the human periostin gene results in 6 isoforms lacking sequences between exons 17 and 21, in addition to full-length periostin. We previously showed that exosomes (Exo) secreted by human cardiac explant-derived progenitor cells (CPC) carried periostin. Here, we aimed to investigate their cell cycle activity.
   Methods: CPC were derived as the cellular outgrowth of ex vivo cultured cardiac atrial explants. Exo were purified from CPC conditioned medium using size exclusion chromatography. Exosomal periostin was analyzed by Western blotting using a pair of antibodies (one raised against aa 537-836, and one raised against amino acids mapping at exon 17 of human periostin), by ELISA, and by cryo-EM with immune-gold labeling. Cell cycle activity was assessed in neonatal rat cardiomyocytes, in human induced pluripotent stem cell (iPS)-derived cardiomyocytes, and in adult rat cardiomyocytes after myocardial infarction. The role of periostin in cell cycle activity was investigated by transfecting donor CPC with a siRNA against this protein.
   Results: Periostin expression in CPC-secreted exosomes was detected using the antibody raised against aa 537-836 of the human protein, but not with the exon 17-specific antibody, consistent with an isoform lacking exon 17. Periostin was visualized on vesicle surfaces by cryo-EM and immune-gold labeling. CPC-derived exosomes induced cell proliferation in neonatal rat cardiomyocytes both in vitro and in vivo, in human iPS-derived cardiomyocytes, and in adult rat cardiomyocytes after myocardial infarction. Exo promoted phosphorylation of focal adhesion kinase (FAK), actin polymerization, and nuclear translocation of Yes-associated protein (YAP) in cardiomyocytes. Knocking down of periostin or YAP, or blocking FAK phosphorylation with PF-573228 nullified Exo-induced proliferation. A truncated human periostin peptide (aa 22-669), but not recombinant human full-length periostin, mimicked the pro-proliferative activity of exosomes.
   Conclusions: Our results show, for the first time, that CPC-secreted exosomes promote cardiomyocyte cell cycle-reentry via a short periostin isoform expressed on their surfaces, whereas recombinant full-length periostin does not. These findings highlight isoform-specific roles of periostin in cardiomyocyte proliferation.
C1 [Balbi, Carolina; Milano, Giuseppina; Bolis, Sara; Vassalli, Giuseppe] Ist Cardioctr Ticino, Lab Cellular & Mol Cardiol, Via Tesserete 48, CH-6900 Lugano, Switzerland.
   [Balbi, Carolina; Luescher, Thomas F.; Vassalli, Giuseppe] Univ Zurich, Ctr Mol Cardiol, Zurich, Switzerland.
   [Milano, Giuseppina] Lausanne Univ Hosp, Lab Cardiovasc Res, Lausanne, Switzerland.
   [Fertig, Tudor E.; Gherghiceanu, Mihaela] Victor Babes Natl Inst Pathol, Bucharest, Romania.
   [Lazzarini, Edoardo; Bolis, Sara; Barile, Lucio] Ist Cardioctr Ticino, Lab Cardiovasc Theranost, Lugano, Switzerland.
   [Taniyama, Yoshiaki; Sanada, Fumihiro] Osaka Univ, Dept Clin Gene Therapy, Grad Sch Med, Suita, Osaka, Japan.
   [Di Silvestre, Dario; Mauri, Pierluigi] ITB CNR, Prote & Metabol Lab, Segrate, Italy.
   [Luescher, Thomas F.] Imperial Coll, Royal Brompton & Harefield Hosp, London, England.
   [Barile, Lucio] Scuola Super Sant Anna, Inst Life Sci, Pisa, Italy.
   [Barile, Lucio; Vassalli, Giuseppe] Univ Svizzera Italiana USI, Fac Biomed, Lugano, Switzerland.
C3 University of Zurich; University of Lausanne; Centre Hospitalier
   Universitaire Vaudois (CHUV); Victor Babes National Institute of
   Pathology; The University of Osaka; Consiglio Nazionale delle Ricerche
   (CNR); Istituto di Tecnologie Biomediche (ITB-CNR); Royal Brompton
   Hospital; Imperial College London; Royal Brompton & Harefield NHS
   Foundation Trust; Harefield Hospital; Scuola Superiore Sant'Anna;
   Universita della Svizzera Italiana
RP Balbi, C; Vassalli, G (corresponding author), Ist Cardioctr Ticino, Lab Cellular & Mol Cardiol, Via Tesserete 48, CH-6900 Lugano, Switzerland.
EM carolina.balbi@cardiocentro.org; giuseppe.vassalli@cardiocentro.org
RI Lazzarini, Edoardo/J-8459-2018; di silvestre, dario/AAB-5037-2022;
   Gherghiceanu, Mihaela/G-4621-2016; Mauri, Pietro/AAC-3095-2019; Barile,
   Lucio/AGA-1735-2022; Fertig, Tudor Emanuel/AAL-8492-2020
OI di silvestre, dario/0000-0002-7143-6229; Bolis,
   Sara/0000-0002-8514-9773; Balbi, Carolina/0000-0002-7394-1173; Barile,
   Lucio/0000-0002-5827-0439; Fertig, Tudor Emanuel/0000-0003-0251-3865
FU Swiss National Science Foundation [169194]; UEFISCDI
   [PN-III-P1-1.2PCCDI-2017-0527]; MEC [7PFE/2018]
FX G. V. was supported by Swiss National Science Foundation grant no.
   169194. M.G. and E.T.F. were supported by UEFISCDI grant no.
   PN-III-P1-1.2PCCDI-2017-0527 and MEC grant no. 7PFE/2018.
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NR 42
TC 25
Z9 27
U1 2
U2 9
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2021
VL 11
IS 12
BP 5634
EP 5649
DI 10.7150/thno.57243
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA RJ0WI
UT WOS:000637324000002
PM 33897872
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Pathare, G
   Tutakhel, OAZ
   van der Wel, MC
   Shelton, LM
   Deinum, J
   Lenders, JWM
   Hoenderop, JGJ
   Bindels, RJM
AF Pathare, Ganesh
   Tutakhel, Omar A. Z.
   van der Wel, Mark C.
   Shelton, Luke M.
   Deinum, Jaap
   Lenders, Jacques W. M.
   Hoenderop, Joost G. J.
   Bindels, Rene J. M.
TI Hydrochlorothiazide treatment increases the abundance of the NaCl
   cotransporter in urinary extracellular vesicles of essential
   hypertensive patients
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE hypertension; NaCl cotransporter; thiazide diuretics; urinary
   extracellular vesicles; kidney
ID SODIUM-CHLORIDE COTRANSPORTER; CL COTRANSPORTER; DIURETIC TREATMENT;
   GITELMAN-SYNDROME; DIETARY-SODIUM; BLOOD-PRESSURE; THIAZIDE; MUTATIONS;
   MECHANISMS; EXPRESSION
AB The thiazide-sensitive NaCl cotransporter (NCC), located apically in distal convoluted tubule epithelia, regulates the fine-tuning of renal sodium excretion. Three isoforms of NCC are generated through alternative splicing of the transcript, of which the third isoform has been the most extensively investigated in pathophysiological conditions. The aim of this study was to investigate the effect of different anti-hypertensive treatments on the abundance and phosphorylation of all three NCC isoforms in urinary extracellular vesicles (uEVs) of essential hypertensive patients. In uEVs isolated from patients (n = 23) before and after hydrochlorothiazide or valsartan treatment, the abundance and phosphorylation of the NCC isoforms was determined. Additionally, clinical biochemistry and blood pressure of the patients was assessed. Our results show that NCC detected in human uEVs has a glycosylated and oligomeric structure, comparable to NCC present in human kidney membrane fractions. Despite the inhibitory action of hydrochlorothiazide on NCC activity, immunoblot analysis of uEVs showed significantly increased abundance of NCC isoforms 1 and 2 (NCC1/2), total NCC (NCC1-3), and the phosphorylated form of total NCC (pNCC(1-3)-T55/T60) in essential hypertensive patients treated with hydrochlorothiazide but not with valsartan. This study highlights that NCC1/2, NCC1-3, and pNCC(1-3)-T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.
C1 [Pathare, Ganesh; Tutakhel, Omar A. Z.; Shelton, Luke M.; Hoenderop, Joost G. J.; Bindels, Rene J. M.] Radboud Univ Nijmegen, Med Ctr, Dept Physiol, Nijmegen, Netherlands.
   [van der Wel, Mark C.] Radboud Univ Nijmegen, Med Ctr, Dept Primary & Community Care, Nijmegen, Netherlands.
   [Deinum, Jaap; Lenders, Jacques W. M.] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, Radboud Inst Mol Life Sci, Nijmegen, Netherlands.
   [Lenders, Jacques W. M.] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Med 3, Dresden, Germany.
C3 Radboud University Nijmegen; Radboud University Nijmegen; Radboud
   University Nijmegen; Technische Universitat Dresden; Carl Gustav Carus
   University Hospital
RP Bindels, RJM (corresponding author), Radboud Univ Nijmegen, Med Ctr, Radboud Inst Mol Life Sci, Dept Physiol 286, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM rene.bindels@radboudumc.nl
RI Hoenderop, Joost/H-8047-2014; Tutakhel, Omar/AAW-6591-2021; van der Wel,
   M.C./L-4750-2015; Shelton, Luke/G-6149-2016; Deinum, J./L-4261-2015;
   Lenders, J.W.M./L-4487-2015; Pathare, Ganesh/KHV-5113-2024; Bindels,
   Rene/B-9824-2013
OI Bindels, Rene/0000-0003-1167-1339; Shelton, Luke/0009-0006-3929-6496;
   Pathare, Ganesh/0000-0001-6916-5880
FU European Society of Hypertension; EURenOmics project from the European
   Union seventh Framework Programme (FP7) [305608]; Netherlands
   Organization for Scientific Research (VENI ZonMw) [916.12.046]; Dutch
   Kidney Foundation [PHD12.14, 16OI04]
FX This study was supported by the European Society of Hypertension
   (2011-2013 Fellowship), the EURenOmics project from the European Union
   seventh Framework Programme (FP7/2007-2013, agreement no. 305608), the
   Netherlands Organization for Scientific Research (VENI ZonMw
   916.12.046), and the Dutch Kidney Foundation (PHD12.14 and 16OI04).
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NR 47
TC 17
Z9 18
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
EI 1522-1466
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD JUN
PY 2017
VL 312
IS 6
BP F1063
EP F1072
DI 10.1152/ajprenal.00644.2016
PG 10
WC Physiology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology; Urology & Nephrology
GA EZ0DI
UT WOS:000404369100013
PM 28274929
DA 2025-04-10
ER

PT J
AU Braz, SO
   Acquaire, J
   Gourdon, G
   Gomes-Pereira, M
AF Braz, Sandra O.
   Acquaire, Julien
   Gourdon, Genevieve
   Gomes-Pereira, Mario
TI Of Mice and Men: Advances in the Understanding of Neuromuscular Aspects
   of Myotonic Dystrophy
SO FRONTIERS IN NEUROLOGY
LA English
DT Review
DE myotonic dystrophy; mouse; trinucleotide DNA repeat; skeletal muscle;
   cardiac muscle; central nervous system; brain; RNA toxicity
ID RNA-BINDING PROTEIN; TRIPLET REPEAT RNA; SKELETAL-MUSCLE ATROPHY;
   TRANSGENIC MOUSE MODEL; EXPANDED CTG REPEATS; MESSENGER-RNA; IN-VIVO;
   TRINUCLEOTIDE-REPEAT; SMALL MOLECULES; NUCLEAR FOCI
AB Intensive effort has been directed toward the modeling of myotonic dystrophy (DM) in mice, in order to reproduce human disease and to provide useful tools to investigate molecular and cellular pathogenesis and test efficient therapies. Mouse models have contributed to dissect the multifaceted impact of the DM mutation in various tissues, cell types and in a pleiotropy of pathways, through the expression of toxic RNA transcripts. Changes in alternative splicing, transcription, translation, intracellular RNA localization, polyadenylation, miRNA metabolism and phosphorylation of disease intermediates have been described in different tissues. Some of these events have been directly associated with specific disease symptoms in the skeletal muscle and heart of mice, offering the molecular explanation for individual disease phenotypes. In the central nervous system (CNS), however, the situation is more complex. We still do not know how the molecular abnormalities described translate into CNS dysfunction, nor do we know if the correction of individualmolecular events will provide significant therapeutic benefits. The variability in model design and phenotypes described so far requires a thorough and critical analysis. In this review we discuss the recent contributions of mouse models to the understanding of neuromuscular aspects of disease, therapy development, and we provide a reflective assessment of our current limitations and pressing questions that remain unanswered.
C1 [Braz, Sandra O.; Acquaire, Julien; Gourdon, Genevieve; Gomes-Pereira, Mario] INSERM, UMR1163, Lab CTGDM, Paris, France.
   [Braz, Sandra O.; Acquaire, Julien; Gourdon, Genevieve; Gomes-Pereira, Mario] Univ Paris 05, Sorbonne Paris Cite, Inst Imagine, Paris, France.
C3 Universite Paris Cite; Institut National de la Sante et de la Recherche
   Medicale (Inserm); Universite Paris Cite; Institut National de la Sante
   et de la Recherche Medicale (Inserm)
RP Gomes-Pereira, M (corresponding author), INSERM, UMR1163, Lab CTGDM, Paris, France.; Gomes-Pereira, M (corresponding author), Univ Paris 05, Sorbonne Paris Cite, Inst Imagine, Paris, France.
EM mario.pereira@inserm.fr
RI Braz, Sandra/ABA-7191-2020; Gomes-Pereira, Mario/B-5242-2014; Gourdon,
   Genevieve/F-2996-2013
OI Gomes-Pereira, Mario/0000-0002-3533-0873; Braz,
   Sandra/0000-0002-4734-9651; Gourdon, Genevieve/0000-0002-3319-1347
FU AFM-Telethon (France) [19920]; ANR (France); Imagine Foundation
   (France); INSERM (France); Paris Descartes-Sorbonne Paris Cite
   University (France); National Research Agency, under the Investments or
   the Future program [ANR-10-IAHU-01, ANR-10 BLAN-1121-01]; Agence
   Nationale de la Recherche (ANR) [ANR-10-BLAN-1121] Funding Source:
   Agence Nationale de la Recherche (ANR)
FX We would like to acknowledge the AFM-Telethon (France; Project Grant
   19920), ANR (France), Imagine Foundation (France), INSERM (France) and
   Paris Descartes-Sorbonne Paris Cite University (France) for financial
   support. Our research has received a state subsidy managed by the
   National Research Agency, under the Investments or the Future program
   bearing the reference ANR-10-IAHU-01 and under the program ANR-10
   BLAN-1121-01.
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NR 177
TC 31
Z9 32
U1 0
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-2295
J9 FRONT NEUROL
JI Front. Neurol.
PD JUL 10
PY 2018
VL 9
AR 519
DI 10.3389/fneur.2018.00519
PG 20
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA GM4MP
UT WOS:000438095200001
PM 30050493
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Pereira, JAAS
   Greaser, M
   Moss, RL
AF Pereira, JAAS
   Greaser, M
   Moss, RL
TI Pulse electrophoresis of muscle myosin heavy chains in sodium dodecyl
   sulfate-polyacrylamide gels
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE SDS-PAGE; pulse electrophoresis; myosin heavy chains
ID DEVELOPING CHICKEN HEART; RAT SKELETAL-MUSCLE; SHORTENING VELOCITY;
   EXPRESSION; PROTEINS; ISOFORMS; MYOCYTES; ADULT; MOTOR
AB We have developed a new method that provides enhanced resolution of myosin heavy chain (MHC) isoforms by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The key feature of this protocol involves the application of current to slab SDS gels in a pulsatile, repetitive manner rather than continuously as in standard gel systems. This protocol, designated pulse electrophoresis, was achieved by means of a device that intermittently gates the output of a conventional power supply. When used in long (32 cm) separating gels, pulse electrophoresis not only significantly improves the resolution of MHC isoforms compared to conventional systems, but also reduces common artifacts associated with long running times, such as blurred bands and comingling of closely spaced bands. In addition to the increased resolution of protein bands, pulse electrophoresis also allows detection of bands corresponding to previously unidentified MHC isoforms in mammalian and avian tissue. In rat myocardium, for example, pulse electrophoresis revealed three MHC isoform bands, two of which appeared to correspond to two alpha-MHC subspecies. Alternative splicing of the rat alpha-MHC gene is known to generate two isoform species differing by inclusion (or exclusion) of a single glutamine residue, whose relative levels of expression correspond nicely with the amounts of each band identified in this study. Therefore, we cannot rule out that the system presented here may be sufficiently sensitive to differentiate between high molecular weight proteins differing in a single amino acid. (C) 2001 Academic Press.
C1 Univ Wisconsin, Dept Physiol, Sch Med, Madison, WI 53706 USA.
   Muscle Biol Lab, Madison, WI 53706 USA.
C3 University of Wisconsin System; University of Wisconsin Madison
RP Moss, RL (corresponding author), Univ Wisconsin, Dept Physiol, Sch Med, Madison, WI 53706 USA.
RI Greaser, Marion/C-6147-2012
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NR 25
TC 14
Z9 16
U1 0
U2 6
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD APR 15
PY 2001
VL 291
IS 2
BP 229
EP 236
DI 10.1006/abio.2001.5018
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
   Chemistry, Analytical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 424VZ
UT WOS:000168255800005
PM 11401296
DA 2025-04-10
ER

PT J
AU Mikhail, AI
   Nagy, PL
   Manta, K
   Rouse, N
   Manta, A
   Ng, SY
   Nagy, MF
   Smith, P
   Lu, JQ
   Nederveen, JP
   Ljubicic, V
   Tarnopolsky, MA
AF Mikhail, Andrew I.
   Nagy, Peter L.
   Manta, Katherine
   Rouse, Nicholas
   Manta, Alexander
   Ng, Sean Y.
   Nagy, Michael F.
   Smith, Paul
   Lu, Jian-Qiang
   Nederveen, Joshua P.
   Ljubicic, Vladimir
   Tarnopolsky, Mark A.
TI Aerobic exercise elicits clinical adaptations in myotonic dystrophy type
   1 patients independently of pathophysiological changes
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID SKELETAL-MUSCLE; MESSENGER-RNA; MITOCHONDRIAL DYSFUNCTION; STRENGTH;
   CELLS; METABOLISM; STRATEGIES; BIOMARKERS; RESISTANCE; PATHOLOGY
AB BACKGROUND. Myotonic dystrophy type 1 (DM1) is a complex life-limiting neuromuscular disorder characterized by severe skeletal muscle atrophy, weakness, and cardiorespiratory defects. Exercised DM1 mice exhibit numerous physiological benefits that are underpinned by reduced CUG foci and improved alternative splicing. However, the efficacy of physical activity in patients is unknown. METHODS. Eleven genetically diagnosed DM1 patients were recruited to examine the extent to which 12 weeks of cycling can recuperate clinical and physiological metrics. Furthermore, we studied the underlying molecular mechanisms through which exercise elicits benefits in skeletal muscle of DM1 patients. RESULTS. DM1 was associated with impaired muscle function, fitness, and lung capacity. Cycling evoked several clinical, physical, and metabolic advantages in DM1 patients. We highlight that exercise-induced molecular and cellular alterations in patients do not conform with previously published data in murine models and propose a significant role of mitochondrial function in DM1 pathology. Finally, we discovered a subset of small nucleolar RNAs (snoRNAs) that correlated to indicators of disease severity. CONCLUSION. With no available cures, our data support the efficacy of exercise as a primary intervention to partially mitigate the clinical progression of DM1. Additionally, we provide evidence for the involvement of snoRNAs and other noncoding RNAs in DM1 pathophysiology. TRIAL REGISTRATION. This trial was approved by the HiREB committee (no. 7901) and registered under ClinicalTrials.gov (NCT04187482). FUNDING. Neil and Leanne Petroff. Canadian Institutes of Health Research Foundation (no. 143325).
C1 [Mikhail, Andrew I.; Manta, Alexander; Ng, Sean Y.; Ljubicic, Vladimir] McMaster Univ, Dept Kinesiol, Hamilton, ON, Canada.
   [Nagy, Peter L.; Rouse, Nicholas; Smith, Paul] Praxis Genom LLC, Atlanta, GA USA.
   [Manta, Katherine; Nederveen, Joshua P.; Tarnopolsky, Mark A.] McMaster Univ, Dept Pediat, Childrens Hosp, Hamilton, ON, Canada.
   [Lu, Jian-Qiang] McMaster Univ, Dept Pathol & Mol Med Neuropathol, Hamilton, ON, Canada.
   [Tarnopolsky, Mark A.] McMaster Univ, Med Ctr, Exerkine Corp, Hamilton, ON, Canada.
C3 McMaster University; McMaster University; McMaster University Hospital;
   McMaster University; McMaster University
RP Tarnopolsky, MA (corresponding author), 1200 Main St West, Hamilton, ON L8N3Z5, Canada.
EM tarnopol@mcmaster.ca
RI LU, JIAN-QIANG/AAL-1634-2020; Nagy, Peter/AAT-6055-2020
OI Nagy, Peter Lajos/0000-0002-7461-8415; Smith, Paul/0000-0002-0940-4314;
   Mikhail, Andrew I/0000-0001-8977-2055; Lu,
   Jian-Qiang/0000-0003-1945-5569
FU Canadian Institutes of Health Research (CIHR) Foundation [143325];
   Ontario Graduate Scholarship; CIHR Canada Graduate Scholarship
FX The authors thank the study participants for their time and effort
   throughout. Additionally, we would like to acknowledge Neil and Leanne
   Petroff for their kind donation supporting this project. This study was
   also supported by a Canadian Institutes of Health Research (CIHR)
   Foundation grant (143325 to MAT). AIM received an Ontario Graduate
   Scholarship and a CIHR Canada Graduate Scholarship during this study.
   The authors express their appreciation to Bart Hettinga, Lauren Brady,
   Kirsten Barnard, Erin Hatcher, Linda Brandt, Emily Ma, Milla
   Tarnopolsky, and Alex Bak for their support in this study and recognize
   Jeff Healey for comments on the electrocardiography. Finally, the
   authors would also like to acknowledge Donald Xhuti for his assistance
   with the graphical abstract created with BioRender.com.
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NR 69
TC 28
Z9 28
U1 0
U2 1
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD MAY 16
PY 2022
VL 132
IS 10
AR e156125
DI 10.1172/JCI156125
PG 19
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 1U0JU
UT WOS:000805108300006
PM 35316212
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU He, KY
   Li, XY
   Kelly, TN
   Liang, J
   Cade, BE
   Assimes, TL
   Becker, LC
   Beitelshees, AL
   Bress, AP
   Chang, YPC
   Chen, YDI
   de Vries, PS
   Fox, ER
   Franceschini, N
   Furniss, A
   Gao, Y
   Guo, XQ
   Haessler, J
   Hwang, SJ
   Irvin, MR
   Kalyani, RR
   Liu, CT
   Liu, CY
   Martin, LW
   Montasser, ME
   Muntner, PM
   Mwasongwe, S
   Palmas, W
   Reiner, AP
   Shimbo, D
   Smith, JA
   Snively, BM
   Yanek, LR
   Boerwinkle, E
   Correa, A
   Cupples, LA
   He, J
   Kardia, SLR
   Kooperberg, C
   Mathias, RA
   Mitchell, BD
   Psaty, BM
   Vasan, RS
   Rao, DC
   Rich, SS
   Rotter, JI
   Wilson, JG
   Chakravarti, A
   Morrison, AC
   Levy, D
   Arnett, DK
   Redline, S
   Zhu, XF
AF He, Karen Y.
   Li, Xiaoyin
   Kelly, Tanika N.
   Liang, Jingjing
   Cade, Brian E.
   Assimes, Themistocles L.
   Becker, Lewis C.
   Beitelshees, Amber L.
   Bress, Adam P.
   Chang, Yen-Pei Christy
   Chen, Yii-Der Ida
   de Vries, Paul S.
   Fox, Ervin R.
   Franceschini, Nora
   Furniss, Anna
   Gao, Yan
   Guo, Xiuqing
   Haessler, Jeffrey
   Hwang, Shih-Jen
   Irvin, Marguerite Ryan
   Kalyani, Rita R.
   Liu, Ching-Ti
   Liu, Chunyu
   Martin, Lisa Warsinger
   Montasser, May E.
   Muntner, Paul M.
   Mwasongwe, Stanford
   Palmas, Walter
   Reiner, Alex P.
   Shimbo, Daichi
   Smith, Jennifer A.
   Snively, Beverly M.
   Yanek, Lisa R.
   Boerwinkle, Eric
   Correa, Adolfo
   Cupples, L. Adrienne
   He, Jiang
   Kardia, Sharon L. R.
   Kooperberg, Charles
   Mathias, Rasika A.
   Mitchell, Braxton D.
   Psaty, Bruce M.
   Vasan, Ramachandran S.
   Rao, D. C.
   Rich, Stephen S.
   Rotter, Jerome I.
   Wilson, James G.
   Chakravarti, Aravinda
   Morrison, Alanna C.
   Levy, Daniel
   Arnett, Donna K.
   Redline, Susan
   Zhu, Xiaofeng
CA NHLBI Trans-Omics Precision
   TOPMed Blood Pressure Working Grp
TI Leveraging linkage evidence to identify low-frequency and rare variants
   on 16p13 associated with blood pressure using TOPMed whole genome
   sequencing data
SO HUMAN GENETICS
LA English
DT Article
ID BODY-MASS INDEX; WIDE ASSOCIATION; TRAITS; LOCI; HERITABILITY;
   METAANALYSIS; COMMON; POWER; SCAN
AB In this study, we investigated low-frequency and rare variants associated with blood pressure (BP) by focusing on a linkage region on chromosome 16p13. We used whole genome sequencing (WGS) data obtained through the NHLBI Trans-Omics for Precision Medicine (TOPMed) program on 395 Cleveland Family Study (CFS) European Americans (CFS-EA). By analyzing functional coding variants and non-coding rare variants with CADD score>10 residing within the chromosomal region in families with linkage evidence, we observed 25 genes with nominal statistical evidence (burden or SKAT p<0.05). One of the genes is RBFOX1, an evolutionarily conserved RNA-binding protein that regulates tissue-specific alternative splicing that we previously reported to be associated with BP using exome array data in CFS. After follow-up analysis of the 25 genes in ten independent TOPMed studies with individuals of European, African, and East Asian ancestry, and Hispanics (N=29,988), we identified variants in SLX4 (p=2.19x10(-4)) to be significantly associated with BP traits when accounting for multiple testing. We also replicated the associations previously reported for RBFOX1 (p=0.007). Follow-up analysis with GTEx eQTL data shows SLX4 variants are associated with gene expression in coronary artery, multiple brain tissues, and right atrial appendage of the heart. Our study demonstrates that linkage analysis of family data can provide an efficient approach for detecting rare variants associated with complex traits in WGS data.
C1 [He, Karen Y.; Li, Xiaoyin; Liang, Jingjing; Zhu, Xiaofeng] Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Cleveland, OH 44106 USA.
   [Kelly, Tanika N.; He, Jiang] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA 70112 USA.
   [Cade, Brian E.; Redline, Susan] Brigham & Womens Hosp, Div Sleep & Circadian Disorders, 75 Francis St, Boston, MA 02115 USA.
   [Cade, Brian E.; Redline, Susan] Harvard Med Sch, Div Sleep Med, Boston, MA 02115 USA.
   [Assimes, Themistocles L.] Stanford Univ, Dept Med, Palo Alto, CA 94305 USA.
   [Becker, Lewis C.] Johns Hopkins Univ, Sch Med, GeneSTAR Res Program, Div Cardiol, Baltimore, MD 21205 USA.
   [Becker, Lewis C.] Johns Hopkins Univ, Sch Med, Div Gen Internal Med, Dept Med, Baltimore, MD 21205 USA.
   [Beitelshees, Amber L.; Chang, Yen-Pei Christy; Montasser, May E.; Mitchell, Braxton D.] Univ Maryland, Div Endocrinol Diabet & Nutr, Program Personalized & Genom Med, Dept Med,Sch Med, Baltimore, MD 21201 USA.
   [Bress, Adam P.] Univ Utah, Sch Med, Dept Populat Hlth Sci, Salt Lake City, UT 84132 USA.
   [Chen, Yii-Der Ida; Guo, Xiuqing; Rotter, Jerome I.] Harbor UCLA Med Ctr, Inst Translat Genom & Populat Sci, LABioMed, Dept Pediat, Torrance, CA 90502 USA.
   [Chen, Yii-Der Ida; Guo, Xiuqing; Rotter, Jerome I.] Harbor UCLA Med Ctr, Inst Translat Genom & Populat Sci, LABioMed, Dept Med, Torrance, CA 90502 USA.
   [de Vries, Paul S.; Boerwinkle, Eric; Morrison, Alanna C.] Univ Texas Hlth Sci Ctr Houston, Ctr Human Genet, Sch Publ Hlth, Dept Epidemiol Human Genet & Environm Sci, Houston, TX 77030 USA.
   [Fox, Ervin R.] Univ Mississippi, Med Ctr, Dept Med, Div Cardiovasc Dis, Jackson, MS 39216 USA.
   [Franceschini, Nora] UNC Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
   [Furniss, Anna; Correa, Adolfo] Univ Mississippi, Med Ctr, Jackson Heart Study, Jackson, MS 39216 USA.
   [Gao, Yan; Wilson, James G.] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA.
   [Haessler, Jeffrey; Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
   [Hwang, Shih-Jen; Liu, Ching-Ti; Liu, Chunyu; Cupples, L. Adrienne; Vasan, Ramachandran S.; Levy, Daniel] Boston Univ, Framingham, MA 01702 USA.
   [Hwang, Shih-Jen; Liu, Ching-Ti; Liu, Chunyu; Cupples, L. Adrienne; Vasan, Ramachandran S.; Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
   [Irvin, Marguerite Ryan; Muntner, Paul M.] Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL 35294 USA.
   [Kalyani, Rita R.] Johns Hopkins Univ, Sch Med, Div Endocrinol Diabet & Metab, GeneSTAR Res Program,Dept Med, Baltimore, MD 21205 USA.
   [Martin, Lisa Warsinger] George Washington Univ, Dept Med, Div Cardiol, Washington, DC 20052 USA.
   [Mwasongwe, Stanford] Jackson State Univ, Jackson Heart Study, Jackson, MS 39217 USA.
   [Palmas, Walter; Shimbo, Daichi] Columbia Univ, Med Ctr, Div Gen Med, New York, NY 10032 USA.
   [Reiner, Alex P.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Smith, Jennifer A.; Kardia, Sharon L. R.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
   [Snively, Beverly M.] Wake Forest Univ, Sch Med, Dept Biostat Sci, Winston Salem, NC 27101 USA.
   [Yanek, Lisa R.] Johns Hopkins Univ, Div Gen Internal Med, GeneSTAR Res Program, Dept Med,Sch Med, Baltimore, MD 21205 USA.
   [Boerwinkle, Eric] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
   [Mathias, Rasika A.] Johns Hopkins Univ, GeneSTAR Res Program, Div Allergy & Clin Immunol, Baltimore, MD 21205 USA.
   [Mathias, Rasika A.] Johns Hopkins Univ, Div Gen Internal Med, Dept Med, Sch Med, Baltimore, MD 21205 USA.
   [Mitchell, Braxton D.] Vet Affairs Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21201 USA.
   [Psaty, Bruce M.] Univ Washington, Cardiovasc Hlth Res Unit, Dept Med, Seattle, WA 98195 USA.
   [Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
   [Psaty, Bruce M.] Kaiser Permanente Washington Hlth Res Inst, Seattle, WA 98101 USA.
   [Rao, D. C.] Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA.
   [Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA 22908 USA.
   [Chakravarti, Aravinda] NYU, Langone Hlth, Ctr Human Genet & Genom, Dept Med, New York, NY 10016 USA.
   [Levy, Daniel] NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
   [Arnett, Donna K.] Univ Kentucky, Coll Publ Hlth, Lexington, KY 40508 USA.
   [Redline, Susan] Beth Israel Deaconess Med Ctr, Div Pulm Crit Care & Sleep Med, Boston, MA 02215 USA.
C3 University System of Ohio; Case Western Reserve University; Tulane
   University; Harvard University; Harvard University Medical Affiliates;
   Brigham & Women's Hospital; Harvard University; Harvard Medical School;
   Stanford University; Johns Hopkins University; Johns Hopkins University;
   University System of Maryland; University of Maryland Baltimore; Utah
   System of Higher Education; University of Utah; University of California
   System; University of California Los Angeles; University of California
   Los Angeles Medical Center; University of California System; University
   of California Los Angeles; University of California Los Angeles Medical
   Center; University of Texas System; University of Texas Health Science
   Center Houston; University of Texas School Public Health; University of
   Mississippi Medical Center; University of Mississippi; University of
   North Carolina; University of North Carolina Chapel Hill; University of
   Mississippi; University of Mississippi Medical Center; University of
   Mississippi Medical Center; University of Mississippi; Fred Hutchinson
   Cancer Center; Boston University; Framingham Heart Study; National
   Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood
   Institute (NHLBI); University of Alabama System; University of Alabama
   Birmingham; Johns Hopkins University; George Washington University;
   Jackson State University; University of Mississippi Medical Center;
   Columbia University; University of Washington; University of Washington
   Seattle; University of Michigan System; University of Michigan; Wake
   Forest University; Johns Hopkins University; Baylor College of Medicine;
   Johns Hopkins University; Johns Hopkins University; Geriatric Research
   Education & Clinical Center; US Department of Veterans Affairs; Veterans
   Health Administration (VHA); University of Washington; University of
   Washington Seattle; University of Washington; University of Washington
   Seattle; University of Washington; University of Washington Seattle;
   Kaiser Permanente; Washington University (WUSTL); University of
   Virginia; New York University; National Institutes of Health (NIH) -
   USA; NIH National Heart Lung & Blood Institute (NHLBI); University of
   Kentucky; Harvard University; Harvard University Medical Affiliates;
   Beth Israel Deaconess Medical Center
RP Zhu, XF (corresponding author), Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Cleveland, OH 44106 USA.
EM xxz10@case.edu
RI Rotter, Jerome/AAY-6598-2021; Boerwinkle, Eric/B-9599-2015; Zhu,
   Xiaofeng/O-6874-2019; Ramachandran, Vasan/Y-2527-2019; Levy,
   Daniel/ABB-2752-2021; He, Jiang/AAF-5303-2020; Mitchell,
   Braxton/CAF-0876-2022; Smith, Albert Vernon/AHC-3838-2022; Mwasongwe,
   Stanford/K-5822-2019; Lin, Chih-Cheng/IQT-4912-2023; Mathias,
   Rasika/IAM-5259-2023; Beitelshees, Amber/IVV-2872-2023; Ford,
   James/A-4284-2013; Liu, Li-Ping/ADB-6833-2022; Muntner,
   Paul/ACC-1358-2022; Cade, Brian/J-6770-2019; Assimes,
   Themistocles/D-9696-2015
OI Cade, Brian/0000-0003-1424-0673; Zhu, Xiaofeng/0000-0003-0037-411X;
   Arnett, Donna/0000-0003-2219-657X; Rich, Stephen/0000-0003-3872-7793;
   Franceschini, Nora/0009-0001-8346-3662; mathias,
   Rasika/0000-0002-2282-9042; Smith, Jennifer Ann/0000-0002-3575-5468;
   Kelly, Tanika/0000-0002-7348-4451; Levy, Daniel/0000-0003-1843-8724;
   Liu, Ching-Ti/0000-0002-0703-0742; Assimes,
   Themistocles/0000-0003-2349-0009
FU National Heart, Lung, and Blood Institute (NHLBI) [T32 HL007567,
   HL113338, HL086694]; National Human Genome Research Institute (NHGRI)
   [HG003054]; National Heart, Lung, and Blood Institute, National
   Institutes of Health, Department of Health and Human Services
   [HHSN268201700001I, HHSN268201700002I, HHSN268201700003I,
   HHSN268201700004I, HHSN268201700005I]; NIH [HL113338, R01 AG18728, U01
   HL072515, R01 HL088119, R01 HL121007, P30 DK072488, HL 046389,
   1R35HL135818]; National Institutes of Health/National Heart, Lung, and
   Blood Institute [U01 HL72518, HL087698, HL49762, HL58625, HL071025,
   HL112064]; National Institutes of Health/National Institute of Nursing
   Research [NR0224103]; National Institutes of Health/National Center for
   Research Resources [M01-RR000052]; National Heart, Lung and Blood
   Institute of the National Institutes of Health [HL054457, HL054464,
   HL054481, HL087660]; National Heart, Lung and Blood Institute, National
   Institutes of Health, Bethesda, MD [U01HL072507, R01HL087263,
   R01HL090682]; Jackson State University from the National Heart, Lung,
   and Blood Institute (NHLBI) [HHSN268201800013I]; Tougaloo College from
   the National Heart, Lung, and Blood Institute (NHLBI)
   [HHSN268201800014I]; Mississippi State Department of Health from the
   National Heart, Lung, and Blood Institute (NHLBI)
   [HHSN268201800015I/HHSN26800001]; University of Mississippi Medical
   Center from the National Heart, Lung, and Blood Institute (NHLBI)
   [HHSN268201800010I, HHSN268201800011I, HHSN268201800012I]; National
   Heart, Lung, and Blood Institute, National Institutes of Health, U.S.
   Department of Health and Human Services [HHSN268201600018C,
   HHSN268201600001C, HHSN268201600002C, HHSN268201600003C,
   HHSN268201600004C]; National Heart, Lung, and Blood Institute, Bethesda,
   MD [K01HL133468]; National Institute of Diabetes and Digestive Kidney
   Diseases (NIDDK) [DK117445]; National Institute on Minority Health and
   Health Disparities (NIMHD) [MD012765]; Jackson State University from the
   National Institute for Minority Health and Health Disparities (NIMHD)
   [HHSN268201800013I]; Tougaloo College from the National Institute for
   Minority Health and Health Disparities (NIMHD) [HHSN268201800014I];
   Mississippi State Department of Health from the National Institute for
   Minority Health and Health Disparities (NIMHD)
   [HHSN268201800015I/HHSN26800001]; University of Mississippi Medical
   Center from the National Institute for Minority Health and Health
   Disparities (NIMHD) [HHSN268201800010I, HHSN268201800011I,
   HHSN268201800012I];  [N01-HC-25195];  [HHSN268201500001I];  [R01
   HL092577];  [HHSN268201500003I];  [N01-HC-95159];  [N01-HC-95160]; 
   [N01-HC-95161];  [N01-HC-95162];  [N01-HC-95163];  [N01-HC-95164]; 
   [N01-HC-95165];  [N01-HC-95166];  [N01-HC-95167];  [N01-HC-95168]; 
   [N01-HC-95169];  [UL1-TR-000040];  [UL1-TR-001079];  [UL1-TR-001420]; 
   [UL1-TR-001881];  [DK063491]
FX This work was supported by Grants T32 HL007567, HL113338 and HL086694
   from the National Heart, Lung, and Blood Institute (NHLBI) and HG003054
   from the National Human Genome Research Institute (NHGRI). Whole genome
   sequencing (WGS) for the Trans-Omics in Precision Medicine (TOPMed)
   program was supported by the National Heart, Lung and Blood Institute
   (NHLBI). WGS for "NHLBI TOPMed: Atherosclerosis Risk in Communities"
   (phs001211.v1.p1) was performed at the Baylor College of Medicine Human
   Genome Sequencing Center (HHSN268201500015C, 3U54HG003273-12S2). WGS for
   "NHLBI TOPMed: The Framingham Heart Study" (phs000974.v2.p2) was
   performed at the Broad Institute of MIT and Harvard (HHSN268201500014C).
   WGS for "NHLBI TOPMed: Genetics of Cardiometabolic Health in the Amish"
   (phs000956.v2.p1) was performed at the Broad Institute of MIT and
   Harvard (3R01HL121007-01S1). WGS for "NHLBI TOPMed: The Jackson Heart
   Study" (phs000964.v2.p1) was performed at the University of Washington
   Northwest Genomics Center (HHSN268201100037C). WGS for "NHLBI TOPMed:
   The Cleveland Family Study" (phs000954.v1.p1) was performed at the
   University of Washington Northwest Genomics Center (3R01HL098433-05S1).
   WGS for "NHLBI TOPMed: Multi-Ethnic Study of Atherosclerosis (MESA)"
   (phs001416.v1.p1) was performed at the Broad Institute of MIT and
   Harvard (3U54HG003067-13S1). WGS for "NHLBI TOPMed: Hypertension Genetic
   Epidemiology Network and Genetic Epidemiology Network of Arteriopathy"
   (phs001293.v1.p1) was performed at the University of Washington
   Northwest Genomics Center (3R01HL055673-18S1). WGS for "NHLBI TOPMed:
   Genetic Epidemiology Network of Arteriopathy" (phs001345.v1.p1) was
   performed at the University of Washington Northwest Genomics Center
   (3R01HL055673-18S1). WGS for "NHLBI TOPMed: Genetic Studies of
   Atherosclerosis Risk" (phs001218.v1.p1) was performed at the Macrogen
   and the Broad Institute of MIT and Harvard (HHSN268201500014C). WGS for
   "NHLBI TOPMed: Genetic Epidemiology Network of Salt Sensitivity"
   (phs001217.v1.p1) was performed at the Baylor College of Medicine Human
   Genome Sequencing Center (HHSN268201500015C). WGS for "NHLBI TOPMed:
   Women's Health Initiative" (phs001237.v1.p1) was performed at the Broad
   Institute of MIT and Harvard (HHSN268201500014C). Centralized read
   mapping and genotype calling, along with variant quality metrics and
   filtering, were provided by the TOPMed Informatics Research Center
   (3R01HL-117626-02S1). Phenotype harmonization, data management,
   sample-identity QC, and general study coordination were provided by the
   TOPMed Data Coordinating Center (3R01HL-120393-02S1). We gratefully
   acknowledge the studies and participants who provided biological samples
   and data for TOPMed. The Atherosclerosis Risk in Communities study has
   been funded in whole or in part with Federal funds from the National
   Heart, Lung, and Blood Institute, National Institutes of Health,
   Department of Health and Human Services (contract numbers
   HHSN268201700001I, HHSN268201700002I, HHSN268201700003I,
   HHSN268201700004I and HHSN268201700005I). The authors thank the staff
   and participants of the ARIC study for their important contributions.
   The Amish studies upon which these data are based were supported by NIH
   Grants R01 AG18728, U01 HL072515, R01 HL088119, R01 HL121007, and P30
   DK072488. See publication: PMID: 18440328. Support for the Cleveland
   Family Study was provided by NIH Grants HL 046389, HL113338, and
   1R35HL135818. The Framingham Heart Study has been supported by contracts
   N01-HC-25195 and HHSN268201500001I and Grant R01 HL092577.The Framingham
   Heart Study thanks the study participants and the multitude of
   investigators who over its 70-year history continue to contribute so
   much to further our knowledge of heart, lung, blood, and sleep disorders
   and associated traits. GeneSTAR was supported by Grants from the
   National Institutes of Health/National Heart, Lung, and Blood Institute
   (U01 HL72518, HL087698, HL49762, HL58625, HL071025, HL112064), the
   National Institutes of Health/National Institute of Nursing Research
   (NR0224103), and by a Grant from the National Institutes of
   Health/National Center for Research Resources (M01-RR000052) to the
   Johns Hopkins General Clinical Research Center. Support for GENOA was
   provided by the National Heart, Lung and Blood Institute (HL054457,
   HL054464, HL054481, and HL087660) of the National Institutes of Health.
   The Genetic Epidemiology Network of Salt-Sensitivity (GenSalt) was
   supported by research Grants (U01HL072507, R01HL087263, and R01HL090682)
   from the National Heart, Lung and Blood Institute, National Institutes
   of Health, Bethesda, MD. The Jackson Heart Study (JHS) is supported and
   conducted in collaboration with Jackson State University
   (HHSN268201800013I), Tougaloo College (HHSN268201800014I), the
   Mississippi State Department of Health (HHSN268201800015I/HHSN26800001)
   and the University of Mississippi Medical Center (HHSN268201800010I,
   HHSN268201800011I and HHSN268201800012I) contracts from the National
   Heart, Lung, and Blood Institute (NHLBI) and the National Institute for
   Minority Health and Health Disparities (NIMHD). The authors also wish to
   thank the staffs and participants of the JHS. MESA and the MESA SHARe
   project are conducted and supported by the National Heart, Lung, and
   Blood Institute (NHLBI) in collaboration with MESA investigators.
   Support for MESA is provided by contracts HHSN268201500003I,
   N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163,
   N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168,
   N01-HC-95169, UL1-TR-000040, UL1-TR-001079, UL1-TR-001420,
   UL1-TR-001881, and DK063491. The WHI program is funded by the National
   Heart, Lung, and Blood Institute, National Institutes of Health, U.S.
   Department of Health and Human Services through contracts
   HHSN268201600018C, HHSN268201600001C, HHSN268201600002C,
   HHSN268201600003C, and HHSN268201600004C. Dr. Bress is supported by
   K01HL133468 from the National Heart, Lung, and Blood Institute,
   Bethesda, MD. Dr. Franceschini is supported by DK117445 from the
   National Institute of Diabetes and Digestive Kidney Diseases (NIDDK) and
   MD012765 from the National Institute on Minority Health and Health
   Disparities (NIMHD). The authors would like to acknowledge contributions
   from the investigators of the NHLBI TOPMed Consortium
   (https://www.nhlbiwgs.org/topmed-banner-authorship).
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   Zhu XF, 2015, AM J HUM GENET, V96, P21, DOI 10.1016/j.ajhg.2014.11.011
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NR 39
TC 20
Z9 21
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0340-6717
EI 1432-1203
J9 HUM GENET
JI Hum. Genet.
PD FEB
PY 2019
VL 138
IS 2
BP 199
EP 210
DI 10.1007/s00439-019-01975-0
PG 12
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA HL1CY
UT WOS:000458432800007
PM 30671673
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Camacho-Jiménez, L
   Sánchez-Castrejón, E
   Ponce-Rivas, E
   Muñoz-Márquez, ME
   Aguilar, MB
   Re, AD
   Díaz, F
AF Camacho-Jimenez, Laura
   Sanchez-Castrejon, Edna
   Ponce-Rivas, Elizabeth
   Enriqueta Munoz-Marquez, Ma.
   Aguilar, Manuel B.
   Denisse Re, Ana
   Diaz, Fernando
TI Hyperglycemic activity of the recombinant crustacean hyperglycemic
   hormone B1 isoform (CHH-B1) of the Pacific white shrimp Litopenaeus
   vannamei
SO PEPTIDES
LA English
DT Article
DE Crustacean hyperglycemic hormone; Crustacean neurohormone; Recombinant
   expression; Dose-response hyperglycemic analysis; Litopenaeus vannamei
ID CRAYFISH PROCAMBARUS-CLARKII; GONAD-INHIBITING HORMONE; PERICARDIAL
   ORGAN; KURUMA PRAWN; MACROBRACHIUM-ROSENBERGII; STRUCTURAL VARIANTS;
   MOLECULAR-CLONING; PENAEUS-MONODON; GENE-EXPRESSION; SHORE CRAB
AB Crustacean hyperglycemic hormone (CHH) is the most abundant neuropeptide produced by the X-organ/sinus gland (XO/SG) complex in the crustacean eyestalk. CHH plays a principal role in the control of glucose metabolism. The CHH-B1 isoform is produced in the eyestalk of Litopenaeus vannamei by alternative splicing of the chhB gene and its cDNA sequence has revealed that this isoform has a nonamidated C-terminal residue (CHH-like peptide). In this work, a recombinant CHH-B1 (rCHH-B1) with a sequence identical to the native hormone was expressed in the methylotrophic yeast Pichia pastoris X-33 and purified from the culture medium by RP-HPLC. The identity of the purified rCHH-B1 was confirmed by N-terminal sequencing and by using an anti-CHH-B1 polyclonal antibody. An in vivo assay showed that the hyperglycemic effect was dependant of the dosage of rCHH-B1, and the maximal hyperglycemic response was obtained with 250 pmol treatment. These results suggest that the amino acid sequence of the C-terminus and its correct structure are both important for the hyperglycemic activity of naturally occurring non-amidated CHH peptides, such as CHH-B1. CHH-B1 appears to be the first reported CHH-like peptide with significant hyperglycemic activity produced in the sinus gland of a penaeid shrimp. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Camacho-Jimenez, Laura; Sanchez-Castrejon, Edna; Ponce-Rivas, Elizabeth] Ctr Invest Cient & Educ Super Ensenada CICESE, Dept Biotecnol Marina, Lab Biol Celular & Mol, Ensenada 22860, Baja California, Mexico.
   [Enriqueta Munoz-Marquez, Ma.] Univ Autonoma Baja California UABC, Fac Ciencias Quim & Ingn, Tijuana 22390, Baja California, Mexico.
   [Aguilar, Manuel B.] Univ Nacl Autonoma Mexico, Inst Neurobiol, Lab Neurofarmacol Marina, Juriquilla 76230, Queretaro, Mexico.
   [Denisse Re, Ana; Diaz, Fernando] Ctr Invest Cient & Educ Super Ensenada CICESE, Dept Biotecnol Marina, Lab Ecofisiol Organismos Acuat, Ensenada 22860, Baja California, Mexico.
C3 CICESE - Centro de Investigacion Cientifica y de Educacion Superior de
   Ensenada; Universidad Nacional Autonoma de Mexico; CICESE - Centro de
   Investigacion Cientifica y de Educacion Superior de Ensenada
RP Ponce-Rivas, E (corresponding author), Ctr Invest Cient & Educ Super Ensenada CICESE, Dept Biotecnol Marina, Lab Biol Celular & Mol, Carretera Ensenada Tijuana 3918, Ensenada 22860, Baja California, Mexico.
EM eponce@cicese.mx
RI Ponce-Rivas, Elizabeth/K-3278-2016; Aguilar, Manuel/AAI-2847-2021; Diaz,
   Fernando/X-1430-2019; Camacho-Jimenez, Laura/L-4313-2018; Sanchez,
   Edna/B-7850-2016
OI Ponce-Rivas, Elizabeth/0000-0002-2842-7300; Camacho-Jimenez,
   Laura/0000-0002-0278-5943; Re Araujo, Ana Denise/0000-0002-9639-9866;
   Sanchez, Edna/0000-0002-7375-1468
FU National Council for Science and Technology of Mexico (CONACyT); CONACyT
   [CB2009-133958-Z]
FX We thank Dr. John van der Meer for his helpful suggestions and his
   valuable help in polishing the English in the manuscript. The
   scholarship of the first author of this study was granted by the
   National Council for Science and Technology of Mexico (CONACyT). This
   work was funded by CONACyT (grant CB2009-133958-Z).
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NR 53
TC 16
Z9 16
U1 0
U2 17
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0196-9781
EI 1873-5169
J9 PEPTIDES
JI Peptides
PD SEP
PY 2015
VL 71
BP 32
EP 39
DI 10.1016/j.peptides.2015.05.014
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
   Pharmacology & Pharmacy
GA CS1PA
UT WOS:000361837800005
PM 26079393
DA 2025-04-10
ER

PT J
AU Qi, JW
   Qin, TT
   Xu, LX
   Zhang, K
   Yang, GL
   Li, J
   Xiao, HY
   Zhang, ZS
   Li, LY
AF Qi, Jian-Wei
   Qin, Ting-Ting
   Xu, Li-Xia
   Zhang, Kun
   Yang, Gui-Li
   Li, Jie
   Xiao, Huai-Yuan
   Zhang, Zhi-Song
   Li, Lu-Yuan
TI TNFSF15 inhibits vasculogenesis by regulating relative levels of
   membrane-bound and soluble isoforms of VEGF receptor 1
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE angiogenesis; protein degradation
ID ENDOTHELIAL PROGENITOR CELLS; TUMOR ANGIOGENESIS; GROWTH INHIBITOR;
   MYOCARDIAL-INFARCTION; TYROSINE KINASE-1; RECRUITMENT; FLT1;
   NEOVASCULARIZATION; DIFFERENTIATION; EXPRESSION
AB Mouse bone marrow-derived Lin(-)-Sca-1(+) endothelial progenitor cell (EPC) has pluripotent abilities such as supporting neovascularization. Vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) (Flt1) recognizes various VEGF isoforms and is critically implicated in a wide range of physiological and pathological settings, including vasculogenesis. Mouse EPC expresses two isoforms of VEGFR1: mFlt1, which transmits ligand-induced signals; and sFlt1, which acts as a negative regulator by sequestering ligands of VEGF receptors. How the relative levels of mFlt1 and sFlt1 are regulated is not yet clear. We report here that tumor necrosis factor superfamily 15 (TNFSF15) (also known as VEGI or TL1A), an endothelial cell-secreted cytokine, simultaneously promotes mFlt1 degradation and up-regulates sFlt1 expression in EPC, giving rise to disruption of VEGF-or PlGF-induced activation of eNOS and MAPK p38 and effective inhibition of VEGF-driven, EPC-supported vasculogenesis in a murine Matrigel implant model. TNFSF15 treatment of EPC cultures facilitates Akt deactivation-dependent, ubiquitin-assisted degradation of mFlt1 and stimulates sFlt1 expression by activating the PKC, Src, and Erk1/2 signaling pathway. Additionally, TNFSF15 promotes alternative splicing of the Flt1 gene in favor of sFlt1 production by down-regulating nuclear protein Jumonji domain-containing protein 6 (Jmjd6), thus alleviating Jmjd6-inhibited sFlt1 expression. These findings indicate that TNFSF15 is a key component of a molecular mechanism that negatively modulates EPC-supported vasculogenesis through regulation of the relative levels of mFlt1 and sFlt1 in EPC.
C1 [Qi, Jian-Wei; Qin, Ting-Ting; Xu, Li-Xia; Zhang, Kun; Yang, Gui-Li; Li, Jie; Xiao, Huai-Yuan; Zhang, Zhi-Song; Li, Lu-Yuan] State Key Lab Med Chem Biol, Tianjin 300071, Peoples R China.
   [Qi, Jian-Wei; Qin, Ting-Ting; Xu, Li-Xia; Zhang, Kun; Yang, Gui-Li; Li, Jie; Xiao, Huai-Yuan; Zhang, Zhi-Song; Li, Lu-Yuan] Nankai Univ, Coll Pharm, Tianjin 300071, Peoples R China.
   [Qi, Jian-Wei; Qin, Ting-Ting; Xu, Li-Xia; Zhang, Kun; Yang, Gui-Li; Li, Jie; Xiao, Huai-Yuan; Zhang, Zhi-Song; Li, Lu-Yuan] Nankai Univ, Tianjin Key Lab Mol Drug Res, Tianjin 300071, Peoples R China.
C3 Nankai University; Nankai University
RP Li, LY (corresponding author), State Key Lab Med Chem Biol, Tianjin 300071, Peoples R China.
EM zzs@nankai.edu.cn; liluyuan@nankai.edu.cn
RI li, jie/ABG-7099-2021; Xu, Lixia/CAJ-5305-2022
OI Xu, Lixia/0000-0002-1843-0127; li, jie/0000-0002-4732-5967
FU Ministry of Science and Technology of China [2009CB918901,
   2013ZX09103003-013]; Natural Science Foundation of China [81272356,
   81101709]; Tianjin Municipality Science and Technology Commission
   [10ZCKFSH00100]
FX This study was supported in part by grants from The Ministry of Science
   and Technology of China (2009CB918901 and 2013ZX09103003-013 to
   L.-Y.L.), Natural Science Foundation of China (81272356 to L.-Y.L. and
   81101709 to Z.-S.Z.), and Tianjin Municipality Science and Technology
   Commission (10ZCKFSH00100 to L.-Y.L.).
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NR 51
TC 48
Z9 53
U1 0
U2 14
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD AUG 20
PY 2013
VL 110
IS 34
BP 13863
EP 13868
DI 10.1073/pnas.1304529110
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 203DU
UT WOS:000323271400048
PM 23918400
OA Green Published, Bronze
DA 2025-04-10
ER

PT J
AU Luo, CX
   Zhu, DY
AF Luo, Chun-Xia
   Zhu, Dong-Ya
TI Research progress on neurobiology of neuronal nitric oxide synthase
SO NEUROSCIENCE BULLETIN
LA English
DT Review
DE neuronal nitric oxide synthase; cAMP response element-binding protein;
   post-synaptic density protein 95; synaptogenesis; neurogenesis
ID LONG-TERM POTENTIATION; FOCAL CEREBRAL-ISCHEMIA;
   AMYOTROPHIC-LATERAL-SCLEROSIS; MOUSE SUBVENTRICULAR ZONE; TRANSIENT
   GLOBAL-ISCHEMIA; CENTRAL-NERVOUS-SYSTEM; ADULT DENTATE GYRUS; NEURAL
   STEM-CELLS; ALZHEIMERS-DISEASE; HIPPOCAMPAL NEUROGENESIS
AB Neuronal nitric oxide synthase (nNOS) is mainly expressed in neurons, to some extent in astrocytes and neuronal stem cells. The alternative splicing of nNOS mRNA generates 5 isoforms of nNOS, including nNOS-alpha, nNOS-beta, nNOS-mu, nNOS-gamma and nNOS-2. Monomer of nNOS is inactive, and dimer is the active form. Dimerization requires tetrahydrobiopterin (BH4), heme and L-arginine binding. Regulation of nNOS expression relies largely on cAMP response element-binding protein (CREB) activity, and nNOS activity is regulated by heat shock protein 90 (HSP90)/HSP70, calmodulin (CaM), phosphorylation and dephosphorylation at Ser847 and Ser1412, and the protein inhibitor of nNOS (PIN). There are primarily 9 nNOS- interacting proteins, including post-synaptic density protein 95 (PSD95), clathrin assembly lymphoid leukemia (CALM), calcium/calmodulin-dependent protein kinase II alpha (CAMKIIA), Disks large homolog 4 (DLG4), DLG2, 6-phosphofructokinase, muscle type (PFK-M), carboxy-terminal PDZ ligand of nNOS (CAPON) protein, syntrophin and dynein light chain (LC). Among them, PSD95, CAPON and PFK-M are important nNOS adapter proteins in neurons. The interaction of PSD95 with nNOS controls synapse formation and is implicated in N-methyl-D-aspartic acid-induced neuronal death. nNOS- derived NO is implicated in synapse loss-mediated early cognitive/motor deficits in several neuropathological states, and negatively regulates neurogenesis under physiological and pathological conditions.
C1 [Luo, Chun-Xia; Zhu, Dong-Ya] Nanjing Med Univ, Lab Cerebrovasc Dis, Sch Pharm, Dept Pharmacol, Nanjing 210029, Peoples R China.
C3 Nanjing Medical University
RP Zhu, DY (corresponding author), Nanjing Med Univ, Lab Cerebrovasc Dis, Sch Pharm, Dept Pharmacol, Nanjing 210029, Peoples R China.
EM dyzhu@njmu.edu.cn
FU National Natural Science Foundation of China [30971021, 81030023,
   30901550]
FX This work was supported by the National Natural Science Foundation of
   China (No. 30971021, 81030023 and 30901550).
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NR 130
TC 45
Z9 58
U1 2
U2 55
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1673-7067
EI 1995-8218
J9 NEUROSCI BULL
JI Neurosci. Bull.
PD FEB
PY 2011
VL 27
IS 1
BP 23
EP 35
DI 10.1007/s12264-011-1038-0
PG 13
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 831JP
UT WOS:000295726900004
PM 21270901
OA Green Published
DA 2025-04-10
ER

PT J
AU Osborne, RJ
   Welle, S
   Venance, SL
   Thornton, CA
   Tawil, R
AF Osborne, R. J.
   Welle, S.
   Venance, S. L.
   Thornton, C. A.
   Tawil, R.
TI Expression profile of FSHD supports a link between retinal vasculopathy
   and muscular dystrophy
SO NEUROLOGY
LA English
DT Article
ID GENE-EXPRESSION; FUNCTIONAL ISCHEMIA; DNA REARRANGEMENTS; OXIDATIVE
   STRESS; SKELETAL-MUSCLE; D4Z4; LOCUS; FRG1; HYPOMETHYLATION;
   IDENTIFICATION
AB Background: Facioscapulohumeral muscular dystrophy ( FSHD) is caused by deletions within a tandem array of D4Z4 repeats on chromosome 4q35. In addition to muscle degeneration, most patients with FSHD develop abnormalities of the retinal vasculature. Previous work has suggested that muscle degeneration in FSHD results from increased expression of genes proximal to the deletion, including FRG1. Objectives: To reexamine this mechanism and identify pathways that are abnormally regulated early in the disease process. Methods: We prospectively studied gene expression in skeletal muscle in patients with FSHD (n = 19) vs healthy individuals (n = 30) and patients with myotonic dystrophy type 1 (n = 12). We used oligonucleotide microarrays for global analysis of gene expression and reverse transcriptase-PCR (RT-PCR) to assess expression or alternative splicing for particular genes. Results: Expression of FRG1 was not increased in patients with FSHD, either by microarray analysis or quantitative RT-PCR. Among genes on 4q35, only LRP2BP showed upregulation that was specific to FSHD. However, neither LRP2BP nor FRG1 showed imbalance of allelic expression by RT-PCR. After filtering out genes that showed similar dysregulation in other forms of muscular dystrophy, only 44 genes were specifically upregulated early in FSHD. Among these, 34 genes were characterized or partially characterized, of which 11 (32%) had a role in vascular smooth muscle or endothelial cells. Conclusion: Expression of genes on chromosome 4q35 was normally regulated in the early stages of facioscapulohumeral muscular dystrophy. Our results support a possible link between muscular dystrophy and retinal vasculopathy in facioscapulohumeral muscular dystrophy.
C1 Univ Rochester, Sch Med & Dent, Neuromuscular Dis Ctr, Dept Neurol, Rochester, NY 14642 USA.
   Univ Rochester, Sch Med & Dent, Dept Med, Rochester, NY 14642 USA.
   London Hlth Sci Ctr, Dept Clin Neurol Sci, London, ON, Canada.
C3 University of Rochester; University of Rochester; London Health Sciences
   Centre
RP Tawil, R (corresponding author), Univ Rochester, Sch Med & Dent, Neuromuscular Dis Ctr, Dept Neurol, 601 Elmwood Ave,Box 673, Rochester, NY 14642 USA.
EM rabi_tawil@urmc.rochester.edu
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NR 46
TC 108
Z9 122
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD FEB 20
PY 2007
VL 68
IS 8
BP 569
EP 577
DI 10.1212/01.wnl.0000251269.31442.d9
PG 9
WC Clinical Neurology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 137DT
UT WOS:000244273900007
PM 17151338
DA 2025-04-10
ER

PT J
AU Berman, JM
   Brand, C
   Awayda, MS
AF Berman, Jonathan M.
   Brand, Cristin
   Awayda, Mouhamed S.
TI A long isoform of the epithelial sodium channel alpha subunit forms a
   highly active channel
SO CHANNELS
LA English
DT Article
DE alternative splicing; electrophysiology; epithelial sodium channel
   (ENaC); hypertension; ion channels; protease
ID NA+ CHANNEL; ION CHANNELS; ENAC; ACTIVATION; INHIBITION; EXPRESSION;
   DEPENDENCE; TRANSPORT; EXOSOMES; VOLTAGE
AB A long isoform of the human Epithelial Sodium Channel (ENaC) alpha subunit has been identified, but little data exist regarding the properties or regulation of channels formed by alpha(728). The baseline whole cell conductance of oocytes expressing trimeric alpha(728)beta gamma channels was 898.1 +/- 277.2 and 49.59 +/- 13.2 mu S in low and high sodium solutions, respectively, and was 11 and 2 fold higher than the conductances of alpha(669)beta gamma in same solutions. alpha(728)beta gamma channels were also 2 to 5 fold less sensitive to activation by the serine proteases subtilisin and trypsin than alpha(669)beta gamma in low and high Na+ conditions. The long isoform exhibited lower levels of full length and cleaved protein at the plasma membrane and a rightward shifted sensitivity to inhibition by increases of [Na+](i). Both channels displayed similar single channel conductances of 4 pS, and both were activated to a similar extent by reducing temperature, altogether indicating that activation of baseline conductance of alpha(728)beta gamma was likely mediated by enhanced channel activity or open probability. Expression of alpha(728) in native kidneys was validated in human urinary exosomes. These data demonstrate that the long isoform of alpha ENaC forms the structural basis of a channel with different activity and regulation, which may not be easily distinguishable in native tissue, but may underlie sodium hyperabsorption and salt sensitive differences in humans.
C1 [Berman, Jonathan M.; Brand, Cristin; Awayda, Mouhamed S.] SUNY Buffalo, Dept Physiol & Biophys, Buffalo, NY 14260 USA.
C3 State University of New York (SUNY) System; University at Buffalo, SUNY
RP Awayda, MS (corresponding author), SUNY Buffalo, Dept Physiol & Biophys, Buffalo, NY 14260 USA.
EM awayda@buffalo.edu
OI Berman, Jonathan/0000-0001-6547-9647; Beumer,
   Cristin/0009-0006-5032-6414
FU NIH [DK55626]; John R. Oishei Foundation
FX This work was supported by NIH grant DK55626, and by the John R. Oishei
   Foundation.
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NR 47
TC 5
Z9 6
U1 0
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6950
EI 1933-6969
J9 CHANNELS
JI Channels
PD JAN-FEB
PY 2015
VL 9
IS 1
BP 30
EP 43
DI 10.4161/19336950.2014.985478
PG 14
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA CG3HH
UT WOS:000353169700006
PM 25517724
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU McCright, B
   Gao, X
   Shen, LY
   Lozier, J
   Lan, Y
   Maguire, M
   Herzlinger, D
   Weinmaster, G
   Jiang, RL
   Gridley, T
AF McCright, B
   Gao, X
   Shen, LY
   Lozier, J
   Lan, Y
   Maguire, M
   Herzlinger, D
   Weinmaster, G
   Jiang, RL
   Gridley, T
TI Defects in development of the kidney, heart and eye vasculature in mice
   homozygous for a hypomorphic Notch2 mutation
SO DEVELOPMENT
LA English
DT Article
DE Notch2; glomerulogenesis; kidney; hypomorphic mutation; persistent
   hyperplastic primary vitreous; mouse
ID STAFFORDSHIRE BULL TERRIER; ENDOTHELIAL GROWTH-FACTOR; DELTA-HOMOLOG;
   MOLECULAR REGULATION; EMBRYONIC LETHALITY; ALAGILLE-SYNDROME; NEUROGENIC
   GENES; MOUSE EMBRYO; EXPRESSION; RECEPTOR
AB The Notch gene family encodes large transmembrane receptors that are components of an evolutionarily conserved intercellular signaling mechanism. To assess the in vivo role of the Notch2 gene, we constructed a targeted mutation, Notch2(del1), Unexpectedly, we found that alternative splicing of the Notch2(del1) mutant allele leads to the production of two different in-frame transcripts that delete either one or two EGF repeats of the Notch2 protein, suggesting that this allele is a hypomorphic Notch2 mutation. Mice homozygous for the Notch2(del1) mutation died perinatally from defects in glomerular development in the kidney. Notch2(del1)/Notch2(del1) mutant kidneys were hypoplastic and mutant glomeruli lacked a normal capillary tuft, The Notch ligand encoded by the Jag1 gene was expressed in developing glomeruli in cells adjacent to Notch2-expressing cells, We show that mice heterozygous for both the Notch2(del1) and Jag1(dDSL) mutations exhibit a glomerular defect similar to, but less severe than, that of Notch2(del1)/Notch2(del1) homozygotes. The co-localization and genetic interaction of Jag1 and Notch2 imply that this ligand and receptor physically interact, forming part of the signal transduction pathway required for glomerular differentiation and patterning, NotCh2(del1)/Notch2(del1) homozygotes also display myocardial hypoplasia, edema and hyperplasia of cells associated with the hyaloid vasculature of the eye, These data identify novel developmental roles for Notch2 in kidney, heart and eye development.
C1 Jackson Lab, Bar Harbor, ME 04609 USA.
   Roche Inst Mol Biol, Roche Res Ctr, Nutley, NJ 07110 USA.
   Cornell Univ Med Coll, Dept Physiol & Biophys, New York, NY 10021 USA.
   Cornell Univ Med Coll, Dept Urol, New York, NY 10021 USA.
   Univ Calif Los Angeles, Sch Med, Dept Biol Chem, Los Angeles, CA 90024 USA.
C3 Jackson Laboratory; Roche Holding; Roche Holding USA; Cornell
   University; Cornell University; University of California System;
   University of California Los Angeles; University of California Los
   Angeles Medical Center; David Geffen School of Medicine at UCLA
RP Gridley, T (corresponding author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
OI Jiang, Rulang/0000-0001-7842-4696
FU NCI NIH HHS [CA34196] Funding Source: Medline; NINDS NIH HHS [NS36437]
   Funding Source: Medline
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NR 63
TC 284
Z9 359
U1 0
U2 13
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
   CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD FEB
PY 2001
VL 128
IS 4
BP 491
EP 502
PG 12
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA 407VF
UT WOS:000167290900004
PM 11171333
DA 2025-04-10
ER

PT J
AU Small, TW
   Penalva, LO
   Pickering, JG
AF Small, Theodore W.
   Penalva, Luiz O.
   Pickering, J. Geoffrey
TI Vascular biology and the sex of flies: Regulation of vascular smooth
   muscle cell proliferation by Wilms' tumor 1-associating protein
SO TRENDS IN CARDIOVASCULAR MEDICINE
LA English
DT Article
ID PRE-MESSENGER-RNA; DROSOPHILA-MELANOGASTER; IN-VIVO; PROTEOMIC ANALYSIS;
   SUPPRESSOR WT1; FL(2)D GENE; EXPRESSION; DIFFERENTIATION; AMPHIREGULIN;
   APOPTOSIS
AB Smooth muscle cells (SMCS) are called on to proliferate during vascular repair but must return to a nonproliferative state if remodeling is to terminate appropriately. One gene that has recently been implicated in the acquisition of SMC replicative quiescence is Wilms' tumor 1-associating protein (WTAP). Wilms' tumor 1-associating protein is a nuclear constituent of uncertain function that, as the name implies ' interacts with the Wilms' tumor 1 tumor suppressor gene product (WTI). Wilms' tumor 1-associating protein is essential for embryonic development, and recent data suggest that WTAP regulates the proliferation of both SMCs and endothelial cells. In SMCs, WTAP appears to be antiproliferative, inhibiting G(1)-to-S phase cell cycle transition and also promoting apoptosis. These effects could be the result of WTAP suppressing the transcriptional activity of WT1 in SMCs. Interestingly, the Drosophila homologue of WTAP, fl(2)d, is a protein essential for alternative splicing regulation and sexual determination in this species. Wilms' tumor 1-associating protein may thus also play a role in messenger RNA processing in mammalian cells, either dependent on or independent of its interaction with WT1. The putative actions of WTAP as a regulator of transcriptional and posttranscriptional events and emerging evidence for a WTAP-WT1 axis in vascular cells suggest that WTAP is a vital and multifaceted regulator of vascular remodeling. (Trends Cardiovasc Med 2007;17:230-234) (c) 2007, Elsevier Inc.
C1 Univ Western Ontario, London Hlth Sci Ctr, Robarts Res Inst, Dept Med Cardiol, London, ON N6A 5K8, Canada.
   Univ Western Ontario, London Hlth Sci Ctr, Robarts Res Inst, Dept Biochem, London, ON N6A 5K8, Canada.
   Univ Western Ontario, London Hlth Sci Ctr, Robarts Res Inst, Dept Med Biophys, London, ON N6A 5K8, Canada.
   Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
C3 Western University (University of Western Ontario); University Western
   Ontario Hospital; London Health Sciences Centre; London Health Sciences
   Centre; Western University (University of Western Ontario); University
   Western Ontario Hospital; London Health Sciences Centre; Western
   University (University of Western Ontario); University Western Ontario
   Hospital; University of Texas System; University of Texas Health Science
   Center at San Antonio
RP Pickering, JG (corresponding author), London Hlth Sci Ctr, 339 Windermere Rd, London, ON N6A 5A5, Canada.
EM gpickering@robarts.ca
RI ; Pickering, J. Geoffrey/G-3341-2011
OI Penalva, Luiz/0000-0003-4491-6769; Pickering, J.
   Geoffrey/0000-0001-6474-3274
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NR 37
TC 18
Z9 21
U1 0
U2 6
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1050-1738
J9 TRENDS CARDIOVAS MED
JI Trends Cardiovasc. Med.
PD OCT
PY 2007
VL 17
IS 7
BP 230
EP 234
DI 10.1016/j.tcm.2007.08.002
PG 5
WC Cardiac & Cardiovascular Systems
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA 224AS
UT WOS:000250418000003
PM 17936204
DA 2025-04-10
ER

PT J
AU Matthews, V
   Schuster, B
   Schütze, S
   Bussmeyer, I
   Ludwig, A
   Hundhausen, C
   Sadowski, T
   Saftig, P
   Hartmann, D
   Kallen, KJ
   Rose-John, S
AF Matthews, V
   Schuster, B
   Schütze, S
   Bussmeyer, I
   Ludwig, A
   Hundhausen, C
   Sadowski, T
   Saftig, P
   Hartmann, D
   Kallen, KJ
   Rose-John, S
TI Cellular cholesterol depletion triggers shedding of the human
   interleukin-6 receptor by ADAM10 and ADAM17 (TACE)
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; HUMAN IL-6 RECEPTOR; KINASE-C-DELTA;
   CONVERTING-ENZYME; T-CELL; SOLUBLE RECEPTOR; CLEAVAGE; PROTEIN;
   SECRETASE; CYTOKINE
AB Interleukin-6 (IL-6) activates cells by binding to the membrane-bound IL-6 receptor (IL-6R) and subsequent formation of a glycoprotein 130 homodimer. Cells that express glycoprotein 130, but not the IL-6R, can be activated by IL-6 and the soluble IL-6R which is generated by shedding from the cell surface or by alternative splicing. Here we show that cholesterol depletion of cells with methyl-beta-cyclodextrin increases IL-6R shedding independent of protein kinase C activation and thus differs from phorbol ester-induced shedding. Contrary to cholesterol depletion, cholesterol enrichment did not increase IL-6R shedding. Shedding of the IL-6R because of cholesterol depletion is highly dependent on the metalloproteinase ADAM17 (tumor necrosis factor-alpha-converting enzyme), and the related ADAM10, which is identified here for the first time as an enzyme involved in constitutive and induced shedding of the human IL-6R. When combined with protein kinase C inhibition by staurosporine or rottlerin, breakdown of plasma membrane sphingomyelin or enrichment of the plasma membrane with ceramide also increased IL-6R shedding. The effect of cholesterol depletion was confirmed in human THP-1 and Hep3B cells and in primary human peripheral blood monocytes, which naturally express the IL-6R. For decades, high cholesterol levels have been considered harmful. This study indicates that low cholesterol levels may play a role in shedding of the membrane-bound IL-6R and thereby in the immuno-pathogenesis of human diseases.
C1 Univ Kiel, Inst Biochem, D-24098 Kiel, Germany.
   Univ Kiel, Inst Immunol, D-24105 Kiel, Germany.
   Leuven & Flanders Interuniv, Ctr Human Genet, B-3000 Louvain, Belgium.
C3 University of Kiel; University of Kiel; KU Leuven
RP Univ Kiel, Inst Biochem, Olshaussenstr 40, D-24098 Kiel, Germany.
EM rosejohn@biochem.uni-kiel.de
RI Hundhausen, Christian/F-2539-2011; Schütze, Stefan/C-8596-2011; Saftig,
   Paul/A-7966-2010; Schuster, Bjorn/G-6339-2014; Ludwig,
   Andreas/I-5685-2012; Rose-John, Stefan/A-7998-2010
OI Ludwig, Andreas/0000-0001-8536-4986; Rose-John,
   Stefan/0000-0002-7519-3279
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NR 71
TC 324
Z9 354
U1 0
U2 14
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 3
PY 2003
VL 278
IS 40
BP 38829
EP 38839
DI 10.1074/jbc.M210584200
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 726AM
UT WOS:000185575100091
PM 12832423
OA hybrid
DA 2025-04-10
ER

PT J
AU Yamak, A
   Georges, RO
   Sheikh-Hassani, M
   Morin, M
   Komati, H
   Nemer, M
AF Yamak, Abir
   Georges, Romain O.
   Sheikh-Hassani, Massomeh
   Morin, Martin
   Komati, Hiba
   Nemer, Mona
TI Novel Exons in the Tbx5 Gene Locus Generate Protein Isoforms with
   Distinct Expression Domains and Function
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HOLT-ORAM-SYNDROME; TRANSCRIPTION FACTOR; NUCLEAR-LOCALIZATION;
   MUTATIONS; GATA4; DIFFERENTIATION; HEART; CARDIOGENESIS; MORPHOGENESIS;
   NKX2-5
AB TBX5 is the gene mutated in Holt-Oran syndrome, an autosomal dominant disorder with complex heart and limb deformities. Its protein product is a member of the T-box family of transcription factors and an evolutionarily conserved dosage-sensitive regulator of heart and limb development. Understanding TBX5 regulation is therefore of paramount importance. Here we uncover the existence of novel exons and provide evidence that TBX5 activity may be extensively regulated through alternative splicing to produce protein isoforms with differing N- and C-terminal domains. These isoforms are also present in human heart, indicative of an evolutionarily conserved regulatory mechanism. The newly identified isoforms have different transcriptional properties and can antagonize TBX5a target gene activation. Droplet Digital PCI1 as well as immunohistochemistry with isoform-specific antibodies reveal differential as well as overlapping expression domains. In particular, we find that the predominant isoform in skeletal myoblasts is Tbx5c, and we show that it is dramatically up-regulated in differentiating myotubes and is essential for myotube formation. Mechanistically, TBX5c antagonizes TBX5a activation of pro-proliferative signals such as IGF-1, FGF-10, and BMP4. The results provide new insight into Tbx5 regulation and function that will further our understanding of its role in health and disease. The finding of new exons in the Tbx5 locus may also be relevant to mutational screening especially in the 30% of Holt-Oram syndrome patients with no mutations in the known TBX5a exons.
C1 [Yamak, Abir; Sheikh-Hassani, Massomeh; Komati, Hiba; Nemer, Mona] Univ Ottawa, Dept Biochem Microbiol & Immunol, Lab Mol Genet & Cardiac Regenerat, Ottawa, ON K1N 6N5, Canada.
   [Georges, Romain O.; Morin, Martin; Nemer, Mona] Univ Montreal, Inst Rech Clin Montreal, Grad Program Mol Biol, Montreal, PQ H2W 1R7, Canada.
C3 University of Ottawa; Institut de Recherche Clinique de Montreal (IRCM);
   Universite de Montreal
RP Nemer, M (corresponding author), Univ Ottawa, 550 Cumberland,Rm 246, Ottawa, ON K1N 6N5, Canada.
EM mona.nemer@uottawa.ca
FU Canadian Heart and Stroke Foundation; McCain Foundation
FX This work was supported by a grant from the Canadian Heart and Stroke
   Foundation and the McCain Foundation.
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NR 31
TC 7
Z9 8
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAR 13
PY 2015
VL 290
IS 11
BP 6844
EP 6856
DI 10.1074/jbc.M114.634451
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA CD3PP
UT WOS:000350991500020
PM 25623069
OA hybrid, Green Published
DA 2025-04-10
ER

PT J
AU Rogers, HT
   Melby, JA
   Ehlers, LE
   Fischer, MS
   Larson, EJ
   Gao, Z
   Rossler, KJ
   Wang, DJ
   Alpert, AJ
   Ge, Y
AF Rogers, Holden T.
   Melby, Jake A.
   Ehlers, Lauren E.
   Fischer, Matthew S.
   Larson, Eli J.
   Gao, Zhan
   Rossler, Kalina J.
   Wang, Daojing
   Alpert, Andrew J.
   Ge, Ying
TI Small-Scale Serial Size Exclusion Chromatography (s<SUP>3</SUP>SEC) for
   High Sensitivity Top-Down Proteomics of Large Proteoforms
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID PROTEINS; SDS
AB Top-down-mass spectrometry (MS)-based proteomics has emerged as a premier technology to examine proteins at the proteoform level, enabling characterization of genetic mutations, alternative splicing, and post-translational modifications. However, significant challenges that remain in top-down proteomics include the analysis of large proteoforms and the sensitivity required to examine proteoforms from minimal amounts of sample. To address these challenges, we have developed a new method termed "small-scale serial Size Exclusion Chromatography" (s(3)SEC), which incorporates a small-scale protein extraction (1 mg of tissue) and serial SEC without postfractionation sample handling, coupled with online high sensitivity capillary reversed-phase liquid chromatography tandem MS (RPLC-MS/MS) for analysis of large proteoforms. The s(3)SEC-RPLC-MS/MS method significantly enhanced the sensitivity and reduced the proteome complexity across the fractions, enabling the detection of high MW proteoforms previously undetected in one-dimensional (1D)-RPLC analysis. Importantly, we observed a drastic improvement in the signal intensity of high MW proteoforms in early fractions when using the s(3)SEC-RPLC method. Moreover, we demonstrate that this s(3)SEC-RPLC-MS/MS method also allows the analysis of lower MW proteoforms in subsequent fractions without significant alteration in proteoform abundance and equivalent or improved fragmentation efficiency to that of the 1D-RPLC approach. Although this study focuses on the use of cardiac tissue, the s(3)SEC-RPLC-MS/MS method could be broadly applicable to other systems with limited sample inputs.
C1 [Rogers, Holden T.; Melby, Jake A.; Ehlers, Lauren E.; Fischer, Matthew S.; Larson, Eli J.; Ge, Ying] Univ Wisconsin, Dept Chem, Madison, WI 53706 USA.
   [Gao, Zhan; Rossler, Kalina J.; Ge, Ying] Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI 53705 USA.
   [Wang, Daojing] Newomics Inc, Berkeley, CA 94710 USA.
   [Alpert, Andrew J.] PolyLC Inc, Columbia, MD 21045 USA.
   [Ge, Ying] Univ Wisconsin, Sch Med & Publ Hlth, Human Prote Program, Madison, WI 53705 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison
RP Ge, Y (corresponding author), Univ Wisconsin, Dept Chem, Madison, WI 53706 USA.; Ge, Y (corresponding author), Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI 53705 USA.; Ge, Y (corresponding author), Univ Wisconsin, Sch Med & Publ Hlth, Human Prote Program, Madison, WI 53705 USA.
EM ying.ge@wisc.edu
OI Melby, Jake/0000-0003-1499-9508; Ehlers, Lauren/0009-0004-8156-1973;
   Fischer, Matthew/0009-0005-7713-8205; Larson, Eli/0000-0002-1354-0722;
   Rogers, Holden/0000-0003-0870-0127
FU , National Institutes of Health [R01 GM125085, R01 HL096971, S10
   OD018475]; NIH [T32 HL007936-20, T32 HL007936-21]; Training Program in
   Translational Cardiovascular Science [DGE-1747503]; National Science
   Foundation Graduate Research Fellowship Program; Graduate School; Office
   of the Vice Chancellor for Research and Graduate Education at the
   University of Wisconsin-Madison - Wisconsin Alumni Research Foundation
FX This research is supported by NIH R01 HL109810-06 (Y.G.). Y.G. would
   like to acknowledge NIH R01 GM125085, R01 HL096971, and S10 OD018475.
   J.A.M. acknowledges the support from the Training Program in
   Translational Cardiovascular Science, T32 HL007936-20 and T32
   HL007936-21, for funding during the duration of this project. K.J.R.
   acknowledges the National Science Foundation Graduate Research
   Fellowship Program under Grant No. DGE-1747503 and the Graduate School
   and the Office of the Vice Chancellor for Research and Graduate
   Education at the University of Wisconsin-Madison, funded by Wisconsin
   Alumni Research Foundation. Graphics in Figure 1 and the TOC/Abstract
   were created with clipart from BioRender.com.
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NR 31
TC 3
Z9 4
U1 3
U2 19
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
EI 1520-6882
J9 ANAL CHEM
JI Anal. Chem.
PD FEB 5
PY 2024
VL 96
IS 7
BP 2748
EP 2753
DI 10.1021/acs.analchem.3c05733
EA FEB 2024
PG 6
WC Chemistry, Analytical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA JL8B7
UT WOS:001163328600001
PM 38315630
DA 2025-04-10
ER

PT J
AU Rajaratinam, H
   Mokhtar, NF
   Asma-Abdullah, N
   Fuad, WEM
AF Rajaratinam, Harishini
   Mokhtar, Noor Fatmawati
   Asma-Abdullah, Nurul
   Fuad, Wan Ezumi Mohd
TI Discovering the Triad between Nav1.5, Breast Cancer, and the Immune
   System: A Fundamental Review and Future Perspectives
SO BIOMOLECULES
LA English
DT Review
DE SCN5A; Nav1; 5; neonatal Nav1; immune system; breast cancer;
   immunotherapy
ID GATED SODIUM-CHANNEL; TUMOR-INFILTRATING LYMPHOCYTES;
   EPITHELIAL-MESENCHYMAL TRANSITION; ADOPTIVE CELLULAR THERAPY; SIGNALING
   PATHWAY; GENE-EXPRESSION; CLASS-I; DIFFERENTIAL EXPRESSION;
   ESTROGEN-RECEPTOR; S3-S4 LINKER
AB Nav1.5 is one of the nine voltage-gated sodium channel-alpha subunit (VGSC-alpha) family members. The Nav1.5 channel typically carries an inward sodium ion current that depolarises the membrane potential during the upstroke of the cardiac action potential. The neonatal isoform of Nav1.5, nNav1.5, is produced via VGSC-alpha alternative splicing. nNav1.5 is known to potentiate breast cancer metastasis. Despite their well-known biological functions, the immunological perspectives of these channels are poorly explored. The current review has attempted to summarise the triad between Nav1.5 (nNav1.5), breast cancer, and the immune system. To date, there is no such review available that encompasses these three components as most reviews focus on the molecular and pharmacological prospects of Nav1.5. This review is divided into three major subsections: (1) the review highlights the roles of Nav1.5 and nNav1.5 in potentiating the progression of breast cancer, (2) focuses on the general connection between breast cancer and the immune system, and finally (3) the review emphasises the involvements of Nav1.5 and nNav1.5 in the functionality of the immune system and the immunogenicity. Compared to the other subsections, section three is pretty unexploited; it would be interesting to study this subsection as it completes the triad.
C1 [Rajaratinam, Harishini; Asma-Abdullah, Nurul; Fuad, Wan Ezumi Mohd] Univ Sains Malaysia USM, Sch Hlth Sci, Hlth Campus, Kubang Kerian 16150, Kelantan, Malaysia.
   [Mokhtar, Noor Fatmawati] Univ Sains Malaysia USM, Inst Res Mol Med INFORMM, Hlth Campus, Kubang Kerian 16150, Kelantan, Malaysia.
C3 Universiti Sains Malaysia; Universiti Sains Malaysia
RP Fuad, WEM (corresponding author), Univ Sains Malaysia USM, Sch Hlth Sci, Hlth Campus, Kubang Kerian 16150, Kelantan, Malaysia.
EM harishinir@student.usm.my; fatmawati@usm.my; nurulasma@usm.my;
   wanezumi@usm.my
RI Rajaratinam, Harishini/KIL-1971-2024; Mokhtar, Noor/GLU-2437-2022;
   nurul, asma/AAK-7939-2021
OI Rajaratinam, Harishini/0000-0002-8012-1624; Mokhtar, Noor
   Fatmawati/0000-0003-0349-4096; Nurul, Asma Abdullah/0000-0003-1180-8809
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NR 176
TC 4
Z9 4
U1 1
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD FEB
PY 2022
VL 12
IS 2
AR 310
DI 10.3390/biom12020310
PG 29
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA ZR4WP
UT WOS:000767785500001
PM 35204811
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Chen, P
   Zhang, K
   Zhou, B
   Zhang, Z
   Song, YP
   Pu, Y
   Yang, Y
   Zhang, YY
   Zhou, R
   Wang, T
   Zhang, L
AF Chen, Peng
   Zhang, Kui
   Zhou, Bin
   Zhang, Zhu
   Song, Yaping
   Pu, Yan
   Yang, Yan
   Zhang, Yanyan
   Zhou, Rong
   Wang, Tao
   Zhang, Lin
TI The variations in the IL1RL1 gene and susceptibility to
   preeclampsia
SO IMMUNOLOGICAL INVESTIGATIONS
LA English
DT Article
DE Association; IL1RL1; preeclampsia; polymorphisms
ID SOLUBLE ST2 PROTEIN; IL-33; PREGNANCY; INTERLEUKIN-33; IDENTIFICATION;
   POLYMORPHISMS; HYPERTENSION; PATHOGENESIS; INFLAMMATION; EXPRESSION
AB The IL1RL1, which encodes at least three isoforms by alternative splicing, has been identified to be involved in the initiation and perpetuation of inflammation. In spite of being a main contributor of maternal and perinatal mortality, the mechanism responsible for the pathophysiology of preeclampsia has not yet been well addressed. To investigate the relationship between IL1RL1 polymorphisms and preeclampsia risk, we identified the correlation between three tag SNPs (rs13017455, rs1420103 and rs17027006) in IL1RL1 with preeclampsia risk in a case-control study. A total of 214 cases and 208 controls were recruited to participate in this study. Genotypes of the three SNPs were determined with the use of polymerase chain reaction-restriction fragment length polymorphism assay. Significantly reduced preeclampsia risk was found to be associated with the CT genotype of rs13017455 (p = 0. 032, OR = 0. 66, 95% CI = 0.45-0.97) in overdominant model. Differences were particularly significant in the severe preeclampsia subgroup (p = 0.045, OR = 0.66, 95% CI = 0.44-0.99) and the early-onset severe preeclampsia subgroup (p = 0.0097, OR = 0.47, 95% CI = 0.26-0.84). Significantly increased mild preeclampsia risk was observed associated with GG genotype of rs1420103 polymorphisms (p = 0.029, OR = 2.18, 95% CI = 1.09-4.34), while reducing late-onset severe preeclampsia susceptibility was associated with TT genotype of rs1420103 (p = 0.02, OR = 0.49, 95% CI = 0.26-0.92).
C1 [Chen, Peng; Zhang, Kui; Pu, Yan; Yang, Yan; Zhang, Lin] Sichuan Univ, Dept Forens Biol, West China Sch Preclin & Forens Med, Chengdu 610041, Peoples R China.
   [Zhou, Bin; Song, Yaping; Wang, Tao; Zhang, Lin] Sichuan Univ, West China Inst Women & Childrens Hlth,Minist Edu, Lab Mol Translat Med,West China Univ Hosp 2, Key Lab Obstetr & Gynecol & Pediat Dis & Birth De, Chengdu 610041, Peoples R China.
   [Zhang, Zhu; Zhang, Yanyan; Zhou, Rong] Sichuan Univ, West China Second Univ Hosp, Dept Obstet & Gynecol, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Zhang, L (corresponding author), Sichuan Univ, Dept Forens Biol, West China Sch Preclin & Forens Med, Chengdu 610041, Peoples R China.
EM zhanglin@scu.edu.cn
RI chen, peng/HMD-1278-2023; ZHANG, LIN/GYD-9123-2022
OI Chen, Peng/0000-0001-8462-2875
FU National Natural Science Foundation of China [81172440, 81172494,
   81272821]; Science Foundation for The Excellent Youth Scholars of
   Sichuan University [2011SCU04A16]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81172440, No. 81172494 and No. 81272821); and the Science
   Foundation for The Excellent Youth Scholars of Sichuan University (No.
   2011SCU04A16).
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NR 36
TC 7
Z9 9
U1 0
U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0882-0139
EI 1532-4311
J9 IMMUNOL INVEST
JI Immunol. Invest.
PY 2014
VL 43
IS 5
BP 424
EP 435
DI 10.3109/08820139.2013.879173
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AH8NR
UT WOS:000336395300002
PM 24564816
DA 2025-04-10
ER

PT J
AU Abali, S
   Tamura, M
   Turan, S
   Atay, Z
   Isguven, P
   Guran, T
   Haliloglu, B
   Bas, S
   Isojima, T
   Kitanaka, S
   Bereket, A
AF Abali, Saygin
   Tamura, Mayuko
   Turan, Serap
   Atay, Zeynep
   Isguven, Pinar
   Guran, Tulay
   Haliloglu, Belma
   Bas, Serpil
   Isojima, Tsuyoshi
   Kitanaka, Sachiko
   Bereket, Abdullah
TI Hereditary vitamin D-resistant rickets: a report of four cases with two
   novel variants in the VDR gene and successful use of intermittent
   intravenous calcium via a peripheral route
SO JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM
LA English
DT Article
DE calcium; hereditary vitamin D-resistant rickets; VDR gene; vitamin D
   receptor
ID D-DEPENDENT RICKETS; BINDING DOMAIN; MUTATION; HORMONE; SERVER
AB Background: Hereditary vitamin D-resistant rickets (HVDRR) is caused by vitamin D receptor (VDR) defects. Patients with HVDRR do not respond to standard doses of calcitriol and oral calcium (Ca) treatment and need to be treated with intravenous Ca (IV-Ca) via a central route. However, central catheter-related complications can cause significant morbidity.
   Case presentation: Four unrelated patients with HVDRR presenting with rickets and alopecia totalis were administered intermittent IV-Ca treatment (2-5 times/week) through a peripheral route. No complications such as infection, extravasation or arrhythmias were detected upon peripheral infusion. Peripheral 1-22 months'-duration of IV-Ca normalized parathyroid hormone (PTH) and alkaline phosphatase (ALP) in all patients, after which, oral Ca of 200-400 mg/kg/day and calcitriol of 0.5 mu g/kg/day were sufficient to maintain normal PTH levels. Molecular studies on the VDR gene showed a previously reported homozygous c.454C > T (p.Q152*) pathogenic variant in two patients. Two novel homozygous variants in the other two patients were detected: (1) c.756-2A > G, which affects the splice acceptor site, and (2) c.66dupG (p.I23Dfs*20) variant leading to a frameshift that results in a premature stop codon.
   Conclusions: Peripheral IV-Ca treatment is an effective and practical alternative treatment mode that provides dramatic clinical benefit in patients with HVDRR.
C1 [Abali, Saygin; Turan, Serap; Atay, Zeynep; Guran, Tulay; Haliloglu, Belma; Bas, Serpil; Bereket, Abdullah] Marmara Univ, Dept Pediat Endocrinol & Diabet, Sch Med, Dr Faruk Ayanoglu Caddesi 50-11,PC34726, Istanbul, Turkey.
   [Abali, Saygin] Acibadem Mehmet Ali Aydinlar Univ, Dept Pediat, Sch Med, Istanbul, Turkey.
   [Tamura, Mayuko; Isojima, Tsuyoshi; Kitanaka, Sachiko] Univ Tokyo, Dept Pediat, Grad Sch Med, Tokyo, Japan.
   [Isguven, Pinar] Sakarya Univ, Dept Pediat Endocrinol, Sch Med, Sakarya, Turkey.
C3 Marmara University; Acibadem University; University of Tokyo; Sakarya
   University
RP Bereket, A (corresponding author), Marmara Univ, Dept Pediat Endocrinol & Diabet, Sch Med, Dr Faruk Ayanoglu Caddesi 50-11,PC34726, Istanbul, Turkey.
EM abdullahbereket@gmail.com
RI bereket, abdullah/V-3793-2018; Haliloglu, Belma/AGO-1638-2022; ABALI,
   SAYGIN/JAN-7810-2023; Demircioglu, Serap/U-7195-2018; ABALI,
   SAYGIN/T-7809-2017
OI Isojima, Tsuyoshi/0000-0003-0011-0325; Bereket,
   Abdullah/0000-0002-6584-9043; GURAN, TULAY/0000-0003-2658-6866;
   Demircioglu, Serap/0000-0002-5172-5402; Tamura,
   Mayuko/0000-0003-1634-9648; ABALI, SAYGIN/0000-0001-6552-2801
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NR 19
TC 2
Z9 2
U1 1
U2 5
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 0334-018X
EI 2191-0251
J9 J PEDIATR ENDOCR MET
JI J. Pediatr. Endocrinol. Metab.
PD APR
PY 2020
VL 33
IS 4
BP 557
EP 562
DI 10.1515/jpem-2019-0466
PG 6
WC Endocrinology & Metabolism; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Pediatrics
GA LB1NQ
UT WOS:000524402800016
PM 32049653
DA 2025-04-10
ER

PT J
AU Gianfrancesco, F
   Esposito, T
   Casu, G
   Maninchedda, G
   Roberto, R
   Pirastu, M
AF Gianfrancesco, F
   Esposito, T
   Casu, G
   Maninchedda, G
   Roberto, R
   Pirastu, M
TI Emergence of Talanin protein associated with human uric acid
   nephrolithiasis in the Hominidae lineage
SO GENE
LA English
DT Article
DE evolution; primates; uric acid; nephrolithiasis
ID ESSENTIAL-HYPERTENSION; URATE OXIDASE; EVOLUTION; RISK
AB Recently, we identified a susceptibility locus for human uric acid nephrolithiasis (UAN) on 10q21-q22 and demonstrated that a novel gene (ZNF365) included in this region produces through alternative splicing several transcripts coding for four protein isoforms. Mutation analysis showed that one of them (Talanin) is associated with UAN. We examined the evolutionary conservation of ZNF365 gene through a comparative genomic approach. Searching for mouse homologs of ZNF365 transcripts, we identified a highly conserved mouse ortholog of ZNF365A transcript, expressed specifically in brain. We did not found a mouse homolog for ZNF365D transcript encoding the Talanin protein, even if we were able to identify the corresponding genomic region in mouse and rat not yet organized in canonical gene structure suggesting that ZNF365D was originated after the branching of hominoid from rodent lineage. In mouse and in most mammals, a functional uricase degrades the uric acid to allantoin, but uricase activity was lost during the Miocene epoch in hominoids. Searching for the presence of Talanin in Primates, we found a canonical intron-exon structure with several stop codons preventing protein production in Old World and New World monkeys. In humans, we observe expression and we have evidence that ZNF365D transcript produces a functional protein. It seems therefore that ZNF365D transcript emerged during primate evolution from a noncoding genomic sequence that evolved in a standard gene structure and assumed its role in parallel with the disappearance of uricase, probably against a disadvantageous excessive hyperuricemia. (C) 2004 Elsevier B.V. All rights reserved.
C1 CNR, Inst Populat Genet, Alghero, Italy.
   Shardna Life Sci, Cagliari, Italy.
   Univ Bari, Inst Genet, I-70121 Bari, Italy.
C3 Consiglio Nazionale delle Ricerche (CNR); Universita degli Studi di Bari
   Aldo Moro
RP CNR, Ist Sci Alimentaz, 52 A-C, I-83100 Avellino, Italy.
EM fgianfrancesco@isa.cnr.it
RI Esposito, Teresa/AAA-5488-2019; Gianfrancesco, Fernando/P-6853-2014
OI Esposito, Teresa/0000-0002-7879-8441; Gianfrancesco,
   Fernando/0000-0002-3812-2471
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NR 27
TC 8
Z9 13
U1 0
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-1119
EI 1879-0038
J9 GENE
JI Gene
PD SEP 15
PY 2004
VL 339
BP 131
EP 138
DI 10.1016/j.gene.2004.06.030
PG 8
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 858EN
UT WOS:000224173200014
PM 15363853
DA 2025-04-10
ER

PT J
AU He, DN
   Meloche, CA
   Dumas, NA
   Frost, AR
   Falany, CN
AF He, DN
   Meloche, CA
   Dumas, NA
   Frost, AR
   Falany, CN
TI Different subcellular localization of sulphotranse erase 2B1b in human
   placenta and prostate
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE [1,2,6,7-H-3(N)]dehydroepiandrosterone (DHEA); placenta; prostate;
   sulphation; sulphotransferase (SULT); SULT2B1b
ID HYDROXYSTEROID SULFOTRANSFERASE SULT2B1; DEHYDROEPIANDROSTERONE
   SULFOTRANSFERASE; EXPRESSION; CHOLESTEROL; GENE; INTRACRINOLOGY;
   METABOLISM; INDUCE
AB The human hydroxysteroid SULT (sulphotransferase) 2B1 subfamily consists of two isoforms, SULT2B1a and SULT2B1b. These two isoenzymes are transcribed from the same gene by alternative splicing of their first exons and share 94 % amino acid sequence identity. The SULT2B1 isoforms are highly selective for the sulphation of 3beta-hydroxysteroids. Immunoblot analysis of SULT2B1 expression in several human tissues indicates the presence of only SULT2B1b protein. Immunoreactive SULT2B1b protein was detected in human prostate, skin, placenta and lung tissue. SULT2B1b mRNA expression was detected in RNA isolated from term placenta, normal prostate, prostate carcinoma, benign prostate hyperplasia, LNCaP prostate cancer cells, breast cancer specimens and MCF-7 breast cancer cells. Immunohistochemical localization of SULT2B1b, in terms placental and prostate tissues, detected it in nuclei of placental syncytiotrophoblasts and cytoplasm of epithelial cells in prostate tissues. Immunoreactive and catalytically active SULT2B1b was identified in nuclei isolated from term human placenta. Also SULT2B1b was capable of translocating to nuclei in BeWo placental cells after stable transfection and differentiation. In contrast, immunohistochemical analysis of human prostate showed only cytosolic localization of SULT2B1b in the basal and luminal prostate epithelial cells. SULT2B1b was not detected in isolated nuclei from LNCaP prostate cancer cells but was present in the cytosolic fraction. Differential subcellular localization of SULT2B1b in prostate and placenta suggests that SULT2B1b may be differentially regulated and have different physiological functions in these two hormonally responsive human tissues.
C1 Univ Alabama, Dept Pharmacol & Toxicol, Birmingham, AL 35294 USA.
   Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham
RP Univ Alabama, Dept Pharmacol & Toxicol, 1670 Univ Blvd, Birmingham, AL 35294 USA.
EM Charles.Falany@ccc.uab.edu
RI He, Dong/LBH-8540-2024
FU NIGMS NIH HHS [GM38953] Funding Source: Medline
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NR 21
TC 56
Z9 65
U1 0
U2 1
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0264-6021
EI 1470-8728
J9 BIOCHEM J
JI Biochem. J.
PD MAY 1
PY 2004
VL 379
BP 533
EP 540
DI 10.1042/BJ20031524
PN 3
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 822JJ
UT WOS:000221535000003
PM 14741047
OA Green Published
DA 2025-04-10
ER

PT J
AU Isom, LL
AF Isom, LL
TI Sodium channel β subunits:: Anything but auxiliary
SO NEUROSCIENTIST
LA English
DT Review
DE cell adhesion; voltage-gated ion channel; node of Ranvier; cytoskeleton
ID GATED ION CHANNELS; NA+-CHANNEL; RAT-BRAIN; ALPHA-SUBUNIT;
   MESSENGER-RNA; TENASCIN-R; MOLECULAR DETERMINANTS; EXTRACELLULAR DOMAIN;
   ADHESION MOLECULE; ANKYRIN-BINDING
AB Voltage-gated sodium channels are glycoprotein complexes responsible for initiation and propagation of action potentials in excitable cells such as central and peripheral neurons, cardiac and skeletal muscle myocytes, and neuroendocrine cells. Mammalian sodium channels are heterotrimers, composed of a central, pore-forming alpha subunit and two auxiliary beta subunits, The alpha subunits form a gene family with at least 10 members. Mutations in alpha subunit genes have been linked to paroxysmal disorders such as epilepsy, long QT syndrome, and hyperkalemic periodic paralysis in humans, and motor endplate disease and cerebellar ataxia in mice. Three genes encode sodium channel beta subunits with at least one alternative splice product. A mutation in the beta1 subunit gene has been linked to generalized epilepsy with febrile seizures plus type 1 (GEFS + 1) in a human family with this disease. Sodium channel beta subunits are multifunctional, They modulate channel gating and regulate the level of channel expression at the plasma membrane. More recently, they have been shown to function as cell adhesion molecules in terms of interaction with extracellular matrix, regulation of cell migration, cellular aggregation, and interaction with the cytoskeleton, Structure-function studies have resulted in the preliminary assignment of functional domains in the beta1 subunit. A sodium channel signaling complex is proposed that involves beta subunits as channel modulators as well as cell adhesion molecules, other cell adhesion molecules such as neurofascin and contactin, RPTP beta, and extracellular matrix molecules such as tenascin.
C1 Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan
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NR 58
TC 280
Z9 354
U1 0
U2 25
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-8584
J9 NEUROSCIENTIST
JI Neuroscientist
PD FEB
PY 2001
VL 7
IS 1
BP 42
EP 54
DI 10.1177/107385840100700108
PG 13
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 395RD
UT WOS:000166594300013
PM 11486343
DA 2025-04-10
ER

PT J
AU Shimizu, C
   Fuda, H
   Yanai, H
   Strott, CA
AF Shimizu, C
   Fuda, H
   Yanai, H
   Strott, CA
TI Conservation of the hydroxysteroid sulfotransferase SULT2B1 gene
   structure in the mouse:: Pre- and postnatal expression, kinetic analysis
   of isoforms, and comparison with prototypical SULT2A1
SO ENDOCRINOLOGY
LA English
DT Article
ID HUMAN CYTOSOLIC SULFOTRANSFERASES; CHOLESTEROL SULFATE; RAT-BRAIN;
   DEHYDROEPIANDROSTERONE SULFOTRANSFERASE; TISSUE DISTRIBUTION;
   MOLECULAR-CLONING; CRYSTAL-STRUCTURE; FROG BRAIN; NEUROSTEROIDS;
   KERATINOCYTES
AB A novel mouse hydroxysteroid sulfotransferase cDNA has been cloned, and organization of its gene structure has been determined. The new mouse sulfotransferase, SULT2B1a, and its closely related isoform, SULT2B1b, are derived from a single SULT2B1 gene as a result of an alternative exon I and differential splicing. Thus, the only structural distinction between the two SULT2B1 isoforms is at their amino-terminal ends. Importantly, in contrast to the prototypical mouse hydroxysteroid sulfotransferase SULT2A1, the SULT2B1 isoforms have a predilection for cholesterol. Real-time RT-PCR reveals that the SULT2B1a isoform is most abundantly expressed in the brain and spinal cord, whereas SULT2B1b and SULT2A1 are weakly, if at all, expressed in the central nervous system. On the other hand, the SULT2B1b isoform is the most prominent hydroxysteroid sulfotransferase expressed in skin, whereas SULT2A1 is strikingly expressed in the liver. The substrate specificities and differential expression patterns of the three SULT2 isozymes strongly suggest that they have distinct biologic roles to play. Of further interest, the mouse SULT2B1 and SULT2A1 genes are differentially expressed during embryonic development, with the former being expressed at all stages from E8.5-E19, whereas the latter is not expressed until E19. It is speculated that, during embryonic development, SULT2B1b is required for production of cholesterol sulfate essential for normal skin development, whereas SULT2B1a produces pregnenolone sulfate, an essential neurosteroid during development of the central nervous system.
C1 NICHHD, Sect Steroid Regulat Endocrinol & Reprod, Res Branch, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH Eunice Kennedy Shriver
   National Institute of Child Health & Human Development (NICHD)
RP Strott, CA (corresponding author), NICHHD, Sect Steroid Regulat Endocrinol & Reprod, Res Branch, NIH, Bldg 49,Room 6A36, Bethesda, MD 20892 USA.
RI Yanai, Hidekatsu/AFN-9517-2022
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NR 36
TC 54
Z9 70
U1 0
U2 4
PU ENDOCRINE SOC
PI BETHESDA
PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD APR
PY 2003
VL 144
IS 4
BP 1186
EP 1193
DI 10.1210/en.2002-221011
PG 8
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 666QX
UT WOS:000182188900008
PM 12639899
DA 2025-04-10
ER

PT J
AU Zieseniss, A
   Schroeder, U
   Buchmeier, S
   Schoenenberger, CA
   van den Heuvel, J
   Jockusch, BM
   Illenberger, S
AF Zieseniss, Anke
   Schroeder, Ulrich
   Buchmeier, Sabine
   Schoenenberger, Cora-Ann
   van den Heuvel, Joop
   Jockusch, Brigitte M.
   Illenberger, Susanne
TI Raver1 is an integral component of muscle contractile elements
SO CELL AND TISSUE RESEARCH
LA English
DT Article
DE hnRNP; striated muscle; smooth muscle; sarcomere; myofibril; mouse
ID SKELETAL-MUSCLE; GENE-EXPRESSION; STRIATED-MUSCLE; CARDIAC-MUSCLE;
   MESSENGER-RNAS; PROTEIN; CELLS; LOCALIZATION; SARCOMERE; TURNOVER
AB Raver1, a ubiquitously expressed protein, was originally identified as a ligand for metavinculin, the muscle-specific isoform of the microfilament-associated protein vinculin. The protein resides primarily in the nucleus, where it colocalises and may interact with polypyrimidine-tract-binding protein, which is involved in alternative splicing processes. During skeletal muscle differentiation, raver1 translocates to the cytoplasm and eventually targets the Z-line of sarcomeres. Here, it colocalises with metavinculin, vinculin and alpha-actinin, all of which have biochemically been identified as raver1 ligands. To obtain more information about the potential role of raver1 in muscle structure and function, we have investigated its distribution and fine localisation in mouse striated and smooth muscle, by using three monoclonal antibodies that recognise epitopes in different regions of the raver1 protein. Our immunofluorescence and immunoelectron-microscopic results indicate that the cytoplasmic accumulation of raver1 is not confined to skeletal muscle but also occurs in heart and smooth muscle. Unlike vinculin and metavinculin, cytoplasmic raver1 is not restricted to costameres but additionally represents an integral part of the sarcomere. In isolated myofibrils and in ultrathin sections of skeletal muscle, raver1 has been found concentrated at the I-Z-I band. A minor fraction of raver1 is present in the nuclei of all three types of muscle. These data indicate that, during muscle differentiation, raver1 might link gene expression with structural functions of the contractile machinery of muscle.
C1 Tech Univ Carolo Wilhelmina Braunschweig, Inst Zool, Bioctr, D-38092 Braunschweig, Germany.
   Univ Basel, Biozentrum, Maurice E Mueller Inst Struct Biol, CH-4056 Basel, Switzerland.
   Helmholtz Ctr Infect Res, Div Struct Biol, D-38124 Braunschweig, Germany.
   Univ Arizona, Dept Cell Biol & Anat, Tucson, AZ 85724 USA.
C3 Braunschweig University of Technology; University of Basel; Helmholtz
   Association; Helmholtz-Center for Infection Research; University of
   Arizona
RP Illenberger, S (corresponding author), Tech Univ Carolo Wilhelmina Braunschweig, Inst Zool, Bioctr, Spielmann Str 7, D-38092 Braunschweig, Germany.
EM S.Illenberger@tu-bs.de
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NR 34
TC 13
Z9 14
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013 USA
SN 0302-766X
J9 CELL TISSUE RES
JI Cell Tissue Res.
PD MAR
PY 2007
VL 327
IS 3
BP 583
EP 594
DI 10.1007/s00441-006-0322-1
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 134NW
UT WOS:000244091100015
PM 17096167
DA 2025-04-10
ER

PT J
AU Li, J
   Harata-Lee, Y
   Denton, MD
   Feng, QJ
   Rathjen, JR
   Qu, ZP
   Adelson, DL
AF Li, Jun
   Harata-Lee, Yuka
   Denton, Matthew D.
   Feng, Qianjin
   Rathjen, Judith R.
   Qu, Zhipeng
   Adelson, David L.
TI Long read reference genome-free reconstruction of a full-length
   transcriptome from Astragalus membranaceus reveals transcript
   variants involved in bioactive compound biosynthesis
SO CELL DISCOVERY
LA English
DT Article
DE Astragalus membranaceus; transcriptome; Iso-Seq; biosynthesis;
   alternative splicing
ID VAR. MONGHOLICUS; RNA-SEQ; SEQUENCE; CALYCOSIN-7-O-BETA-D-GLUCOSIDE;
   CALYCOSIN; GENE; ACCUMULATION; ANNOTATION; EXPRESSION; ACCURACY
AB Astragalus membranaceus, also known as Huangqi in China, is one of the most widely used medicinal herbs in Traditional Chinese Medicine. Traditional Chinese Medicine formulations from Astragalus membranaceus have been used to treat a wide range of illnesses, such as cardiovascular disease, type 2 diabetes, nephritis and cancers. Pharmacological studies have shown that immunomodulating, anti-hyperglycemic, anti-inflammatory, antioxidant and antiviral activities exist in the extract of Astragalus membranaceus. Therefore, characterising the biosynthesis of bioactive compounds in Astragalus membranaceus, such as Astragalosides, Calycosin and Calycosin-7-O-beta-D-glucoside, is of particular importance for further genetic studies of Astragalus membranaceus. In this study, we reconstructed the Astragalus membranaceus full-length transcriptomes from leaf and root tissues using PacBio Iso-Seq long reads. We identified 27 975 and 22 343 full-length unique transcript models in each tissue respectively. Compared with previous studies that used short read sequencing, our reconstructed transcripts are longer, and are more likely to be full-length and include numerous transcript variants. Moreover, we also re-characterised and identified potential transcript variants of genes involved in Astragalosides, Calycosin and Calycosin-7-O-beta-D-glucoside biosynthesis. In conclusion, our study provides a practical pipeline to characterise the full-length transcriptome for species without a reference genome and a useful genomic resource for exploring the biosynthesis of active compounds in Astragalus membranaceus.
C1 [Li, Jun; Harata-Lee, Yuka; Qu, Zhipeng; Adelson, David L.] Univ Adelaide, Sch Biol Sci, Dept Genet & Evolut, Adelaide, SA, Australia.
   [Li, Jun; Harata-Lee, Yuka; Qu, Zhipeng; Adelson, David L.] Univ Adelaide, Sch Biol Sci, Zhendong Ctr Mol Basis Tradit Chinese Med, Adelaide, SA, Australia.
   [Denton, Matthew D.; Rathjen, Judith R.] Univ Adelaide, Sch Agr Food & Wine, Adelaide, SA, Australia.
   [Feng, Qianjin] Shanxi Univ Tradit Chinese Med, Shanxi Modern Chinese Med Engn Lab, Taiyuan, Shanxi, Peoples R China.
C3 University of Adelaide; University of Adelaide; University of Adelaide
RP Qu, ZP; Adelson, DL (corresponding author), Univ Adelaide, Sch Biol Sci, Dept Genet & Evolut, Adelaide, SA, Australia.; Qu, ZP; Adelson, DL (corresponding author), Univ Adelaide, Sch Biol Sci, Zhendong Ctr Mol Basis Tradit Chinese Med, Adelaide, SA, Australia.
EM zhipeng.qu@adelaide.edu.au; david.adelson@adelaide.edu.au
RI Denton, Matthew/D-9697-2011; Feng, Qianjin/Y-5438-2019; Adelson,
   David/E-5506-2011
OI Adelson, David/0000-0003-2404-5636; Denton, Matthew/0000-0002-2804-0384;
   Qu, Zhipeng/0000-0002-6841-0773; Li, Jun/0000-0001-9988-9409
FU National Special Program for International S&T Cooperation Projects of
   China [2013DFA30700]; Shanxi Provincial Project of Astragalus Resources
   Industrialisation and Industry Internationalisation Collaborative
   Innovation Center [HQXTCXZX2016-006]; University of Adelaide
FX This research was partly supported by the National Special Program for
   International S&T Cooperation Projects of China (2013DFA30700), the
   Shanxi Provincial Project of Astragalus Resources Industrialisation and
   Industry Internationalisation Collaborative Innovation Center
   (HQXTCXZX2016-006), and The University of Adelaide.
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NR 39
TC 86
Z9 95
U1 1
U2 69
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2056-5968
J9 CELL DISCOV
JI Cell Discov.
PD AUG 29
PY 2017
VL 3
AR 17031
DI 10.1038/celldisc.2017.31
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FM3RZ
UT WOS:000414926300001
PM 28861277
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Liu, T
   Kamiyoshi, A
   Sakurai, T
   Ichikawa-Shindo, Y
   Kawate, H
   Yang, L
   Tanaka, M
   Xian, X
   Imai, A
   Zhai, LY
   Hirabayashi, K
   Dai, K
   Tanimura, K
   Liu, T
   Cui, NQ
   Igarashi, K
   Yamauchi, A
   Shindo, T
AF Liu, Tian
   Kamiyoshi, Akiko
   Sakurai, Takayuki
   Ichikawa-Shindo, Yuka
   Kawate, Hisaka
   Yang, Lei
   Tanaka, Megumu
   Xian, Xian
   Imai, Akira
   Zhai, Liuyu
   Hirabayashi, Kazutaka
   Dai, Kun
   Tanimura, Keiya
   Liu, Teng
   Cui, Nanqi
   Igarashi, Kyoko
   Yamauchi, Akihiro
   Shindo, Takayuki
TI Endogenous Calcitonin Gene-Related Peptide Regulates Lipid Metabolism
   and Energy Homeostasis in Male Mice
SO ENDOCRINOLOGY
LA English
DT Article
ID DIET-INDUCED OBESITY; CGRP; RATS; RECEPTORS; PATHOPHYSIOLOGY;
   STREPTOZOTOCIN; NEUROPEPTIDES; VASODILATOR; RESISTANCE; PHYSIOLOGY
AB Calcitonin gene-related peptide (CGRP) is a bioactive peptide produced by alternative splicing of the primary transcript of the calcitonin/CGRP gene. CGRP is largely distributed in the cardiovascular and nervous systems, where it acts as a regulatory factor. CGRP is also expressed in organs and tissues involved in metabolic regulation, including white adipose tissue (WAT), where its function is largely unknown. In this study, we examined the effects of endogenous CGRP on metabolic function. When we administered a high-fat diet to CGRP-specific knockout (CGRP(-/-)) and wild-type (WT) mice for 10 weeks, we observed that food intake did not differ between the two groups, but body weight and visceral fat weight were significantly lower in CGRP(-/-) mice. Fatty liver changes were less severe in CGRP(-/-) mice, which also showed lower serum insulin and leptin levels. Glucose tolerance and insulin sensitivity were better in CGRP(-/-) than WT mice, and expired gas analysis revealed greater oxygen consumption by CGRP(-/-) mice. Adipocyte hypertrophy was suppressed in CGRP(-/-) mice, while expression of beta-3-adrenergic receptor, hormone-sensitive lipase and adiponectin was enhanced. Isoproterenol-induced glycerol release from WAT was higher in CGRP(-/-) than WT mice, and CGRP(-/-) mice showed elevated sympathetic nervous activity. beta-receptor-blockade canceled the beneficial effects of CGRP deletion on obesity. These results suggest that, in addition to its actions in the cardiovascular system, endogenous CGRP is a key regulator of metabolism and energy homeostasis in vivo.
C1 [Liu, Tian; Kamiyoshi, Akiko; Sakurai, Takayuki; Ichikawa-Shindo, Yuka; Kawate, Hisaka; Yang, Lei; Tanaka, Megumu; Xian, Xian; Imai, Akira; Zhai, Liuyu; Hirabayashi, Kazutaka; Dai, Kun; Tanimura, Keiya; Liu, Teng; Cui, Nanqi; Shindo, Takayuki] Shinshu Univ, Dept Cardiovasc Res, Grad Sch Med, Asahi 3-1-1, Matsumoto, Nagano 3908621, Japan.
   [Igarashi, Kyoko; Yamauchi, Akihiro] Japan Bio Prod Co Ltd, Tokyo 1510063, Japan.
C3 Shinshu University
RP Kamiyoshi, A (corresponding author), Shinshu Univ, Dept Cardiovasc Res, Grad Sch Med, Asahi 3-1-1, Matsumoto, Nagano 3908621, Japan.
EM organregen@shinshu-u.ac.jp
RI Xian, Xunde/B-9490-2012
OI Hirabayashi, Kazutaka/0000-0002-1342-6700; Sakurai,
   Takayuki/0000-0002-7220-5940
FU Core Research for Evolutionary Science and Technology of Japan Science
   and Technology Agency; Japan Agency for Medical Research and
   Development; Public Trust Fund for Clinical Cancer Research; Mitsui Life
   Social Welfare Foundation; Takeda Science Foundation research grant;
   Opto-Science and Technology research grant; Takeda Medical Research
   Foundation; Elderly Eye Disease Research Foundation; Novartis Foundation
   for Gerontological Research grant; Cosmetology Research Foundation;
   SENSHIN Medical Research Foundation; Kanzawa Medical Research
   Foundation; Ono Medical Research Foundation; Nagao Memorial Fund;
   Nakatomi Foundation; Japan Vascular Disease Research Foundation;
   YOKOYAMA Foundation for Clinical Pharmacology; Banyu Life Science
   Foundation International; National Cardiovascular Center research grant
   for cardiovascular diseases; Grants-in-Aid for Scientific Research
   [17K09296, 26293085, 17K08588, 16K08545, 16H00679, 26293183] Funding
   Source: KAKEN
FX This study was supported by the Grants-in-Aid for Scientific Research
   (KAKENHI) program, the Core Research for Evolutionary Science and
   Technology of Japan Science and Technology Agency and the Japan Agency
   for Medical Research and Development, a National Cardiovascular Center
   research grant for cardiovascular diseases, grants-in-aid of The Public
   Trust Fund for Clinical Cancer Research, the Mitsui Life Social Welfare
   Foundation, a Takeda Science Foundation research grant, an Opto-Science
   and Technology research grant, a Takeda Medical Research Foundation
   grant, an Elderly Eye Disease Research Foundation grant, a Novartis
   Foundation for Gerontological Research grant, a research grant from the
   Cosmetology Research Foundation, the SENSHIN Medical Research
   Foundation, the Kanzawa Medical Research Foundation, the Ono Medical
   Research Foundation, the Nagao Memorial Fund, the Nakatomi Foundation,
   the Japan Vascular Disease Research Foundation, the YOKOYAMA Foundation
   for Clinical Pharmacology, and Banyu Life Science Foundation
   International.
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NR 37
TC 31
Z9 37
U1 1
U2 6
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD MAY
PY 2017
VL 158
IS 5
BP 1194
EP 1206
DI 10.1210/en.2016-1510
PG 13
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA EW9IC
UT WOS:000402830700017
PM 28324021
OA Bronze, Green Submitted
DA 2025-04-10
ER

PT J
AU Lu, QL
   Rabinowitz, A
   Chen, YC
   Yokota, T
   Yin, HF
   Alter, J
   Jadoon, A
   Bou-Gharios, G
   Partridge, T
AF Lu, QL
   Rabinowitz, A
   Chen, YC
   Yokota, T
   Yin, HF
   Alter, J
   Jadoon, A
   Bou-Gharios, G
   Partridge, T
TI Systemic delivery of antisense oligoribonucleotide restores dystrophin
   expression in body-wide skeletal muscles
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE exon skipping; muscular dystrophy
ID MUSCULAR-DYSTROPHY; EXON; MODEL; MICE; RNA
AB Antisense oligonucleotide-mediated alternative splicing has great potential for treatment of Duchenne muscular dystrophy (DMD) caused by mutations within nonessential regions of the dystrophin gene. We have recently shown in the dystrophic mdx mouse that exon 23, bearing a nonsense mutation, can be skipped after intramuscular injection of a specific 2'-O-methyl phosphorothioate antisense oligoribonucleotide (20MeAO). This skipping created a shortened, but in-frame, transcript that is translated to produce near-normal levels of dystrophin expression. This expression, in turn, led to improved muscle function. However, because DMD affects muscles body-wide, effective treatment requires dystrophin induction ideally in all muscles. Here, we show that systemic delivery of specific 20MeAOs, together with the triblock copolymer F127, induced dystrophin expression in all skeletal muscles but not in cardiac muscle of the mdx dystrophic mice. The highest dystrophin expression was detected in diaphragm, gastrocnemius, and intercostal muscles. Large numbers of fibers with near-normal level of dystrophin were observed in focal areas. Three injections of 20MeAOs at weekly intervals enhanced the levels of dystrophin. Dystrophin mRNA lacking the targeted exon 23 remained detectable 2 weeks after injection. No evidence of tissue damage was detected after 20MeAO and F127 treatment either by serum analysis or histological examination of liver, kidney, lung, and muscles. The simplicity and safety of the antisense protocol provide a realistic prospect for treatment of the majority of DMD mutations. We conclude that a significant therapeutic effect may be achieved by further optimization in dose and regime of administration of antisense oligonucleotide.
C1 Hammersmith Hosp, MRC, Ctr Clin Sci, London W12 0NN, England.
   Carolinas Med Ctr, Neuromuscular Amyotroph Lateral Sclerosis Ctr, Charlotte, NC 28231 USA.
   Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Ultrasound, Wuhan 430030, Peoples R China.
   Univ London Imperial Coll Sci Technol & Med, Div Med, Dept Renal Med, London W12 0NN, England.
C3 Imperial College London; Carolinas Medical Center; Huazhong University
   of Science & Technology; Imperial College London
RP Hammersmith Hosp, MRC, Ctr Clin Sci, Du Cane Rd, London W12 0NN, England.
EM qi.lu@carolinashealthcare.org
OI yokota, toshifumi/0000-0001-6672-6742; Yokota,
   Toshifumi/0000-0001-7316-3546
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NR 22
TC 325
Z9 384
U1 0
U2 30
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD JAN 4
PY 2005
VL 102
IS 1
BP 198
EP 203
DI 10.1073/pnas.0406700102
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 886HB
UT WOS:000226216400036
PM 15608067
OA Green Published
DA 2025-04-10
ER

PT J
AU Oshima, T
   Okada, N
   Joh, T
   Sasaki, M
   Tada, T
   Matsukawa, N
   Nomura, T
   Ohara, H
   Itoh, M
   Okada, H
AF Oshima, T
   Okada, N
   Joh, T
   Sasaki, M
   Tada, T
   Matsukawa, N
   Nomura, T
   Ohara, H
   Itoh, M
   Okada, H
TI Decay-accelerating factor in guinea pig stomachs following ischemia
   reperfusion stress
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID COMPLEMENT REGULATORY PROTEINS; FACTOR DAF; RESTRICTION FACTOR-20;
   MULTIPLE ISOFORMS; EPITHELIAL-CELLS; MEMBRANE; ERYTHROCYTES; EXPRESSION;
   ACTIVATION; PATHWAYS
AB A complement regulatory protein, decay-accelerating factor (DAF, CD55), is known to protect host tissues from autologous complement activation. DAF is present on the apical side of human gastric epithelial cells, and its expression increases during gastritis. To develop an animal model for analysis of DAF expression on gastric cells, a mAb guinea pig DAF was successfully used. Although DAF expression in the mucosal epithelium of the stomach is weak, as judged by immunohistochemical staining with the mAb, it was temporarily up-regulated at 12 and 24 h, and at 3 days after ischemia reperfusion (I/R) (p < 0.05), The DAF mRNA level in gastric tissues was determined by Northern blot analysis and found to be highest at 6 h after I/R, returning to the baseline at 24 h, Strong DAF mRNA expression was observed in the cytoplasm of cells beneath the eroded tissues 6 h after I/R. In guinea pigs, alternative splicing of DAF mRNA generates both GPI-anchored types and transmembrane types of DAF, RT-PCR analysis revealed that mRNAs of the transmembrane types had become significantly dominant by 6 h after I/R, whereas levels for the GPI-anchored types remained unchanged, In guinea pigs depleted of complement by cobra venom factor treatment, the area of erasion and the up-regulation of DAF expression in gastric epithelial cells after VR were significantly limited compared with the normocomplementemic group, indicating that DAF may be up-regulated by an inflammatory stress.
C1 Nagoya City Univ, Sch Med, Dept Mol Biol, Nagoya, Aichi 4678601, Japan.
   Nagoya City Univ, Sch Med, Dept Internal Med 1, Nagoya, Aichi 4678601, Japan.
   Nagoya City Univ, Sch Med, Dept Pathol, Nagoya, Aichi 4678601, Japan.
   Nagoya City Univ, Sch Med, Dept Internal Med 2, Nagoya, Aichi 4678601, Japan.
   Fukushimura Hosp, Choju Med Inst, Toyohashi, Aichi, Japan.
C3 Nagoya City University; Nagoya City University; Nagoya City University;
   Nagoya City University
RP Nagoya City Univ, Sch Med, Dept Mol Biol, Mizuho Cho, Nagoya, Aichi 4678601, Japan.
EM hiokada@med.nagoya-cu.ac.jp
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NR 30
TC 7
Z9 7
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD JAN 15
PY 2000
VL 164
IS 2
BP 1078
EP 1085
DI 10.4049/jimmunol.164.2.1078
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 273LF
UT WOS:000084708600068
PM 10623859
OA Bronze
DA 2025-04-10
ER

PT J
AU Lok, ZSY
   Lyle, AN
AF Lok, Zoe Shin Yee
   Lyle, Alicia N.
TI Osteopontin in Vascular Disease Friend or Foe?
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE atherosclerosis; cytokines; inflammation; osteopontin; risk factors;
   vascular diseases
ID SMOOTH-MUSCLE-CELLS; POTENTIAL CLINICAL-APPLICATIONS; PLASMA
   OSTEOPONTIN; CROSS-LINKING; ACCELERATED ATHEROSCLEROSIS; CIRCULATING
   OSTEOPONTIN; CARDIOVASCULAR-DISEASE; TERMINAL FRAGMENT;
   DIABETES-MELLITUS; DEFICIENT MICE
AB Inflammatory cytokines are necessary for an acute response to injury and the progressive healing process. However, when this acute response does not resolve and becomes chronic, the same proteins that once promoted healing then contribute to chronic inflammatory pathologies, such as atherosclerosis. OPN (Osteopontin) is a secreted matricellular cytokine that signals through integrin and CD44 receptors, is highly upregulated in acute and chronic inflammatory settings, and has been implicated in physiological and pathophysiologic processes. Evidence from the literature suggests that OPN may fit within the Goldilocks paradigm with respect to cardiovascular disease, where acute increases are protective, attenuate vascular calcification, and promote postischemic neovascularization. In contrast, chronic increases in OPN are clinically associated with an increased risk for a major adverse cardiovascular event, and OPN expression is a strong predictor of cardiovascular disease independent of traditional risk factors. With the recent finding that humans express multiple OPN isoforms as the result of alternative splicing and that these isoforms have distinct biologic functions, future studies are required to determine what OPN isoform(s) are expressed in the setting of vascular disease and what role each of these isoforms plays in vascular disease progression. This review aims to discuss our current understanding of the role(s) of OPN in vascular disease pathologies using evidence from in vitro, animal, and clinical studies. Where possible, we discuss what is known about OPN isoform expression and our understanding of OPN isoform contributions to cardiovascular disease pathologies.
C1 [Lyle, Alicia N.] Emory Univ, Sch Med, Dept Med, Div Cardiol, Atlanta, GA USA.
   [Lok, Zoe Shin Yee] Monash Hlth, Sch Clin Sci, Dept Surg, Clayton, Vic, Australia.
C3 Emory University; Monash Health
RP Lyle, AN (corresponding author), Emory Univ, Sch Med, Div Cardiol, 101 Woodruff Cir,WMB 319D, Atlanta, GA 30322 USA.
EM alicia.lyle@emory.edu
OI Lyle, Alicia/0000-0001-7527-9200
FU National Institutes of Health [K99/R00 HL119567]; Georgia Clinical and
   Translational Science Alliance (Georgia CTSA) pilot award through the
   National Center for Advancing Translational Sciences of the National
   Institutes of Health [UL1TR002378]; Emory University's Department of
   Medicine and Division of Cardiology
FX Supported by National Institutes of Health K99/R00 HL119567 (A.N. Lyle),
   a Georgia Clinical and Translational Science Alliance (Georgia CTSA)
   pilot award (A.N. Lyle) through the National Center for Advancing
   Translational Sciences of the National Institutes of Health under Award
   Number UL1TR002378, and funds from Emory University's Department of
   Medicine and Division of Cardiology (to A.N. Lyle).
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NR 119
TC 142
Z9 152
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1079-5642
EI 1524-4636
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD APR
PY 2019
VL 39
IS 4
BP 613
EP 622
DI 10.1161/ATVBAHA.118.311577
PG 10
WC Hematology; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Cardiovascular System & Cardiology
GA IN7OP
UT WOS:000478872000014
PM 30727754
OA Green Accepted, Bronze
DA 2025-04-10
ER

PT J
AU Iizuka, M
   Nishimura, S
   Wakamori, M
   Akiba, I
   Imoto, K
   Barsoumian, EL
AF Iizuka, M
   Nishimura, S
   Wakamori, M
   Akiba, I
   Imoto, K
   Barsoumian, EL
TI The lethal expression of the GluR2flip/GluR4flip AMPA receptor in HEK293
   cells
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE Ca(2+)influx; desensitization; excitotoxicity; flip/flop isoform; Na+
   overload
ID SELECTIVE GLUTAMATE RECEPTORS; RAT HIPPOCAMPAL CULTURES; NA+-CA2+
   EXCHANGER; MEDIATED EXCITOTOXICITY; KAINATE EXCITOTOXICITY; NEOCORTICAL
   NEURONS; CA1 NEURONS; DESENSITIZATION; ISCHEMIA; DEATH
AB alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) -type glutamate receptors play a critical role in excitotoxicity associated with cerebral hypoxia, ischaemia and other acute brain insults. AMPA receptors are composed of GluR1-GluR4 subunits in homomeric and heteromeric assemblies, forming nonselective cation channels. In addition, each subunit has alternative splice variants, flip and flop forms. Heterologous expression studies showed that the AMPA receptor channels exhibit diverse properties depending on subunit/variant composition. For example, the absence of the GluR2 subunit makes AMPA receptor assemblies Ca2+-permeable. Excitotoxicity induced by activating AMPA receptor channels has been linked to excessive Ca2+ influx through the GluR2-lacking channels. Here we demonstrate that coexpression of the AMPA receptor GluR2flip and GluR4flip subunits exerts a lethal effect on HEK293 cells, whereas no lethal activity is observed in other homomeric or heteromeric combinations of AMPA receptor subunits. Patch clamp recordings and Ca2+ imaging analyses have revealed that this GluR2flip/GluR4flip receptor exhibits a low Ca2+ permeability. This subunit combination, however, showed prolonged Na+ influx following AMPA stimulation, even in the absence of cyclothiazide, which attenuates AMPA receptor desensitization. Furthermore, the GluR2flip/GluR4flip-mediated lethality was potentiated by the interruption of cellular Na+ extrusion mechanisms using ouabain or benzamil. These observations suggest that the GluR2flip/GluR4flip receptor-mediated excitotoxicity is attributed to Na+ overload, but not Ca2+ influx.
C1 Nippon Boehringer Ingelheim Co Ltd, Kawanishi Pharma Res Inst, Dept Mol & Cellular Biol, Kawanishi 6660193, Japan.
   Natl Inst Physiol Sci, Dept Informat Physiol, Okazaki, Aichi 444, Japan.
C3 Boehringer Ingelheim; National Institutes of Natural Sciences (NINS) -
   Japan; National Institute for Physiological Sciences (NIPS)
RP Barsoumian, EL (corresponding author), Nippon Boehringer Ingelheim Co Ltd, Kawanishi Pharma Res Inst, Dept Mol & Cellular Biol, 3-10-1 Yato, Kawanishi 6660193, Japan.
RI Wakamori, Minoru/AAE-2661-2019
OI Wakamori, Minoru/0000-0001-8574-3310; Imoto, Keiji/0000-0002-2861-5985
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NR 37
TC 9
Z9 14
U1 0
U2 4
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD NOV
PY 2000
VL 12
IS 11
BP 3900
EP 3908
DI 10.1046/j.1460-9568.2000.00270.x
PG 9
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 378XD
UT WOS:000165609900009
PM 11069585
DA 2025-04-10
ER

PT J
AU Tajbakhsh, A
   Hayat, SMG
   Butler, AE
   Sahebkar, A
AF Tajbakhsh, Amir
   Hayat, Seyed Mohammad Gheibi
   Butler, Alexandra E.
   Sahebkar, Amirhossein
TI Effect of soluble cleavage products of important receptors/ligands on
   efferocytosis: Their role in inflammatory, autoimmune and cardiovascular
   disease
SO AGEING RESEARCH REVIEWS
LA English
DT Article
DE Ectodomain cleavage; Shedding; Target therapy; Atherosclerosis;
   Metalloproteinase; Pharmacological effects
ID GLYCATION END-PRODUCTS; RECEPTOR TYROSINE KINASE; PLASMINOGEN-ACTIVATOR
   RECEPTOR; LIPOPOLYSACCHARIDE-BINDING-PROTEIN; HEMOGLOBIN SCAVENGER
   RECEPTOR; MEMBRANE ATTACK COMPLEX; CELL-ADHESION MOLECULE; APOPTOTIC
   CELLS; UROKINASE RECEPTOR; UP-REGULATION
AB Efferocytosis, the clearance of apoptotic cells (ACs), is a physiologic, multifaceted and dynamic process and a fundamental mechanism for the preservation of tissue homeostasis by avoiding unwanted inflammation and autoimmune responses through special phagocytic receptors. Defective efferocytosis is associated with several disease states, including cardiovascular disease and impaired immune surveillance, as occurs in cancer and autoimmune disease. A major cause of defective efferocytosis is non-functionality of surface receptors on either the phagocytic cells or the ACs, such as TAM family tyrosine kinase, which turns to a soluble form by cleavage/shedding or alternative splicing. Recently, soluble forms have featured prominently as potential biomarkers, indicative of prognosis and enabling targeted therapy using several commonly employed drugs and inhibitors, such as bleomycin, dexamethasone, statins and some matrix metalloproteinase inhibitors such as TAPI-1 and BB3103. Importantly, to design drug carriers with enhanced circulatory durability, the adaptation of soluble forms of physiological receptors/ligands has been purported. Research has shown that soluble forms are more effective than antibody forms in enabling targeted treatment of certain conditions, such as autoimmune diseases. In this review, we sought to summarize the current knowledge of these soluble products, how they are generated, their interactions, roles, and their potential use as biomarkers in prognosis and treatment related to inflammatory, cardiovascular, and autoimmune diseases.
C1 [Tajbakhsh, Amir] Mashhad Univ Med Sci, Sch Med, Dept Modern Sci & Technol, Mashhad, Iran.
   [Hayat, Seyed Mohammad Gheibi] Shahid Sadoughi Univ Med Sci, Sch Med, Dept Genet, Yazd, Iran.
   [Butler, Alexandra E.] Qatar Biomed Res Inst, Diabet Res Ctr, Doha, Qatar.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Iran.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Iran.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Iran.
C3 Mashhad University of Medical Sciences; Qatar Foundation (QF); Hamad Bin
   Khalifa University-Qatar; Qatar Biomedical Research Institute (QBRI);
   Mashhad University of Medical Sciences; Mashhad University of Medical
   Sciences; Mashhad University of Medical Sciences
RP Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Biotechnol Res Ctr, Mashhad 9177948564, Iran.
EM sahebkara@mums.ac.ir
RI Sahebkar, Amirhossein/B-5124-2018; Gheibihayat, Seyed
   Mohammad/T-7187-2017; Tajbakhsh, Amir/AAB-1925-2019; Tajbakhsh,
   Amir/HMV-4969-2023; Gheibihayat, Seyed Mohammad/H-9394-2016
OI Butler, Alexandra/0000-0002-5762-3917; Tajbakhsh,
   Amir/0000-0002-2311-6554; Gheibihayat, Seyed
   Mohammad/0000-0002-1378-118X
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NR 204
TC 42
Z9 43
U1 0
U2 8
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 1568-1637
EI 1872-9649
J9 AGEING RES REV
JI Ageing Res. Rev.
PD MAR
PY 2019
VL 50
BP 43
EP 57
DI 10.1016/j.arr.2019.01.007
PG 15
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA HP1CC
UT WOS:000461402000005
PM 30639340
DA 2025-04-10
ER

PT J
AU La Sala, L
   Micheloni, S
   De Nigris, V
   Prattichizzo, F
   Ceriello, A
AF La Sala, Lucia
   Micheloni, Stefano
   De Nigris, Valeria
   Prattichizzo, Francesco
   Ceriello, Antonio
TI Novel insights into the regulation of miRNA transcriptional control:
   implications for T2D and related complications
SO ACTA DIABETOLOGICA
LA English
DT Review
DE MicroRNAs; Epigenetics; Diabetes and complications
ID DNA METHYLATION; EPIGENETIC REGULATION; MICRORNA EXPRESSION; KAPPA-B;
   INSULIN; GLUCOSE; CELLS; IDENTIFICATION; ASSOCIATION; BIOGENESIS
AB In recent years, epigenetics has emerged as an important form of biological regulation involving chromatin control of gene expression. The mechanisms of this fine-tuned regulation are susceptible to changes forced by environmental stimuli and nutritional factors and may be potentially reversible. Dysregulation of epigenetic processes has important consequences for the pathogenesis of complex and multifactorial diseases such as type 2 diabetes (T2D) and vascular complications. Along with DNA methylation (DNA-me), histone modifications and RNA-based mechanisms as the major epigenetic controllers, small non-coding RNAs known as microRNAs (miRNAs) have their own important implications for the pathogenesis of diabetes. There is increasing evidence supporting the role of miRNAs in modulating gene expression, cumulatively contributing to epigenetic gene silencing by acting either on the methylation status of the cells or in alternative roles. Although significant progress has been made in the characterization of miRNA functions, most miRNA promoters have not yet been characterized, and the transcriptional regulation of miRNAs remains elusive. The present work is centred on the new biological insights pertaining to the epigenetics-miRNA regulatory axis, focusing on the development of T2D and cardiovascular complications, and the ability of these mechanisms to interact in a network of DNA-me regulation. The genomic organization of inter-and intragenic miRNA genes is discussed, and the mutual connections between pre-mRNA splicing and miRNA biogenesis are summarized, along with the discovery of novel miRNA transcriptional regulation sites.
C1 [La Sala, Lucia; Micheloni, Stefano; Prattichizzo, Francesco; Ceriello, Antonio] IRCCS MultiMed, Dept Cardiovasc & Dysmetabol Dis, Via Fantoli 16-15, I-20138 Milan, MI, Italy.
   [De Nigris, Valeria; Ceriello, Antonio] Hosp Clin Barcelona, Inst Invest Biomed August Pi & Sunyer IDIBAPS, Barcelona, Spain.
   [De Nigris, Valeria; Ceriello, Antonio] Hosp Clin Barcelona, Ctr Invest Biomed Red Diabet & Enfermedades Metab, Barcelona, Spain.
C3 IRCCS Multimedica; University of Barcelona; Hospital Clinic de
   Barcelona; IDIBAPS; CIBER - Centro de Investigacion Biomedica en Red;
   CIBERDEM; University of Barcelona; Hospital Clinic de Barcelona
RP La Sala, L (corresponding author), IRCCS MultiMed, Dept Cardiovasc & Dysmetabol Dis, Via Fantoli 16-15, I-20138 Milan, MI, Italy.
EM lucia.lasala@multimedica.it
RI La Sala, Lucia/A-4467-2019; Ceriello, Antonio/J-9575-2016; Prattichizzo,
   Francesco/J-3046-2018; La Sala, Lucia/Q-9969-2016
OI Prattichizzo, Francesco/0000-0002-2959-2658; La Sala,
   Lucia/0000-0002-7580-1377
FU Fondazione Invernizzi, Milan (Italy); European Foundation of the Study
   of Diabetes EFSD/Sanofi programme 2017
FX The authors would like to thank Fondazione Invernizzi, Milan (Italy),
   and European Foundation of the Study of Diabetes EFSD/Sanofi programme
   2017 (to L.L.S.) for the support.
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NR 70
TC 16
Z9 16
U1 1
U2 8
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 0940-5429
EI 1432-5233
J9 ACTA DIABETOL
JI Acta Diabetol.
PD OCT
PY 2018
VL 55
IS 10
BP 989
EP 998
DI 10.1007/s00592-018-1149-4
PG 10
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA GU5VK
UT WOS:000445362800001
PM 29732466
DA 2025-04-10
ER

PT J
AU Zhang, JT
   Li, YY
   Qi, J
   Yu, XF
   Ren, HH
   Zhao, XJ
   Xin, W
   He, SY
   Zheng, XD
   Ma, C
   Zhang, LX
   Wu, BX
   Zhu, DL
AF Zhang, Junting
   Li, Yiying
   Qi, Jing
   Yu, Xiufeng
   Ren, Huanhuan
   Zhao, Xijuan
   Xin, Wei
   He, Siyu
   Zheng, Xiaodong
   Ma, Cui
   Zhang, Lixin
   Wu, Bingxiang
   Zhu, Daling
TI Circ-calm4 Serves as an miR-337-3p Sponge to Regulate
   Myo10 (Myosin 10) and Promote Pulmonary Artery Smooth Muscle
   Proliferation
SO HYPERTENSION
LA English
DT Article
DE animals; hypertension; pulmonary; hypoxia; mice; myocytes; smooth muscle
ID MOLECULAR-MECHANISMS; CIRCULAR RNA; CELLS; HYPOXIA; GROWTH;
   DIFFERENTIATION; HYPERTENSION; MODULATE; ABUNDANT
AB Pulmonary artery smooth muscle cell proliferation is the pathological basis of pulmonary vascular remodeling in hypoxic pulmonary hypertension. Recent studies suggest that circular RNA (circRNA) can regulate various biological processes, including cell proliferation. Therefore, it is possible that circRNA may have important roles in pulmonary artery smooth muscle cell proliferation in hypoxic pulmonary hypertension. In the present study, we aimed to identify functional circRNAs and clarify their roles and mechanisms in pulmonary artery smooth muscle cell proliferation in pulmonary hypertension. RNA sequencing identified 67 circRNAs that were differentially expressed in hypoxic lung tissues of mice. Screening by bioinformatics and quantitative polymerase chain reaction revealed significant elevation of a circRNA derived from alternative splicing of the calmodulin 4 gene (designated circ-calm4). Notably, this circRNA absorbed miR-337-3p. We further identified Myo10 (myosin 10) as a target protein of miR-337-3p. miR-337-3p bound to the 3 '-untranslated region of Myo10 mRNA, thereby attenuating the translation of Myo10. Using loss-of-function and gain-of-function approaches, we found that circ-calm4 regulated cell proliferation by regulating the cell cycle. Additionally, we verified the functions of miR-337-3p and Myo10 in hypoxic pulmonary artery smooth muscle. Our results suggested that the circ-calm4/miR-337-3p/Myo10 signal transduction axis modulated the proliferation of pulmonary artery smooth muscle cells at the molecular level, thus establishing potential targets for the early diagnosis and treatment of pulmonary hypertension.
C1 [Zhang, Junting; Zhao, Xijuan; Ma, Cui; Zhang, Lixin; Zhu, Daling] Harbin Med Univ Daqing, Coll Pharm, Coll Med Lab Sci & Technol, Daqing, Heilongjiang, Peoples R China.
   [Zhang, Junting; Li, Yiying; Qi, Jing; Ren, Huanhuan; Xin, Wei; He, Siyu; Zhu, Daling] Harbin Med Univ Daqing, Coll Pharm, Dept Pharmacol, Daqing, Heilongjiang, Peoples R China.
   [Zhang, Junting; Li, Yiying; Qi, Jing; Yu, Xiufeng; Ren, Huanhuan; Zhao, Xijuan; Xin, Wei; He, Siyu; Zheng, Xiaodong; Ma, Cui; Zhang, Lixin; Zhu, Daling] Harbin Med Univ Daqing, Cent Lab, Daqing, Heilongjiang, Peoples R China.
   [Zhang, Junting; Li, Yiying; Qi, Jing; Yu, Xiufeng; Ren, Huanhuan; Zhao, Xijuan; Xin, Wei; He, Siyu; Zheng, Xiaodong; Ma, Cui; Zhang, Lixin; Zhu, Daling] Harbin Med Univ, Minist Educ, Coll Pharm, Harbin, Peoples R China.
   [Zhu, Daling] Harbin Med Univ, Minist Educ, Key Lab Cardiovasc Med Res, Harbin, Peoples R China.
   [Wu, Bingxiang] Harbin Med Univ, Affiliated Hosp 2, Dept Cardiovasc Med, Harbin, Peoples R China.
   [Zhu, Daling] State Prov Key Labs Biomed Pharmaceut, Prov Key Labs Biomed Pharmaceut, Harbin, Peoples R China.
C3 Harbin Medical University; Harbin Medical University; Harbin Medical
   University; Harbin Medical University; Harbin Medical University; Harbin
   Medical University
RP Zhu, DL (corresponding author), Harbin Med Univ Daqing, Coll Pharm, Xinyang Rd, Daqing 163319, Heilongjiang, Peoples R China.
EM dalingz@yahoo.com
RI zhao, xi/HJY-6017-2023; Zheng, Xiaodong/AAA-4379-2019; Zhang,
   Junting/JVZ-9163-2024
OI daling, Zhu/0000-0001-9763-9772; Zheng, Xiaodong/0000-0002-6103-9836
FU National Natural Science Foundation of China [31820103007, 31771276,
   31471095, 81873412, 81800047, 31500936, 81570041, 81870043]
FX This work was supported by the National Natural Science Foundation of
   China (contract grant No. 31820103007, 31771276, and 31471095 to D. Zhu;
   81873412 to C. Ma; 81800047 to X. Yu; 31500936 to X. Zheng; and 81570041
   and 81870043 to B. Wu).
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NR 45
TC 56
Z9 58
U1 1
U2 27
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0194-911X
EI 1524-4563
J9 HYPERTENSION
JI Hypertension
PD MAR
PY 2020
VL 75
IS 3
BP 668
EP 679
DI 10.1161/HYPERTENSIONAHA.119.13715
PG 12
WC Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA LH5NP
UT WOS:000528832000014
PM 32008463
OA Bronze
DA 2025-04-10
ER

PT J
AU Ile, KE
   Davis, W
   Boyd, JT
   Soulika, AM
   Tew, KD
AF Ile, KE
   Davis, W
   Boyd, JT
   Soulika, AM
   Tew, KD
TI Identification of a novel first exon of the human ABCA2 transporter gene
   encoding a unique N-terminus
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
LA English
DT Article
DE ABC transporter; alternative exon; lysosome; estramustine; drug
   resistance
ID BINDING CASSETTE; MESSENGER-RNAS; PROMOTER REGION; CARCINOMA-CELLS;
   SUBFAMILY-A; ESTRAMUSTINE; CLONING; CHOLESTEROL; REGULATOR; ATP
AB The human ABCA2 transporter is a member of a large family of ATP-binding proteins that transport a variety of molecules across biological membranes. Using RNA ligation-mediated PCR (RLM-PCR), we have identified a novel first exon, which we designate 1B that is located 699 bp upstream of the previously characterized first exon, which we designate 1A. These first exons are alternatively spliced to the second exon of the ABCA2 transcript resulting in a protein that has a unique amino terminus. For exon 1B, the new amino terminus encoded by the first exon is 52 amino acids and for exon 1A, 22 amino acids. We observed that among adult tissues examined, the highest expression of the 1B isoform was in peripheral blood leukocytes (PBL). Laser scanning confocal microscopy revealed that the 1A isoform and the 1B isoform co-localize with lysosome-associated membrane proteins-1 and -2 (LAMP-1 and -2). Cytotoxicity assays suggested a role for ABCA2 in estramustine and estradiol resistance, and overexpression of ABCA2 is seen in an estramustine-resistant prostate carcinoma line. Since both isoforms of the ABCA2 transporter have identical subcellular localization and both are overexpressed in a resistant cell line, we propose that they are also functionally redundant. It is likely that expression of ABCA2 by two independent promoters constitutes locus of regulation controlling expression of the protein to meet requirements in different tissues. (C) 2004 Elsevier B.V. All rights reserved.
C1 Fox Chase Canc Ctr, Dept Pharmacol, Philadelphia, PA 19111 USA.
C3 Fox Chase Cancer Center
RP Fox Chase Canc Ctr, Dept Pharmacol, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM KD_Tew@fccc.edu
FU NCI NIH HHS [CA75266, CA883778, CA06927] Funding Source: Medline
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NR 42
TC 24
Z9 24
U1 0
U2 4
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0167-4781
J9 BBA-GENE STRUCT EXPR
JI Biochim. Biophys. Acta-Gene Struct. Expression
PD APR 16
PY 2004
VL 1678
IS 1
BP 22
EP 32
DI 10.1016/j.bbaexp.2004.01.007
PG 11
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 813ZM
UT WOS:000220945000004
PM 15093135
DA 2025-04-10
ER

PT J
AU Miggin, SM
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AF Miggin, SM
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TI Expression and tissue distribution of the mRNAs encoding the human
   thromboxane A2 receptor (TP) α and β isoforms
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
LA English
DT Article
DE thromboxane A(2); receptor; thromboxane A(2) receptor(alpha);
   thromboxane A(2) receptor(beta); isoform; gene expression
ID VASCULAR SMOOTH-MUSCLE; PROSTANOID FP RECEPTOR; C-TERMINAL TAIL; CDNA
   CLONING; EP3 SUBTYPE; REGULATED EXPRESSION; HUMAN PLATELETS; 2 ISOFORMS;
   IN-VIVO; PROSTAGLANDIN
AB The human thromboxane A(2) receptor (TP), a G protein-coupled receptor, exists as two isoforms, TPalpha and TPbeta, which arise by alternative mRNA splicing and differ exclusively in their carboxyl terminal cytoplasmic regions. In this study, a reverse transcriptase-polymerase chain reaction (RT-PCR)-based strategy was developed to examine the expression of the Tps in tissues of physiologic relevance to TXA(2). Although most of the 17 different cell/tissue types examined expressed both TP isoforms, the liver hepatoblastoma HepG2 cell line was found to exclusively express TPalpha mRNA. In most cell types, TPalpha mRNA predominated over TPbeta mRNA. Moreover, although the levels of TPalpha mRNA expression were similar in most of the cell/tissue types examined, extensive differences in the levels of TPbeta mRNA were observed. Consequently, the relative expression of TPalpha: TPbeta mRNA varied considerably due to extensive differences in TPbeta mRNA expression. Mast strikingly, primary HUVECs were found to express: (i) low levels of TPbeta and (ii) approximately 6-fold greater levels of TPalpha than TPbeta. These data were confirmed in the spontaneously transformed HUVEC derived ECV304 cell line. Expression of TP mRNAs in the various tissue/cells correlated with protein expression, as assessed by radioligand binding using the selective TP antagonist [H-3]SQ29,548. (C) 1998 Elsevier Science B.V. All rights reserved.
C1 Natl Univ Ireland Univ Coll Dublin, Dept Biochem, Dublin 4, Ireland.
C3 University College Dublin
RP Kinsella, BT (corresponding author), Natl Univ Ireland Univ Coll Dublin, Dept Biochem, Merville House, Dublin 4, Ireland.
EM therese.kinsella@ucd.ie
OI Miggin, Sinead/0000-0002-3421-3552; Kinsella, B.
   Therese/0000-0003-3072-941X
FU Wellcome Trust Funding Source: Medline
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NR 68
TC 106
Z9 119
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-4165
J9 BBA-GEN SUBJECTS
JI Biochim. Biophys. Acta-Gen. Subj.
PD NOV 27
PY 1998
VL 1425
IS 3
BP 543
EP 559
DI 10.1016/S0304-4165(98)00109-3
PG 17
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 152MR
UT WOS:000077781800011
PM 9838218
OA Green Accepted, Green Submitted
DA 2025-04-10
ER

PT J
AU Tutakhel, OAZ
   Jelén, S
   Valdez-Flores, M
   Dimke, H
   Piersma, SR
   Jimenez, CR
   Deinum, J
   Lenders, JW
   Hoenderop, JGJ
   Bindels, RJM
AF Tutakhel, Omar A. Z.
   Jelen, Sabina
   Valdez-Flores, Marco
   Dimke, Henrik
   Piersma, Sander R.
   Jimenez, Connie R.
   Deinum, Jaap
   Lenders, Jacques W.
   Hoenderop, Joost G. J.
   Bindels, Rene J. M.
TI Alternative splice variant of the thiazide-sensitive NaCl cotransporter:
   a novel player in renal salt handling
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE hypertension; WNK4; aldosterone-sensitive distal part of the nephron;
   sodium; kidney
ID NA+-CL-COTRANSPORTER; SODIUM-CHLORIDE COTRANSPORTER; ANGIOTENSIN-II;
   DIETARY SALT; PHOSPHORYLATION; HYPERTENSION; PROTEIN; VASOPRESSIN;
   MUTATIONS; ALDOSTERONE
AB The thiazide-sensitive NaCl cotransporter (NCC) is an important pharmacological target in the treatment of hypertension. The human SLC12A3 gene, encoding NCC, gives rise to three isoforms. Only the third isoform has been extensively investigated. The aim of the present study was, therefore, to establish the abundance and localization of the almost identical isoforms 1 and 2 (NCC1/2) in the human kidney and to determine their functional properties and regulation in physiological conditions. Immunohistochemical analysis of NCC1/2 in the human kidney revealed that NCC1/2 localizes to the apical plasma membrane of the distal convoluted tubule. Importantly, NCC1/2 mRNA constitutes similar to 44% of all NCC isoforms in the human kidney. Functional analysis performed in the Xenopus laevis oocyte revealed that thiazide-sensitive Na-22(+) transport of NCC1 was significantly increased compared with NCC3. Mimicking a constitutively active phosphorylation site at residue 811 (S811D) in NCC1 further augmented Na+ transport, while a nonphosphorylatable variant (S811A) of NCC1 prevented this enhanced response. Analysis of human urinary exosomes demonstrated that water loading in human subjects significantly reduces the abundance of NCC1/2 in urinary exosomes. The present study highlights that previously underrepresented NCC1/2 is a fully functional thiazide-sensitive NaCl-transporting protein. Being significantly expressed in the kidney, it may constitute a unique route of renal NaCl reabsorption and could, therefore, play an important role in blood pressure regulation.
C1 [Tutakhel, Omar A. Z.; Jelen, Sabina; Valdez-Flores, Marco; Hoenderop, Joost G. J.; Bindels, Rene J. M.] Radboud Univ Nijmegen, Med Ctr, Dept Physiol, Nijmegen, Netherlands.
   [Deinum, Jaap; Lenders, Jacques W.] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, Nijmegen, Netherlands.
   [Dimke, Henrik] Univ Southern Denmark, Dept Cardiovasc & Renal Res, Odense, Denmark.
   [Lenders, Jacques W.] Tech Univ, Univ Hosp Carl Gustav Carus, Dept Med 3, Dresden, Germany.
   [Piersma, Sander R.; Jimenez, Connie R.] Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, OncoProte Lab, Amsterdam, Netherlands.
C3 Radboud University Nijmegen; Radboud University Nijmegen; University of
   Southern Denmark; Technische Universitat Dresden; Carl Gustav Carus
   University Hospital; Vrije Universiteit Amsterdam
RP Bindels, RJM (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Physiol 286, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM rene.bindels@radboudumc.nl
RI Hoenderop, Joost/H-8047-2014; Flores, Marco/AAG-8838-2020; Deinum,
   J./L-4261-2015; Bindels, René/B-9824-2013; Lenders, J.W.M./L-4487-2015;
   Jimenez, Connie/AAI-3763-2020; Tutakhel, Omar/AAW-6591-2021; Dimke,
   Henrik/M-3319-2019; Dimke, Henrik/G-7970-2011
OI Dimke, Henrik/0000-0002-9170-2168; Jimenez, Connie R/0000-0002-3103-4508
FU European Society of Hypertension; the Netherlands, Organization for
   Scientific Research [VENI ZonMw 916.12.046]; Dutch Kidney Foundation
   [PHD12.14]; European Union [305608]; Novo Nordisk Foundation [11749];
   Carlsberg Foundation [2013_01_0214]
FX This study was supported by the European Society of Hypertension
   (2011-2013 Fellowship), the Netherlands, Organization for Scientific
   Research (VENI ZonMw 916.12.046), the Dutch Kidney Foundation (PHD12.14)
   and the European Union's Seventh Framework Programme (FP7/2007-2013)
   under grant agreement no. 305608 (EURenOmics). H. Dimke is funded by the
   Novo Nordisk Foundation (11749) and the Carlsberg Foundation
   (2013_01_0214).
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NR 49
TC 21
Z9 24
U1 0
U2 8
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
EI 1522-1466
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD FEB 1
PY 2016
VL 310
IS 3
BP F204
EP F216
DI 10.1152/ajprenal.00429.2015
PG 13
WC Physiology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology; Urology & Nephrology
GA DC2TU
UT WOS:000369070400002
PM 26561651
OA Green Published
DA 2025-04-10
ER

PT J
AU Feng, GP
   Steinbach, JH
   Sanes, JR
AF Feng, GP
   Steinbach, JH
   Sanes, JR
TI Rapsyn clusters neuronal acetylcholine receptors but is inessential for
   formation of an interneuronal cholinergic synapse
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE acetylcholine receptor knock-out; mouse; postsynaptic; rapsyn; superior
   cervical ganglion; synaptogenesis
ID SUPERIOR CERVICAL-GANGLION; CENTRAL NERVOUS-SYSTEM; FROG CARDIAC
   GANGLION; NICOTINIC RECEPTORS; 43K PROTEIN; POSTSYNAPTIC MEMBRANES;
   CILIARY GANGLION; INITIAL-STAGES; ALPHA-SUBUNIT; BINDING-SITES
AB Nicotinic acetylcholine receptors (AChRs) are clustered at high density in the postsynaptic membranes of skeletal neuromuscular junctions and cholinergic interneuronal synapses. A cytoplasmic protein, rapsyn, is essential for AChR clustering in muscle. Here, we asked whether rapsyn mediates neuronal AChR clustering at cholinergic synapses in a mammalian sympathetic ganglion, the superior cervical ganglion (SCG). Several observations supported this possibility: (1) AChR clusters containing the alpha 3-5 and beta 2 subunits, homologs of the muscle AChR subunits, are present at SCG synapses; (2) rapsyn RNA is readily detectable in the SCG; and (3) expression of recombinant rapsyn in heterologous cells induces aggregation of coexpressed neuronal AChR subunits. However, rapsyn protein was undetectable at ganglionic synaptic sites. Moreover, aggregates of neuronal AChRs induced in heterologous cells by full-length rapsyn remained intracellular, whereas rapsyn-induced clusters of muscle AChRs reached the cell surface. Additional studies revealed a second rapsyn RNA species in SCG generated by alternative splicing and competent to encode a novel short rapsyn isoform. However, this isoform clustered neither neuronal nor muscle AChRs in heterologous cells. Most telling, the number, size, and density of AChR clusters in SCG did not differ significantly between neonatal mice bearing a targeted mutation of the rapsyn gene and littermate controls. Thus, rapsyn is dispensable for clustering of ganglionic neuronal nicotinic AChRs.
C1 Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA.
   Washington Univ, Sch Med, Dept Anesthesiol, St Louis, MO 63110 USA.
C3 Washington University (WUSTL); Washington University (WUSTL)
RP Washington Univ, Sch Med, Dept Anat & Neurobiol, 660 S Euclid Ave,Box 8108, St Louis, MO 63110 USA.
RI Feng, Guoping/Y-2827-2019
FU NINDS NIH HHS [R01 NS022356] Funding Source: Medline
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NR 57
TC 49
Z9 55
U1 0
U2 1
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD JUN 1
PY 1998
VL 18
IS 11
BP 4166
EP 4176
PG 11
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA ZP487
UT WOS:000073758400017
PM 9592096
DA 2025-04-10
ER

PT J
AU Lancellotti, S
   Rutella, S
   De Filippis, V
   Pozzi, N
   Rocca, B
   De Cristofaro, R
AF Lancellotti, Stefano
   Rutella, Sergio
   De Filippis, Vincenzo
   Pozzi, Nicola
   Rocca, Bianca
   De Cristofaro, Raimondo
TI Fibrinogen-elongated γ Chain Inhibits Thrombin-induced Platelet
   Response, Hindering the Interaction with Different Receptors
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID GLYCOPROTEIN IB-ALPHA; VON-WILLEBRAND-FACTOR; BLOOD-COAGULATION
   PROTEINASES; PEPTIDE CHLOROMETHYL KETONES; II-BINDING INHIBITOR;
   CRYSTAL-STRUCTURE; EXOSITE-II; FRAGMENT-D; MYOCARDIAL-INFARCTION;
   PROTHROMBIN FRAGMENT-2
AB The expression of the elongated fibrinogen gamma chain, termed gamma', derives from alternative splicing of mRNA and causes an insertion sequence of 20 amino acids. This insertion domain interacts with the anion-binding exosite (ABE)-II of thrombin. This study investigated whether and how gamma' chain binding to ABE-II affects thrombin interaction with its platelet receptors, i.e. glycoprotein Ib alpha (GpIb alpha), protease-activated receptor (PAR) 1, and PAR4. Both synthetic gamma' peptide and fibrinogen fragment D*, containing the elongated gamma' chain, inhibited thrombin-induced platelet aggregation up to 70%, with IC50 values of 42 +/- 3.5 and 0.47 +/- 0.03 mu M, respectively. Solid-phase binding and spectrofluorimetric assays showed that both fragment D* and the synthetic gamma' peptide specifically bind to thrombin ABE-II and competitively inhibit the thrombin binding to GpIb alpha with a mean K-i approximate to 0.5 and approximate to 35 mu M, respectively. Both these gamma' chain-containing ligands allosterically inhibited thrombin cleavage of a synthetic PAR1 peptide, of native PAR1 molecules on intact platelets, and of the synthetic chromogenic peptide D-Phe-pipecolyl-Arg-p-nitroanilide. PAR4 cleavage was unaffected. In summary, fibrinogen gamma' chain binds with high affinity to thrombin and inhibits with combined mechanisms the platelet response to thrombin. Thus, its variations in vivo may affect the hemostatic balance in arterial circulation.
C1 [Lancellotti, Stefano; De Cristofaro, Raimondo] Catholic Univ, Sch Med, Haemostasis Res Ctr, Inst Internal Med & Geriatr, I-00168 Rome, Italy.
   [Rutella, Sergio] Catholic Univ, Sch Med, Immunol Lab, Dept Hematol, I-00168 Rome, Italy.
   [De Filippis, Vincenzo; Pozzi, Nicola] Univ Padua, Dept Pharmaceut Sci, I-35131 Padua, Italy.
   [Rocca, Bianca] Catholic Univ, Sch Med, Inst Pharmacol, I-00168 Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   University of Padua; Catholic University of the Sacred Heart; IRCCS
   Policlinico Gemelli
RP De Cristofaro, R (corresponding author), Catholic Univ, Sch Med, Haemostasis Res Ctr, Inst Internal Med & Geriatr, Largo F Vito 1, I-00168 Rome, Italy.
EM rdecristofaro@rm.unicatt.it
RI Pozzi, Nicola/AAE-4910-2020; De Cristofaro, Raimondo/K-3942-2018; rocca,
   bianca/K-3922-2018; Rutella, Sergio/AAF-9187-2020; Lancellotti,
   Stefano/K-3939-2018
OI Pozzi, Nicola/0000-0003-2309-7100; De Cristofaro,
   Raimondo/0000-0002-8066-8849; LANCELLOTTI, Stefano/0000-0002-8090-9040;
   Rutella, Sergio/0000-0003-1970-7375
FU Italian Ministry of University [PRIN-2005]
FX This work was supported by Italian Ministry of University "PRIN-2005."
   The costs of publication of this article were defrayed in part by the
   payment of page charges. This article must therefore be hereby marked
   "advertisement" in accordance with 18 U. S. C. Section 1734 solely to
   indicate this fact.
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NR 61
TC 35
Z9 38
U1 0
U2 8
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 31
PY 2008
VL 283
IS 44
BP 30193
EP 30204
DI 10.1074/jbc.M803659200
PG 12
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 364WS
UT WOS:000260366900064
PM 18779330
OA Green Published, Green Accepted, hybrid
DA 2025-04-10
ER

PT J
AU Schissel, SL
   Schuchman, EH
   Williams, KJ
   Tabas, I
AF Schissel, SL
   Schuchman, EH
   Williams, KJ
   Tabas, I
TI Zn2+-stimulated sphingomyelinase is secreted by many cell types and is a
   product of the acid sphingomyelinase gene
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LOW-DENSITY-LIPOPROTEIN; NIEMANN-PICK DISEASE; MOUSE
   PERITONEAL-MACROPHAGES; NEUTRAL SPHINGOMYELINASE; NUCLEOTIDE-SEQUENCE;
   MISSENSE MUTATION; LYSOSOMAL-ENZYMES; RAT-BRAIN; CHOLESTEROL;
   ACCUMULATION
AB Mammalian sphingomyelinases have been implicated in many important physiological and pathophysiological processes. Although several mammalian sphingomyelinases have been identified and studied, one of these, an acidic Zn2+-stimulated sphingomyelinase (Zn-SMase) originally found in fetal bovine serum, has received little attention since its first and only report 7 years ago. We now show that Zn-SMase activity is secreted by human and murine macrophages, human skin fibroblasts, microglial cells, and several other cells in culture and is markedly up-regulated during differentiation of human monocytes to macrophages. Remarkably, peritoneal macrophages from mice in which the acid SMase gene had been disrupted by homologous recombination secreted no Zn-SMase activity, indicating that this enzyme and the intracellular lysosomal SMase, which is Zn-independent, arise from the same gene, Furthermore, skin fibroblasts from patients with types A and B Niemann-Pick disease, which are known to lack lysosomal SMase activity, also lack Zn-SMase activity in their conditioned media. Chinese hamster ovary cells stably transfected with a cDNA encoding lysosomal SMase massively overexpress both cellular lysosomal SMase and secreted Zn-SMase activities. Thus, Zn-SMase arises independently of alternative splicing, suggesting a post-translational process. In summary, a wide variety of cell types secrete Zn-SMase activity, which arises from the same gene as lysosomal SMase. This secreted enzyme may play roles in physiological and pathophysiological processes involving extracellular sphingomyelin hydrolysis.
C1 COLUMBIA UNIV, DEPT MED, NEW YORK, NY 10032 USA.
   COLUMBIA UNIV, DEPT ANAT & CELL BIOL, NEW YORK, NY 10032 USA.
   CUNY MT SINAI SCH MED, DEPT HUMAN GENET, NEW YORK, NY 10029 USA.
   THOMAS JEFFERSON UNIV, DIV ENDOCRINOL DIABET & METAB DIS, DORRANCE H HAMILTON RES LABS, PHILADELPHIA, PA 19107 USA.
C3 Columbia University; Columbia University; City University of New York
   (CUNY) System; Icahn School of Medicine at Mount Sinai; Thomas Jefferson
   University
RI Williams, Kevin Jon/ISA-4589-2023
OI Williams, Kevin Jon/0000-0002-0000-2159; Tabas, Ira/0000-0003-3429-1515
FU NHLBI NIH HHS [HL39703, HL21006] Funding Source: Medline; NICHD NIH HHS
   [HD28607] Funding Source: Medline
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NR 60
TC 255
Z9 302
U1 0
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD AUG 2
PY 1996
VL 271
IS 31
BP 18431
EP 18436
DI 10.1074/jbc.271.31.18431
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA VB683
UT WOS:A1996VB68300025
PM 8702487
OA hybrid
DA 2025-04-10
ER

PT J
AU Schaffer, LV
   Tucholski, T
   Shortreed, MR
   Ge, Y
   Smith, LM
AF Schaffer, Leah V.
   Tucholski, Trisha
   Shortreed, Michael R.
   Ge, Ying
   Smith, Lloyd M.
TI Intact-Mass Analysis Facilitating the Identification of Large Human
   Heart Proteoforms
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID TOP-DOWN PROTEOMICS; BINDING-PROTEIN-C; PHOSPHORYLATION; ISOFORMS;
   SPECTROMETRY; SOFTWARE; FAMILIES; REVEALS
AB Proteoforms, the primary effectors of biological processes, are the different forms of proteins that arise from molecular processing events such as alternative splicing and post-translational modifications. Heart diseases exhibit changes in proteoform levels, motivating the development of a deeper understanding of the heart proteoform landscape. Our recently developed two-dimensional top-down proteomics platform coupling serial size exclusion chromatography (sSEC) to reversed-phase chromatography (RPC) expanded coverage of the human heart proteome and allowed observation of high molecular weight proteoforms. However, most of these observed proteoforms were not identified due to the difficulty in obtaining quality tandem mass spectrometry (MS2) fragmentation data for large proteoforms from complex biological mixtures on a chromatographic time scale. Herein, we sought to identify human heart proteoforms in this data set using an enhanced version of Proteoform Suite, which identifies proteoforms by intact mass alone. Specifically, we added a new feature to Proteoform Suite to determine candidate identifications for isotopically unresolved proteoforms larger than 50 kDa, enabling subsequent MS2 identification of important high-molecular weight human heart proteoforms such as lamin A (72 kDa) and trifunctional enzyme subunit alpha (79 kDa). With this new workflow for large proteoform identification, endogenous human cardiac myosin binding protein C (140 kDa) was identified for the first time. This study demonstrates the integration of our sSEC-RPC-MS proteomics platform with intact-mass analysis through Proteoform Suite to create a catalog of human heart proteoforms and facilitate the identification of large proteoforms in complex systems.
C1 [Schaffer, Leah V.; Tucholski, Trisha; Shortreed, Michael R.; Ge, Ying; Smith, Lloyd M.] Univ Wisconsin, Dept Chem, Madison, WI 53706 USA.
   [Ge, Ying] Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI 53705 USA.
   [Ge, Ying] Univ Wisconsin, Human Prote Program, Madison, WI 53705 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison
RP Ge, Y; Smith, LM (corresponding author), Univ Wisconsin, Dept Chem, Madison, WI 53706 USA.; Ge, Y (corresponding author), Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI 53705 USA.; Ge, Y (corresponding author), Univ Wisconsin, Human Prote Program, Madison, WI 53705 USA.
EM ge2@wisc.edu; smith@chem.wisc.edu
OI Tucholski, Trisha/0000-0003-1407-6922; Schaffer,
   Leah/0000-0001-6339-9141
FU National Institute of General Medical Sciences of the National
   Institutes of Health (NIH) [R35GM126914, R01HL109810, R01HL096971, R01
   GM125085, S10 OD018475]; NIH Biotechnology Training Program
   [T32GM008349]; NIH Chemistry Biology Interface Training Program
   [T32GM008505]
FX This work was supported by the National Institute of General Medical
   Sciences of the National Institutes of Health (NIH) under Award Number
   R35GM126914 to L.M.S. and R01HL109810, R01HL096971, R01 GM125085, and
   S10 OD018475 to Y.G. L.V.S. was supported by the NIH Biotechnology
   Training Program, T32GM008349. T.T. was supported by the NIH Chemistry
   Biology Interface Training Program, T32GM008505. We thank Yunxiang Dai
   and Emma Schaffer for contributing to our table of contents graphic.
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NR 32
TC 14
Z9 20
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
EI 1520-6882
J9 ANAL CHEM
JI Anal. Chem.
PD SEP 3
PY 2019
VL 91
IS 17
BP 10937
EP 10942
DI 10.1021/acs.analchem.9b02343
PG 6
WC Chemistry, Analytical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA IW0IE
UT WOS:000484644800005
PM 31393705
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Gahete, MD
   Rincón-Fernández, D
   Villa-Osaba, A
   Hormaechea-Agulla, D
   Ibáñez-Costa, A
   Martínez-Fuentes, AJ
   Gracia-Navarro, F
   Castaño, JP
   Luque, RM
AF Gahete, Manuel D.
   Rincon-Fernandez, David
   Villa-Osaba, Alicia
   Hormaechea-Agulla, Daniel
   Ibanez-Costa, Alejandro
   Martinez-Fuentes, Antonio J.
   Gracia-Navarro, Francisco
   Castano, Justo P.
   Luque, Raul M.
TI Ghrelin gene products, receptors, and GOAT enzyme: biological and
   pathophysiological insight
SO JOURNAL OF ENDOCRINOLOGY
LA English
DT Review
DE ghrelin; ghrelin gene splice variants; obestatin; GHSR; GOAT; endocrine
   actions; pathophysiology
ID HORMONE-SECRETAGOGUE RECEPTOR; PITUITARY-ADRENAL AXIS; DES-ACYL GHRELIN;
   GHRELIN/MOTILIN-RELATED PEPTIDE; GONADOTROPIN-RELEASING-HORMONE; INDUCED
   INSULIN-RESISTANCE; ACTIVATED PROTEIN-KINASE; GASTRIC-ACID-SECRETION;
   O-ACYLTRANSFERASE GOAT; PANCREATIC BETA-CELLS
AB Ghrelin is a 28-amino acid acylated hormone, highly expressed in the stomach, which binds to its cognate receptor (GHSR1a) to regulate a plethora of relevant biological processes, including food intake, energy balance, hormonal secretions, learning, inflammation, etc. However, ghrelin is, in fact, the most notorious component of a complex, intricate regulatory system comprised of a growing number of alternative peptides (e. g. obestatin, unacylated ghrelin, and In1-ghrelin, etc.), known (GHSRs) and, necessarily unknown receptors, as well as modifying enzymes (e. g. ghrelin-O-acyl-transferase), which interact among them as well as with other regulatory systems in order to tightly modulate key (patho)-physiological processes. This multiplicity of functions and versatility of the ghrelin system arise from a dual, genetic and functional, complexity. Importantly, a growing body of evidence suggests that dysregulation in some of the components of the ghrelin system can lead to or influence the development and/or progression of highly concerning pathologies such as endocrine-related tumors, inflammatory/cardiovascular diseases, and neurodegeneration, wherein these altered components could be used as diagnostic, prognostic, or therapeutic targets. In this context, the aim of this review is to integrate and comprehensively analyze the multiple components and functions of the ghrelin system described to date in order to define and understand its biological and (patho)-physiological significance.
C1 [Luque, Raul M.] Univ Cordoba, Dept Cell Biol Physiol & Immunol, Cordoba 14014, Spain.
   Univ Cordoba, Inst Maimonides Invest Biomed Cordoba IMIBIC, Cordoba 14014, Spain.
   Reina Sofia Univ Hosp, Cordoba, Spain.
   CIBER Fisiopatol Obesidad & Nutr CIBERobn, Cordoba, Spain.
C3 Universidad de Cordoba; Universidad de Cordoba; Hospital Universitario
   Reina Sofia - Cordoba; CIBER - Centro de Investigacion Biomedica en Red;
   CIBEROBN
RP Luque, RM (corresponding author), Univ Cordoba, Dept Cell Biol Physiol & Immunol, Campus Univ Rabanales,Edificio Severo Ochoa C6,Pl, Cordoba 14014, Spain.
EM raul.luque@uco.es
RI Rincon Fernandez Pacheco, David/ABH-7915-2020; Martinez-Fuentes,
   Antonio/F-8198-2016; Raul, Luque/M-6948-2018; Gahete, Manuel
   D./C-4969-2009; Castano, Justo P/A-7124-2010; Ibanez-Costa,
   Alejandro/L-5323-2013
OI Rincon Fernandez Pacheco, David/0000-0002-6998-4920; Luque, Raul
   M./0000-0002-7585-1913; Gracia Navarro, Francisco/0000-0003-2128-4228;
   Gahete, Manuel D./0000-0002-4578-2179; Martinez Fuentes, Antonio
   Jesus/0000-0003-0994-1037; Castano, Justo P/0000-0002-3145-7287;
   Ibanez-Costa, Alejandro/0000-0003-4649-0095
FU Junta de Andalucia [BIO-0139, CTS-5051, PI-0369-2012]; Ministerio de
   Economia y Competitividad [BFU2008-01136, BFU2010-19300, FPU12/01086];
   FEDER; CIBERobn; Merck Serono Foundation; Instituto de Salud Carlos III
   ('Sara Borrell' program) [CD11/00276]
FX This work has been funded by grants from Junta de Andalucia (BIO-0139,
   CTS-5051 and PI-0369-2012), Ministerio de Economia y Competitividad
   (BFU2008-01136, BFU2010-19300 and FPU12/01086), FEDER, CIBERobn, Merck
   Serono Foundation and Instituto de Salud Carlos III ('Sara Borrell'
   program CD11/00276). CIBER is an initiative of Instituto de Salud Carlos
   III, Ministerio de Sanidad, Servicios Sociales e Igualdad, Spain.
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NR 253
TC 74
Z9 79
U1 1
U2 41
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA STARLING HOUSE, 1600 BRISTOL PARKWAY N, BRISTOL, ENGLAND
SN 0022-0795
EI 1479-6805
J9 J ENDOCRINOL
JI J. Endocrinol.
PD JAN
PY 2014
VL 220
IS 1
BP R1
EP R24
DI 10.1530/JOE-13-0391
PG 24
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 286CI
UT WOS:000329441700001
PM 24194510
OA Bronze
DA 2025-04-10
ER

PT J
AU Xie, J
   Jiang, H
   Wan, YH
   Du, AY
   Guo, KJ
   Liu, T
   Ye, WY
   Niu, X
   Wu, J
   Dong, XQ
   Zhang, XJ
AF Xie, Jing
   Jiang, Hua
   Wan, Yi-Han
   Du, Ai-Ying
   Guo, Kai-Jie
   Liu, Te
   Ye, Wei-Yuan
   Niu, Xin
   Wu, Jun
   Dong, Xiao-Qin
   Zhang, Xue-Jun
TI Induction of a 55 kDa acetylcholinesterase protein during apoptosis and
   its negative regulation by the Akt pathway
SO JOURNAL OF MOLECULAR CELL BIOLOGY
LA English
DT Article
DE acetylcholinesterase; apoptosis; 55 kDa AChE; caspase; PI3K/Akt pathway
ID NONNEURONAL CHOLINERGIC SYSTEM; NEURONAL CELL-DEATH; SURVIVAL SIGNALS;
   EXPRESSION; CANCER; ACHE; PHOSPHORYLATION; CHOLINESTERASES; INHIBITION;
   NEUROLIGIN
AB Acetylcholinesterase (AChE) is emerging as an important contributor to apoptosis in various cell types. However, overexpression of AChE does not initiate apoptosis, and cells which express AChE at basal levels grow normally, suggesting that AChE may function differently between normal and apoptotic conditions. In this study, we determined that an AChE-derived protein (similar to 55 kDa) positively correlated with cellular apoptotic levels. The 55 kDa AChE protein was not a result of a novel splice variant of the AChE primary transcript. Instead, it was determined to be a cleaved fragment of the full-length 68 kDa AChE protein that could not be inhibited by cycloheximide (CHX) but could be suppressed by caspase inhibitors in apoptotic PC-12 cells. Furthermore, activation of the Akt cascade abolished the 55 kDa protein, and both AChE protein forms (68 and 55 kDa) accumulated in the nucleus during apoptosis. In a mouse model for ischemia/reperfusion (I/R)-induced acute renal failure, the 55 kDa AChE protein was detected in the impaired organs but not in the normal ones, and its levels correlated with the genotype of the mice. In summary, a 55 kDa AChE protein resulting from the cleavage of 68 kDa AChE is induced during apoptosis, and it is negatively regulated by the Akt pathway. This study suggests that an alternative form of AChE may play a role in apoptosis.
C1 [Xie, Jing; Jiang, Hua; Wan, Yi-Han; Du, Ai-Ying; Guo, Kai-Jie; Ye, Wei-Yuan; Niu, Xin; Wu, Jun; Dong, Xiao-Qin; Zhang, Xue-Jun] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, Shanghai 200031, Peoples R China.
   [Liu, Te] Jiao Tong Univ, Sch Med, Int Peace Matern & Child Care Ctr, Shanghai 200030, Peoples R China.
C3 Chinese Academy of Sciences; Center for Excellence in Molecular Cell
   Science, CAS; Shanghai Jiao Tong University
RP Zhang, XJ (corresponding author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, 320 YueYang Rd, Shanghai 200031, Peoples R China.
EM xjzhang@sibs.ac.cn
RI Wan, Yuan/J-9029-2012
OI Wan, Yihan/0000-0003-4272-0340
FU National Natural Science Foundation of China [30971481, 31071213]; Major
   State Basic Research Development Program of China (973 Program)
   [2007CB947901]; Chinese Academy of Sciences [KSCX2-YW-R-13]
FX This work was supported in part by the grants from the National Natural
   Science Foundation of China (Nos. 30971481 and 31071213), the Major
   State Basic Research Development Program of China (973 Program) (No.
   2007CB947901) and the Third Phase Creative Program of Chinese Academy of
   Sciences (No. KSCX2-YW-R-13).
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NR 38
TC 31
Z9 39
U1 0
U2 17
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1674-2788
J9 J MOL CELL BIOL
JI J. Mol. Cell Biol.
PD AUG
PY 2011
VL 3
IS 4
BP 250
EP 259
DI 10.1093/jmcb/mjq047
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 804AA
UT WOS:000293624000007
PM 21377978
DA 2025-04-10
ER

PT J
AU Chen, MJ
   Chen, Q
   Li, YR
   Yang, ZJ
   Taylor, EW
   Zhao, LJ
AF Chen, Mengjie
   Chen, Qi
   Li, Yirui
   Yang, Zhenjun
   Taylor, Ethan W.
   Zhao, Lijun
TI A G-quadruplex nanoswitch in the SGK1 promoter regulates isoform
   expression by K<SUP>+</SUP>/Na<SUP>+</SUP> balance and resveratrol
   binding
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
LA English
DT Article
DE G4; Salt-sensitive hypertension; Gene expression; Dietary sodium
   guidelines
ID DIETARY POTASSIUM; BLOOD-PRESSURE; HYPERTENSION; SODIUM; SERUM; VARIANT
AB Background: High sodium intake can up-regulate the level of renal serum- and glucocorticoid-inducible kinase-1 (SGK1), which plays a pivotal role in controlling blood pressure via activation of the epithelial sodium channel (ENaC), which can lead to salt-sensitive hypertension. Increased potassium intake, or a vegetarian diet, counteracts salt-sensitive hypertension, but the underlying mechanisms are not fully understood.
   Methods: Bioinformatics and molecular modeling were used to identify G-quadruplex (G4) and their conformations in the SGK1 promoter. CD spectra and UV melting dynamics were measured to study the stability of G4 as influenced by potassium/sodium balance and resveratrol. RT-PCR and Western blot were employed to study the effects of potassium and resveratrol on the SGK1 isoform expression.
   Results: The SGK1 gene encodes a G4 structure in the proximal upstream of promoter-2; the G4 structure is stabilized by potassium or resveratrol, but destabilized by sodium. Super-physiological levels of sodium stimulate the transcription of all SGK1 isoforms, whereas resveratrol or potassium supplementation inhibits the transcription of iso-2 and iso-3, but not iso-1.
   Conclusions: Stabilizing the G4 by potassium or resveratrol induces alternative promoter usage and/or pre-mRNA splicing in the transcription of SGK1.
   General significance: Potassium/sodium ion balance or resveratrol binding can act to regulate G4 molecular switches for controlling SGK1 gene expression, thereby presenting a new avenue for drug development.
C1 [Chen, Mengjie; Chen, Qi; Li, Yirui; Zhao, Lijun] Shaanxi Normal Univ, Coll Life Sci, Key Lab, Minist Educ Med Plant Resource & Nat Pharmaceut C, Xian 710119, Peoples R China.
   [Yang, Zhenjun] Peking Univ, Sch Pharmaceut Sci, Beijing 100083, Peoples R China.
   [Taylor, Ethan W.] Univ North Carolina Greensboro, Dept Chem & Biochem, Greensboro, NC 27402 USA.
C3 Shaanxi Normal University; Peking University; University of North
   Carolina; University of North Carolina Greensboro
RP Zhao, LJ (corresponding author), Shaanxi Normal Univ, Coll Life Sci, Key Lab, Minist Educ Med Plant Resource & Nat Pharmaceut C, Xian 710119, Peoples R China.
EM ewtaylor@uncg.edu; Zhaolijun@snnu.edu.cn
RI Taylor, Ethan/HLW-2118-2023
FU National Natural Science Foundation of China (NSFC) [81272257, 31170855]
FX This work was supported by grants from National Natural Science
   Foundation of China (NSFC) (No. 81272257 and No.31170855) to Lijun Zhao,
   and by an unrestricted gift to Ethan W. Taylor from the Dr. Arthur and
   Bonnie Ennis Foundation, Decatur, IL, USA.
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NR 44
TC 6
Z9 6
U1 0
U2 34
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0304-4165
EI 1872-8006
J9 BBA-GEN SUBJECTS
JI Biochim. Biophys. Acta-Gen. Subj.
PD FEB
PY 2021
VL 1865
IS 2
AR 129778
DI 10.1016/j.bbagen.2020.129778
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA PG9QY
UT WOS:000600062100004
PM 33144140
DA 2025-04-10
ER

PT J
AU Cox, RH
AF Cox, RH
TI Molecular determinants of voltage-gated potassium currents in vascular
   smooth muscle
SO CELL BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Review
DE vascular smooth muscle cell (VSMC); voltage-gated K+ channels (K-v);
   Ca2+ channels
ID RECTIFIER K+ CURRENT; SPONTANEOUSLY HYPERTENSIVE-RATS; CHANNEL
   ALPHA-SUBUNIT; PROTEIN-KINASE-C; SMALL MESENTERIC-ARTERIES;
   MAMMALIAN-CELL LINES; PULMONARY-ARTERY; BETA-SUBUNIT; CORONARY-ARTERY;
   ANGIOTENSIN-II
AB Voltage-gated K+ channels (K-v) play an important role in regulating contraction of vascular smooth muscle cells (VSMC) through their effects on membrane potential and on voltage-gated Ca2+ channel activity. K-v channels are tetrameric structures consisting of four identical or closely related pore-forming alpha subunits that may be associated with accessory subunits. More than 30 different gene products that contribute to K-v channel complexes have been identified to date, some of which are subject to alternative splicing. Consequently, there is an enormous potential diversity in the molecular composition and properties of possible K-v channel complexes. Electrophysiologic measurements of K+ currents in VSMC suggest the presence of multiple K-v channel assemblies including: (1) rapidly inactivating, 4-aninopyridine-sensitive, (2) slowly inactivating, tetraethylammonium-insensitive, and (3) noninactivating, tetraethylammonium-sensitive components. Based on electrophysiological and expression studies, it is likely that the latter two components are represented by a heteromultimeric complex of Kv1.2 with either Kv1.4 or Kv1.5 and a Kv beta 1 subunit, and by at least Kv2.1, respectively. The identity of the first A-type current component, however, is not clear at this time. The relative abundance of these current components appears to vary in VSMC from different anatomical sites, from animals of different ages, and perhaps in VSMC within specific vascular segments. Expression of numerous K-v alpha and beta subunits has been demonstrated in VSMC at both the gene and protein level. However, the number of expressed subunits appears to be much larger than the number of apparent K-v current components. It remains unclear if all of these transcripts are expressed in VSMC or in other cell types in the tissue, or if expression patterns are homogenous or heterogeneous in VSMC at a given site.
C1 Lankenau Inst Med Res, Jefferson Hlth Syst, Wynnewood, PA 19096 USA.
C3 Thomas Jefferson University; Lankenau Medical Center; Lankenau Institute
   for Medical Research
RP Lankenau Inst Med Res, Jefferson Hlth Syst, 100 W Lancaster Ave, Wynnewood, PA 19096 USA.
EM coxr@mlhs.org
OI Cox, Robert/0000-0001-8884-9540
FU NHLBI NIH HHS [HL28476] Funding Source: Medline
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NR 199
TC 74
Z9 100
U1 0
U2 11
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1085-9195
EI 1559-0283
J9 CELL BIOCHEM BIOPHYS
JI Cell Biochem. Biophys.
PY 2005
VL 42
IS 2
BP 167
EP 195
DI 10.1385/CBB:42:2:167
PG 29
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 931MV
UT WOS:000229490300004
PM 15858231
DA 2025-04-10
ER

PT J
AU Chu, X
   Thompson, D
   Yee, LJ
   Sung, LA
AF Chu, X
   Thompson, D
   Yee, LJ
   Sung, LA
TI Genomic organization of mouse and human erythrocyte tropomodulin genes
   encoding the pointed end capping protein for the actin filaments
SO GENE
LA English
DT Article
DE exon; gene family; intron; sanpodo; sequence alignment; tropomyosin
ID TROPOMYOSIN-BINDING PROTEIN; SKELETAL-MUSCLE; CELL FATE; EXPRESSION;
   ISOFORM; IDENTIFICATION; CLONING; LOCALIZATION; MYOFIBRILS; DROSOPHILA
AB Erythrocyte tropomodulin (E-Tmod), a globular protein of 359 residues, is highly expressed in the erythrocyte, heart and skeletal muscle. By binding to the N-terminus of tropomyosin (TM) and actin, E-Tmod blocks the elongation and depolymerization of the actin filaments at the pointed end. In erythrocytes, the E-Tmod/TM complex contributes to the formation of the short actin protofilament, which in turn defines the geometry of the membrane skeleton. In juvenile mice, over-expression of E-Tmod is associated with dilated cardiomyopathy. We have previously cloned the human E-Tmod cDNA, identified its TM-binding region, and mapped its gene to chromosome 9q22. Through genomic library screening and PCR-based genomic walking we have now cloned the mouse E-Tmod gene, whose coding region spans similar to 60 kb containing nine exons and eight introns. The human Tmod gene obtained by PCR has an identical exon-intron organization. In sanpodo, a Tmod homologue in Drosophila, the exon boundaries are also conserved except that exons 2-5 and 6-7 are 'fused' and alternative splicing of two additional 5' exons and the 3' exons may give rise to several sanpodo isoforms. In a Tmod-like gene of C. elegans, exons 2-3 are 'fused', boundaries of exons 1, 7, 8, and 9 are conserved and exon/intron junctions of exons 4, 5 and 6 are shifted by a few residues. Analyses of 15 Tmod members from six species show no insertions or deletions of residues in the region of exons 6 and 7. A 5' rapid amplification of cDNA ends reveals that mouse E-Tmod transcripts obtained from embryonic stem cells, skeletal muscle and heart, but not smooth muscle, contain an additional 86 bp untranslated cDNA sequence further upstream from exon 1. Thus, alternative promoters may provide a possible mechanism For tissue-specific expression and regulation of E-Tmod. This study is the first to report the exon organization of E-Tmod genes, which allows their regulation, manipulation, and disease relevance to be further investigated. (C) 2000 Published by Elsevier Science B.V. All rights reserved.
C1 Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA.
   Univ Calif San Diego, Ctr Genet Mol, La Jolla, CA 92093 USA.
C3 University of California System; University of California San Diego;
   University of California System; University of California San Diego
RP Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA.
EM amysung@bioeng.ucsd.edu
OI Yee, Leland Jonathan/0000-0002-0369-5878
FU NHLBI NIH HHS [HL07089, P01HL43026-6] Funding Source: Medline
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   [No title captured]
NR 37
TC 20
Z9 24
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-1119
EI 1879-0038
J9 GENE
JI Gene
PD OCT 3
PY 2000
VL 256
IS 1-2
BP 271
EP 281
DI 10.1016/S0378-1119(00)00327-9
PG 11
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 371GG
UT WOS:000165170000029
PM 11054557
DA 2025-04-10
ER

PT J
AU Cheng, XY
   Liu, JX
   Asuncion-Chin, M
   Blaskova, E
   Bannister, JP
   Dopico, AM
   Jaggar, JH
AF Cheng, Xiaoyang
   Liu, Jianxi
   Asuncion-Chin, Maria
   Blaskova, Eva
   Bannister, John P.
   Dopico, Alejandro M.
   Jaggar, Jonathan H.
TI A novel CaV1.2 N terminus expressed in smooth muscle cells of
   resistance size arteries modifies channel regulation by auxiliary
   subunits
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SENSITIVE CALCIUM-CHANNEL; BETA-SUBUNIT; FUNCTIONAL EXPRESSION;
   ALPHA(1C) SUBUNIT; CA2+ CHANNELS; SUBCELLULAR-LOCALIZATION;
   LARGE-CONDUCTANCE; BLOOD-PRESSURE; CLONING; HETEROGENEITY
AB Voltage-dependent L-type Ca2+ (Ca(V)1.2) channels are the principal Ca2+ entry pathway in arterial myocytes. Ca(V)1.2 channels regulate multiple vascular functions and are implicated in the pathogenesis of human disease, including hypertension. However, the molecular identity of Ca(V)1.2 channels expressed in myocytes of myogenic arteries that regulate vascular pressure and blood flow is unknown. Here, we cloned Ca(V)1.2 subunits from resistance size cerebral arteries and demonstrate that myocytes contain a novel, cysteine rich N terminus that is derived from exon 1 (termed "exon 1c"), which is located within CACNA1C, the Ca(V)1.2 gene. Quantitative PCR revealed that exon 1c was predominant in arterial myocytes, but rare in cardiac myocytes, where exon 1a prevailed. When co-expressed with alpha(2)delta subunits, Ca(V)1.2 channels containing the novel exon 1c-derived N terminus exhibited: 1) smaller whole cell current density, 2) more negative voltages of half activation (V-1/2,V-act) and half-inactivation (V-1/2,V-inact), and 3) reduced plasma membrane insertion, when compared with channels containing exon 1b. beta(1b) and beta(2a) subunits caused negative shifts in the V-1/2,V-act and (V1/2,inact) of exon 1b-containing Ca(V)1.2 alpha(1)/alpha(2)delta currents that were larger than those in exon 1c-containing Ca(V)1.2 alpha(1)/alpha(2)delta currents. In contrast, beta(3) similarly shifted V-1/2,V-act and V-1/2,V-inact of currents generated by exon 1b- and exon 1c-containing channels. beta subunits isoform-dependent differences in current inactivation rates were also detected between N-terminal variants. Data indicate that through novel alternative splicing at exon 1, the Ca(V)1.2 N terminus modifies regulation by auxiliary subunits. The novel exon 1c should generate distinct voltage-dependent Ca2+ entry in arterial myocytes, resulting in tissue-specific Ca2+ signaling.
C1 Univ Tennessee, Ctr Hlth Sci, Dept Physiol, Memphis, TN 38163 USA.
   Univ Tennessee, Ctr Hlth Sci, Dept Pharmacol, Memphis, TN 38163 USA.
C3 University of Tennessee System; University of Tennessee Health Science
   Center; University of Tennessee System; University of Tennessee Health
   Science Center
RP Jaggar, JH (corresponding author), Univ Tennessee, Ctr Hlth Sci, Dept Physiol, 894 Union Ave, Memphis, TN 38163 USA.
EM jjaggar@physio1.utmem.edu
RI Cheng, Xiaoyang/M-1257-2017
OI Cheng, Xiaoyang/0000-0003-1446-2815
FU NHLBI NIH HHS [R01 HL077678-03, R01 HL077678, R01 HL077424, R01
   HL067061-05, R01 HL067061, HL77678, HL67061, HL77424] Funding Source:
   Medline; NIAAA NIH HHS [AA11560, R01 AA011560, R29 AA011560, R37
   AA011560] Funding Source: Medline
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NR 46
TC 36
Z9 39
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 5
PY 2007
VL 282
IS 40
BP 29211
EP 29221
DI 10.1074/jbc.M610623200
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 215DH
UT WOS:000249788000017
PM 17699517
OA Green Accepted, hybrid
DA 2025-04-10
ER

PT J
AU Russell, MW
   Raeker, MO
   Korytkowski, KA
   Sonneman, KJ
AF Russell, MW
   Raeker, MO
   Korytkowski, KA
   Sonneman, KJ
TI Identification, tissue expression and chromosomal localization of human
   Obscurin-MLCK, a member of the titin and Dbl families of myosin light
   chain kinases
SO GENE
LA English
DT Article
DE serine-threonine kinase; Rho guanine exchange factor; gene expression;
   skeletal muscle; heart
ID CARDIAC MYOCYTES; EXCHANGE FACTOR; PROTEIN; DOMAINS; RHOA; GENE;
   INVOLVEMENT; BINDING; FAILURE; ALPHA
AB Members of the Db1 family of guanine nucleotide exchange factors (GEFs) have important roles in the organization of actin-based cytoskeletal structures of a wide variety of cell types. Through the activation of members of the Rho family of GTP signaling molecules, these exchange factors elicit cytoskeletal alterations that allow cellular remodeling. As important regulators of RhoGTPase activity, members Of this family are candidates for mediating the RhoGTPase activation and cytoskeletal changes that occur during cardiac development and during the myocardial response to hypertrophic stimuli, In this study, we characterize a novel human gene that is expressed in skeletal and cardiac muscle and has putative functional domains similar to those found in members of both the Db1 family of GEFs and the titin family of myosin light chain kinases (MLCK). The cDNA sequence of this gene, which has been designated Obscurin-myosin light chain kinase (Obscurin-MLCK), would be predicted to encode for at least 68 immunoglobulin domains, two fibronectin domains, one calcium/calmodulin binding domain, a RhoGTP exchange factor domain, and two serine-threonine kinase domains. The combination of the putative Rho GEF and two kinase domains has not been noted in any other members of the titin or Db1 families. Alternative splicing allows the generation of a number of unique Obscurin-MLCK isoforms that contain various combinations of the functional domains. One group of isoforms is comparable to Unc-89, a Caenorhabditis elegans sarcomere-associated protein, in that they contain a putative RhoGEF domain and multiple immunoglobulin repeats. Other isoforms more closely resemble MLCK, containing one or both of the putative carboxy-terminal serine-threonine kinase domains. The modular nature of the Obscurin-MLCK isoforms indicates that it may have an array of functions important to cardiac and skeletal muscle physiology. (C) 2002 Elsevier Science B.V. All rights reserved.
C1 Univ Michigan, Div Pediat Cardiol, Dept Pediat & Communicable Dis, Ann Arbor, MI 48109 USA.
   Univ Wisconsin, Dept Physiol, Madison, WI 53706 USA.
C3 University of Michigan System; University of Michigan; University of
   Wisconsin System; University of Wisconsin Madison
RP Russell, MW (corresponding author), Univ Michigan, Womens Hosp, 1500 E Med Ctr Dr L1242, Ann Arbor, MI 48109 USA.
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NR 23
TC 80
Z9 93
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD JAN 9
PY 2002
VL 282
IS 1-2
BP 237
EP 246
DI 10.1016/S0378-1119(01)00795-8
PG 10
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 521GA
UT WOS:000173829800024
PM 11814696
DA 2025-04-10
ER

PT J
AU Murphy, D
   Konopacka, A
   Hindmarch, C
   Paton, JFR
   Sweedler, JV
   Gillette, MU
   Ueta, Y
   Grinevich, V
   Lozic, M
   Japundzic-Zigon, N
AF Murphy, D.
   Konopacka, A.
   Hindmarch, C.
   Paton, J. F. R.
   Sweedler, J. V.
   Gillette, M. U.
   Ueta, Y.
   Grinevich, V.
   Lozic, M.
   Japundzic-Zigon, N.
TI The Hypothalamic-Neurohypophyseal System: From Genome to Physiology
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Review
DE genome; transcriptome; proteome; neuropeptidome;
   hypothalamic-neurohypophyseal system; oxytocin; vasopressin; transgenic
   rats; viral vectors
ID DIRECT CELLULAR PEPTIDOMICS; PROTEIN FUSION TRANSGENE; PAIR BOND
   FORMATION; GENE-EXPRESSION; PARAVENTRICULAR NUCLEUS; BARORECEPTOR
   REFLEX; HYPOTHALAMONEUROHYPOPHYSEAL SYSTEM; EXAGGERATED RESPONSE;
   VASOPRESSIN NEURONS; MICROARRAY ANALYSIS
AB The elucidation of the genomes of a large number of mammalian species has produced a huge amount of data on which to base physiological studies. These endeavours have also produced surprises, not least of which has been the revelation that the number of protein coding genes needed to make a mammal is only 22 333 (give or take). However, this small number belies an unanticipated complexity that has only recently been revealed as a result of genomic studies. This complexity is evident at a number of levels: (i) cis-regulatory sequences; (ii) noncoding and antisense mRNAs, most of which have no known function; (iii) alternative splicing that results in the generation of multiple, subtly different mature mRNAs from the precursor transcript encoded by a single gene; and (iv) post-translational processing and modification. In this review, we examine the steps being taken to decipher genome complexity in the context of gene expression, regulation and function in the hypothalamic-neurohypophyseal system (HNS). Five unique stories explain: (i) the use of transcriptomics to identify genes involved in the response to physiological (dehydration) and pathological (hypertension) cues; (ii) the use of mass spectrometry for single-cell level identification of biological active peptides in the HNS, and to measure in vitro release; (iii) the use of transgenic lines that express fusion transgenes enabling (by cross-breeding) the generation of double transgenic lines that can be used to study vasopressin (AVP) and oxytocin (OXT) neurones in the HNS, as well as their neuroanatomy, electrophysiology and activation upon exposure to any given stimulus; (iv) the use of viral vectors to demonstrate that somato-dendritically released AVP plays an important role in cardiovascular homeostasis by binding to V1a receptors on local somata and dendrites; and (v) the use of virally-mediated optogenetics to dissect the role of OXT and AVP in the modulation of a wide variety of behaviours.
C1 [Murphy, D.; Konopacka, A.; Hindmarch, C.] Univ Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, Bristol BS1 3NY, Avon, England.
   [Murphy, D.; Lozic, M.; Japundzic-Zigon, N.] Univ Belgrade, Fac Med, Inst Pharmacol Clin Pharmacol & Toxicol, Belgrade, Serbia.
   [Paton, J. F. R.] Univ Bristol, Dept Physiol & Pharmacol, Bristol BS1 3NY, Avon, England.
   [Sweedler, J. V.; Gillette, M. U.] Univ Illinois, Dept Chem, Urbana, IL 61801 USA.
   [Sweedler, J. V.; Gillette, M. U.] Univ Illinois, Dept Cellular & Dev Biol, Urbana, IL 61801 USA.
   [Ueta, Y.] Univ Occupat & Environm Hlth, Sch Med, Dept Physiol, Kitakyushu, Fukuoka 807, Japan.
   [Grinevich, V.] Max Planck Inst Med Res, Dept Mol Neurobiol, Heidelberg, Germany.
C3 University of Bristol; University of Belgrade; University of Bristol;
   University of Illinois System; University of Illinois Urbana-Champaign;
   University of Illinois System; University of Illinois Urbana-Champaign;
   University of Occupational & Environmental Health - Japan; Max Planck
   Society
RP Murphy, D (corresponding author), Univ Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, Dorothy Hodgkin Bldg,Whitson St, Bristol BS1 3NY, Avon, England.
EM d.murphy@bristol.ac.uk
RI Japundzic-Zigon, Nina/AAA-5329-2021; Hindmarch, Charles/AAM-3385-2021;
   Paton, Julian/AAM-2121-2020; Murphy, David/C-3967-2012; Sweedler,
   Jonathan/A-9405-2009
OI Paton, Julian/0000-0001-7410-2913; Grinevich,
   Valery/0000-0002-6337-8866; Hindmarch, Charles/0000-0002-6036-1292;
   Lozic, Maja/0000-0002-8874-9889; Konopacka,
   Agnieszka/0000-0003-2192-1928; Murphy, David/0000-0003-2946-0353;
   Sweedler, Jonathan/0000-0003-3107-9922; Japundzic-Zigon,
   Nina/0000-0002-3036-5321
FU British Heart Foundation [RG/11/6/28714, FS/12/5/29339] Funding Source:
   Medline; Medical Research Council [G0700954] Funding Source: Medline;
   NHLBI NIH HHS [R01 HL092571-01A1, R01 HL092571] Funding Source: Medline;
   NIDA NIH HHS [P30 DA018310, P30 DA018310-01] Funding Source: Medline;
   BBSRC [BB/J01981X/1] Funding Source: UKRI; MRC [G0700954] Funding
   Source: UKRI; Grants-in-Aid for Scientific Research [23659127] Funding
   Source: KAKEN
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NR 107
TC 39
Z9 40
U1 0
U2 24
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-8194
EI 1365-2826
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD APR
PY 2012
VL 24
IS 4
BP 539
EP 553
DI 10.1111/j.1365-2826.2011.02241.x
PG 15
WC Endocrinology & Metabolism; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 914CA
UT WOS:000301925100003
PM 22448850
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Rasper, DM
   Vaillancourt, JP
   Hadano, S
   Houtzager, VM
   Seiden, I
   Keen, SLC
   Tawa, P
   Xanthoudakis, S
   Nasir, J
   Martindale, D
   Koop, BF
   Peterson, EP
   Thornberry, NA
   Huang, JQ
   MacPherson, DP
   Black, SC
   Hornung, F
   Lenardo, MJ
   Hayden, MR
   Roy, S
   Nicholson, DW
AF Rasper, DM
   Vaillancourt, JP
   Hadano, S
   Houtzager, VM
   Seiden, I
   Keen, SLC
   Tawa, P
   Xanthoudakis, S
   Nasir, J
   Martindale, D
   Koop, BF
   Peterson, EP
   Thornberry, NA
   Huang, JQ
   MacPherson, DP
   Black, SC
   Hornung, F
   Lenardo, MJ
   Hayden, MR
   Roy, S
   Nicholson, DW
TI Cell death attenuation by 'Usurpin', a mammalian DED-caspase homologue
   that precludes caspase-8 recruitment and activation by the CD-95 (Fas,
   APO-1) receptor complex
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
DE apoptosis; caspase; CD95 (Fas, APO-1); ischemia/reperfusion injury
ID INTERLEUKIN-1-BETA-CONVERTING ENZYME; ICE/CED-3 PROTEASE; APOPTOSIS;
   INHIBITION; MECHANISMS; INTERACTS; DOMAIN; FAMILY; BRAIN; GENES
AB Apoptotic cell suicide initiated by ligation of CD95 (Fas/APO-1) occurs through recruitment, oligomerization and autocatalytic activation of the cysteine protease, caspase-8 (MACH, FLICE, Mch5). An endogenous mammalian regulator of this process, named Usurpin, has been identified (aliases for Usurpin include CASH, Gasper, CLARP, FLAME-1, FLIP, I-FLICE and MRIT). This protein is ubiquitously expressed and exists as at least three isoforms arising by alternative mRNA splicing. The Usurpin gene is comprised of 13 exons and is clustered within approximately 200 Kb with the caspase-8 and -10 genes on human chromosome 2q33-34. The Usurpin polypeptide has features in common with pro-caspase-8 and -10, including tandem 'death effector domains' on the N-terminus of a large subunit/small subunit caspase-like domain, but it lacks key residues that are necessary for caspase proteolytic activity, including the His and Cys which form the catalytic substrates diad, and residues that stabilize the P-1 aspartic acid in substrates. Retro-mutation of these residues to functional caspase counterparts failed to restore proteolytic activity, indicating that other determinants also ensure the absence of catalytic potential. Usurpin heterodimerized with pro-caspase-8 in vitro and precluded pro-caspase-8 recruitment by the FADD/MORT1 adapter protein. Cell death induced by CD95 (Fas/APO-1) ligation was attenuated in cells transfected with Usurpin. In vivo, a Usurpin deficit was found in cardiac infarcts where TUNEL-positive myocytes and active caspase-3 expression were prominent following ischemia/reperfusion injury. In contrast, abundant Usurpin expression (and a caspase-3 deficit) occurred in surrounding unaffected cardiac tissue, suggesting reciprocal regulation of these pro-and anti-apoptotic molecules in vivo. Usurpin thus appears to be an endogenous modulator of apoptosis sensitivity in mammalian cells, including the susceptibility of cardiac myocytes to apoptotic death following ischemia/reperfusion injury.
C1 Merck Frosst Ctr Therapeut Res, Dept Biochem & Mol Biol, Pointe Claire, PQ H9R 4P8, Canada.
   Merck Frosst Ctr Therapeut Res, Dept Pharmacol, Pointe Claire, PQ H9R 4P8, Canada.
   Merck Res Labs, Dept Enzymol, Rahway, NJ 07065 USA.
   NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
   Univ British Columbia, Dept Med Genet, Canadian Genet Dis Network, Ctr Mol Med & Therapeut, Vancouver, BC V6T 1Z4, Canada.
   Tokai Univ, Sch Med, Japan Sci & Technol Corp, Int Cooperat Res Project, Kanagawa 25911, Japan.
   Univ Victoria, Dept Biol, Ctr Environm Hlth, Victoria, BC V8W 3N5, Canada.
C3 Merck & Company; Merck & Company Canada; Merck & Company; Merck &
   Company Canada; Merck & Company; National Institutes of Health (NIH) -
   USA; NIH National Institute of Allergy & Infectious Diseases (NIAID);
   University of British Columbia; Tokai University; Japan Science &
   Technology Agency (JST); University of Victoria
RP Nicholson, DW (corresponding author), Merck Frosst Ctr Therapeut Res, Dept Biochem & Mol Biol, POB 1005, Pointe Claire, PQ H9R 4P8, Canada.
RI Hadano, Shinji/ABA-5052-2021; Hayden, Michael/D-8581-2011; Koop,
   Ben/A-8151-2008
OI MacPherson, David/0000-0003-3729-907X; Nasir, Jamal/0000-0001-6378-5616;
   Hayden, Michael/0000-0001-5159-1419; Koop, Ben/0000-0003-0045-5200
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NR 50
TC 278
Z9 310
U1 0
U2 5
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND
SN 1350-9047
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD APR
PY 1998
VL 5
IS 4
BP 271
EP 288
DI 10.1038/sj.cdd.4400370
PG 18
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA ZF385
UT WOS:000072892200003
PM 10200473
OA Bronze
DA 2025-04-10
ER

PT J
AU Grover, AK
   Xu, A
   Samson, SE
   Narayanan, N
AF Grover, AK
   Xu, A
   Samson, SE
   Narayanan, N
TI Sarcoplasmic reticulum Ca2+ pump in pig coronary artery smooth muscle is
   regulated by a novel pathway
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE calmodulin; calmodulin kinase; protein kinase; phospholamban; cardiac
   muscle; adenosinetriphosphatase
ID CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE; PHOSPHOLAMBAN PHOSPHORYLATION;
   CALCIUM PUMPS; CA-2+ PUMP; CALMODULIN; ATPASE; RECEPTORS; BINDING;
   IDENTIFICATION; CA2+-ATPASE
AB Coronary artery smooth muscle expresses an alternative splice (SERCA2b) of the sarcoplasmic reticulum (SR) Ca2+ pump gene SERCA2, which is also expressed in cardiac muscle (SERCA2a), but how the activity of this transporter is regulated in the coronary artery is not known. SERCA2a in the cardiac muscle can be regulated via phospholamban or, as recently reported, by a direct phosphorylation of this protein by calmodulin kinase (Xu, A., C. Hawkins, and N. Narayanan. J. Biol. Chem. 268: 8394-8397, 1993). Because both SERCA2a and SERCA2b contain this calmodulin kinase phosphorylation site, we examined the effect of endogenous calmodulin kinase phosphorylation of the SR Ca2+ pump in the coronary artery. SR-enriched membranes were isolated from coronary artery smooth muscle and washed in ethylene glycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid to remove bound calmodulin. When these membranes were incubated with MgATP(2-) in the presence of Ca2+/calmodulin, a 115-kDa protein was phosphorylated. This phosphorylated 115-kDa protein was identified as SERCA2b in Western blots and by immunoprecipitation using a SERCA2-selective antibody. Preincubating the membranes in MgATP(2-) in the presence of Ca2+/calmodulin stimulated the subsequent Ca2+ uptake in the presence of oxalate plus MgATP(2-) and azide. The stimulation of Ca2+ uptake was inhibited by including the SR Ca2+ pump inhibitors thapsigargin and cyclopiazonic acid in the Ca2+ uptake medium or by including the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenes or the calmodulin kinase II peptide fragment 290-309 in the phosphorylation solution. Thus an endogenous calmodulin-dependent kinase phosphorylated SERCA2b and activated it. Phospholamban could not be detected in these membranes in Western blots. Therefore, the regulation of the SR Ca2+ pump activity in coronary artery smooth muscle may involve a direct phosphorylation of the pump protein by an endogenous calmodulin-dependent kinase.
C1 UNIV WESTERN ONTARIO, DEPT PHYSIOL, LONDON, ON N6A 5C1, CANADA.
C3 Western University (University of Western Ontario)
RP Grover, AK (corresponding author), MCMASTER UNIV, DEPT BIOMED SCI, HAMILTON, ON L8N 3Z5, CANADA.
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NR 37
TC 28
Z9 28
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0363-6143
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD JUL
PY 1996
VL 271
IS 1
BP C181
EP C187
DI 10.1152/ajpcell.1996.271.1.C181
PG 7
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA UX534
UT WOS:A1996UX53400019
PM 8760044
DA 2025-04-10
ER

PT J
AU Bertoncini, P
   Schoenauer, R
   Agarkova, I
   Hegner, M
   Perriard, JC
   Güntherodt, HJ
AF Bertoncini, P
   Schoenauer, R
   Agarkova, I
   Hegner, M
   Perriard, JC
   Güntherodt, HJ
TI Study of the mechanical properties of myomesin proteins using dynamic
   force spectroscopy
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE myomesin; EH-myomesin; EH segment; M-band; mechanical unfolding
ID TITIN IMMUNOGLOBULIN DOMAINS; SARCOMERIC M-BAND; STRIATED-MUSCLE;
   MOLECULAR MECHANICS; ENTROPIC ELASTICITY; LASER-TWEEZERS;
   CONTOUR-LENGTH; SINGLE PROTEIN; CARDIAC TITIN; MICROSCOPY
AB Myomesin is the most prominent structural component of the sarcomeric M-Band that is expressed in mammalian heart and skeletal muscles. Like titin, this protein is an intracellular member of the Ig-fibronectin superfamily, which has a flexible filamentous structure and which is largely composed of two types of domain that are similar to immunoglobulin (Ig)-like and fibronectin type III (FNIII) domains. Several myomesin, isoforms have been identified, and their expression patterns are highly regulated both spatially and temporally. Particularly, alternative splicing in the central part of the molecule gives rise to an isoform, EH (embryonic heart)-myomesin, containing a serine and proline-rich insertion with no well-defined secondary structure, the EH segment. EH-myomesin represents the major myomesin isoform at embryonic stages of mammalian heart and is rapidly down-regulated around birth, but it is re-expressed in the heart of patients suffering from dilated cardio-myopathy. Here, in order to facilitate a better understanding of the physiological, and possibly pathological, functions of myomesin proteins, we explore the mechanical stability, elasticity and force-driven structural changes of human myomesin's sub-molecular segments using single-molecule force spectroscopy and protein engineering. We find that human myomesin molecules are composed of modules (Ig and FNIII), that are designed to withstand force and we demonstrate that the human cardiac EH segment functions like an additional elastic stretch in the middle part of the EH-myomesin and behaves like a random coil. Consequently myomesin isoforms (proteins with or without the EH segment) have different elastic properties, the EH-myomesin being the more compliant one. These findings imply that the compliance of the M-band increases with the amount of EH-myomesin it contains. So, we provide the evidence that not only titin but also other sarcomeric proteins have complicated visco-elastic properties depending on the contractile parameters in different muscle types. © 2005 Elsevier Ltd. All rights reserved.
C1 Univ Basel, Inst Phys, CH-4056 Basel, Switzerland.
   ETH Honggerberg, Inst Cell Biol, CH-8093 Zurich, Switzerland.
C3 University of Basel; Swiss Federal Institutes of Technology Domain; ETH
   Zurich
RP Bertoncini, P (corresponding author), Univ Basel, Inst Phys, Klingelbergstr 82, CH-4056 Basel, Switzerland.
EM Bertoncini.Patricia@wanadoo.fr
RI Agarkova, Irina/AAG-2153-2019; Bertoncini, Patricia/K-5398-2015
OI Bertoncini, Patricia/0000-0001-8508-2962; Hegner,
   Martin/0000-0003-1514-3437
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NR 55
TC 20
Z9 23
U1 0
U2 6
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD MAY 20
PY 2005
VL 348
IS 5
BP 1127
EP 1137
DI 10.1016/j.jmb.2005.03.040
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 925LK
UT WOS:000229054400007
PM 15854649
DA 2025-04-10
ER

PT J
AU Gábriel, R
   Pöstyéni, E
   Dénes, V
AF Gabriel, Robert
   Postyeni, Etelka
   Denes, Viktoria
TI Neuroprotective Potential of Pituitary Adenylate Cyclase Activating
   Polypeptide in Retinal Degenerations of Metabolic Origin
SO FRONTIERS IN NEUROSCIENCE
LA English
DT Review
DE PACAP; signaling; retina degeneration; metabolic origin; neuroprotection
ID ENDOTHELIAL GROWTH-FACTOR; PROGRAMMED CELL-DEATH; DIABETIC-RETINOPATHY;
   C-JUN; ULTRASTRUCTURAL-LOCALIZATION; MICROGLIAL ACTIVATION;
   SIGNAL-TRANSDUCTION; VEGF EXPRESSION; PACAP RECEPTORS; SPLICE VARIANTS
AB Pituitary adenylate cyclase-activating polypeptide (PACAP1-38) is a highly conserved member of the secretin/glucagon/VIP family. The repressive effect of PACAP1-38 on the apoptotic machinery has been an area of active research conferring a significant neuroprotective potential onto this peptide. A remarkable number of studies suggest its importance in the etiology of neurodegenerative disorders, particularly in relation to retinal metabolic disorders. In our review, we provide short descriptions of various pathological conditions (diabetic retinopathy, excitotoxic retinal injury and ischemic retinal lesion) in which the remedial effect of PACAP has been well demonstrated in various animal models. Of all the pathological conditions, diabetic retinopathy seems to be the most intriguing as it develops in 75% of patients with type 1 and 50% of patients with type 2 diabetes, with concomitant progression to legal blindness in about 5%. Several animal models have been developed in recent years to study retinal degenerations and out of these glaucoma and age-related retina degeneration models bear human recapitulations. PACAP neuroprotection is thought to operate through enhanced cAMP production upon binding to PAC1R. However, the underlying signaling network that leads to neuroprotection is not fully understood. We observed that (i) PACAP is not equally efficient in the above conditions; (ii) in some cases more than one signaling pathways are activated; (iii) the coupling of PAC1-R and signaling is stage dependent; and (iv) PAC1-R is not the only receptor that must be considered to interpret the effects in our experiments. These observations point to a complex signaling mechanism, that involves alternative routes besides the classical cAMP/protein kinase A pathway to evoke the outstanding neuroprotective action. Consequently, the possible contribution of the other two main receptors (VPAC1-R and VPAC2-R) will also be discussed. Finally, the potential medical use of PACAP in some retinal and ocular disorders will also be reviewed. By taking advantage of, low-cost synthesis technologies today, PACAP may serve as an alternative to the expensive treatment modelities currently available in ocular or retinal conditions.
C1 [Gabriel, Robert; Postyeni, Etelka; Denes, Viktoria] Univ Pecs, Dept Expt Zool & Neurobiol, Pecs, Hungary.
   [Gabriel, Robert] Univ Pecs, Janos Szentagothai Res Ctr, Pecs, Hungary.
C3 University of Pecs; University of Pecs
RP Gábriel, R (corresponding author), Univ Pecs, Dept Expt Zool & Neurobiol, Pecs, Hungary.; Gábriel, R (corresponding author), Univ Pecs, Janos Szentagothai Res Ctr, Pecs, Hungary.
EM gabriel@gamma.ttk.pte.hu
FU Hungarian Scientific Research Fund (NKFIH) [119289,
   EFOP-3.6.2-16-2017-00008]; Academy of Finland (AKA) [119289] Funding
   Source: Academy of Finland (AKA)
FX Funding was provided by the Hungarian Scientific Research Fund (NKFIH)
   (Grant No. 119289) and EFOP-3.6.2-16-2017-00008.
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NR 115
TC 16
Z9 16
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1662-453X
J9 FRONT NEUROSCI-SWITZ
JI Front. Neurosci.
PD OCT 9
PY 2019
VL 13
AR 1031
DI 10.3389/fnins.2019.01031
PG 12
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA JO4UR
UT WOS:000497575900001
PM 31649495
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Dal Lin, C
   Marinova, M
   Brugnolo, L
   Rubino, G
   Plebani, M
   Iliceto, S
   Tona, F
AF Dal Lin, Carlo
   Marinova, Mariela
   Brugnolo, Laura
   Rubino, Giorgio
   Plebani, Mario
   Iliceto, Sabino
   Tona, Francesco
TI Rapid changes of miRNAs-20,-30,-410,-515,-134, and-183 and telomerase
   with psychological activity: A one year study on the relaxation response
   and epistemological considerations
SO JOURNAL OF TRADITIONAL AND COMPLEMENTARY MEDICINE
LA English
DT Article
DE Cardiovascular disease; Inflammation; Epigenetics; Telomerase;
   Meditation; microRNA
ID CELLULAR SENESCENCE; MICRORNAS; STRESS; DISEASE; INFLAMMATION;
   MEDITATION; MECHANISMS; EXPRESSION; INJURY; LENGTH
AB Background and aim: Mental stress represents a pivotal factor in cardiovascular diseases. The mechanism by which stress produces its deleterious effects is still under study, but one of the most explored pathways is inflammation-aging and cell senescence. In this scenario, circulating microRNAs appear to be regulatory elements of the telomerase activity and alternative splicing within the nuclear factor kappa light-chain-enhancer (NF -KB) network. Anti-stress techniques appeared to be able to slow down the inflammatory and aging processes. As we recently verified, the practice of the relaxation response (RR) counteracted psychological stress and determined favorable changes of the NF -KB, p53, and toll-like receptor-4 (TLR-4) gene expression and in neurotransmitters, hormones, cytokines, and inflammatory circulating microRNAs. We aimed to verify a possible change in the serum levels of six other micro-RNAs of cardiovascular interest, involved in cell senescence and in the NF -KB network (miRNAs-20,-30,-410,-515,-134, and-183), and tested the activity of telomerase in peripheral blood mononuclear cells (PBMCs). Experimental procedure: We measured the aforementioned molecules in the serum of patients with ischemic heart disease (and healthy controls) immediately before and after a relaxation response session, three times (after the baseline), in one year of follow-up. Results: According to our data, the miRNA-20 and-30 levels and PBMCs-telomerase activity increased during the RR while the-410 and-515 levels decreased. During the RR sessions, both miRNA-134 and-183 decreased. Conclusion: The mediators considered in this exploratory work appeared to vary rapidly with the psychological activity (in particular when focused on relaxation techniques) showing that psychological activity should be part of the future research on epigenetics. Epistemological perspectives are also discussed. (c) 2021 Center for Food and Biomolecules, National Taiwan University. Production and hosting by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
C1 [Dal Lin, Carlo; Rubino, Giorgio; Iliceto, Sabino; Tona, Francesco] Univ Padua, Sch Med, Dept Cardiac Thorac & Vasc Sci, Via Giustiniani 2, I-35100 Padua, Italy.
   [Marinova, Mariela; Brugnolo, Laura; Plebani, Mario] Univ Padua, Sch Med, Dept Lab Med, Via Giustiniani 2, I-35100 Padua, Italy.
C3 University of Padua; University of Padua
RP Dal Lin, C (corresponding author), Univ Padua, Sch Med, Dept Cardiac Thorac & Vasc Sci, Via Giustiniani 2, I-35100 Padua, Italy.
EM carlodallin@libero.it
RI Tona, Franceso/AAC-3386-2022; Plebani, Mario/AAF-4953-2020
FU Department of Cardiac, Thoracic and Vascular Sciences, Padua University
   School of Medicine, Italy
FX This research received no external funding, the entire study was funded
   by the Department of Cardiac, Thoracic and Vascular Sciences, Padua
   University School of Medicine, Italy.
CR [Anonymous], 2015, J INTEGRATIVE CARDIO, DOI DOI 10.15761/JIC.1000135
   [Anonymous], miRBase by the Griffiths -Jones lab at the faculty of biology, medicine and health
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NR 99
TC 5
Z9 5
U1 0
U2 8
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2225-4110
J9 J TRADIT COMPL MED
JI J. Tradit. Complement. Med.
PD SEP
PY 2021
VL 11
IS 5
BP 409
EP 418
DI 10.1016/j.jtcme.2021.02.005
EA SEP 2021
PG 10
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Integrative & Complementary Medicine
GA US9SG
UT WOS:000697764900004
PM 34522635
OA gold, Green Submitted, Green Published
DA 2025-04-10
ER

PT J
AU Mancuso, DJ
   Jenkins, CM
   Sims, HF
   Cohen, JM
   Yang, JY
   Gross, RW
AF Mancuso, DJ
   Jenkins, CM
   Sims, HF
   Cohen, JM
   Yang, JY
   Gross, RW
TI Complex transcriptional and translational regulation of
   iPLA2γ resulting in multiple gene products containing dual
   competing sites for mitochondrial or peroxisomal localization
SO EUROPEAN JOURNAL OF BIOCHEMISTRY
LA English
DT Article
DE phospholipase; mitochondria; peroxisomes; transcription; translation
ID CALCIUM-INDEPENDENT PHOSPHOLIPASE; ARACHIDONIC-ACID RELEASE;
   PLASMALOGEN-SELECTIVE PHOSPHOLIPASE-A2; MECHANISM-BASED DISCRIMINATION;
   VIRUS EXPRESSION VECTORS; HIGH-LEVEL EXPRESSION; SMOOTH-MUSCLE-CELLS;
   MESSENGER-RNA; CHOLINE GLYCEROPHOSPHOLIPIDS; MYOCARDIAL-ISCHEMIA
AB Membrane-associated calcium-independent phospholipase A(2)gamma (iPLA(2)gamma) contains four potential in-frame methionine start sites (Mancuso, D.J. Jenkins, C.M. & Gross, R.W. (2000) J. Biol. Chem.275, 9937-9945), but the mechanisms regulating the types, amount and subcellular localization of iPLA(2)gamma in cells are incompletely understood. We now: (a) demonstrate the dramatic transcriptional repression of mRNA synthesis encoding iPLA(2)gamma by a nucleotide sequence nested in the coding sequence itself; (b) localize the site of transcriptional repression to the most 5' sequence encoding the iPLA(2)gamma holoprotein; (c) identify the presence of nuclear protein constituents which bind to the repressor region by gel shift analysis; (d) demonstrate the translational regulation of distinct iPLA(2)gamma isoforms; (e) identify multiple novel exons, promoters, and alternative splice variants of human iPLA(2)gamma; (f) document the presence of dual-competing subcellular localization signals in discrete isoforms of iPLA(2)gamma; and (g) demonstrate the functional integrity of an N-terminal mitochondrial localization signal by fluorescence imaging and the presence of iPLA(2)gamma in the mitochondrial compartment of rat myocardium. The intricacy of the regulatory mechanisms of iPLA(2)gamma biosynthesis in rat myocardium is underscored by the identification of seven distinct protein products that utilize multiple mechanisms (transcription, translation and proteolysis) to produce discrete iPLA(2)gamma polypeptides containing either single or dual subcellular localization signals. This unanticipated complex interplay between peroxisomes and mitochondria mediated by competition for uptake of the nascent iPLA(2)gamma polypeptide identifies a new level of phospholipase-mediated metabolic regulation. Because uncoupling protein function is regulated by free fatty acids in mitochondria, these results suggest that iPLA(2)gamma processing contributes to integrating respiration and thermogenesis in mitochondria.
C1 Washington Univ, Sch Med, Div Bioorgan Chem & Mol Pharmacol, St Louis, MO 63110 USA.
   Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
   Washington Univ, Sch Med, Dept Chem, St Louis, MO 63110 USA.
   Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA.
C3 Washington University (WUSTL); Washington University (WUSTL); Washington
   University (WUSTL); Washington University (WUSTL)
RP Washington Univ, Sch Med, Div Bioorgan Chem & Mol Pharmacol, 660 S Euclid Ave,Campus Box 8020, St Louis, MO 63110 USA.
EM rgross@wustl.edu
OI Cohen, Joshua/0000-0002-7550-3791
FU NHLBI NIH HHS [5PO1HL57278-O7, 5R01HL41250-12] Funding Source: Medline
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NR 66
TC 67
Z9 76
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2956
J9 EUR J BIOCHEM
JI Eur. J. Biochem.
PD DEC
PY 2004
VL 271
IS 23-24
BP 4709
EP 4724
DI 10.1111/j.1432-1033.2004.04435.x
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 879WV
UT WOS:000225750800013
PM 15606758
OA Bronze
DA 2025-04-10
ER

PT J
AU Grantham, JA
   Schirger, JA
   Wennberg, PW
   Sandberg, S
   Heublein, DM
   Subkowski, T
   Burnett, JC
AF Grantham, JA
   Schirger, JA
   Wennberg, PW
   Sandberg, S
   Heublein, DM
   Subkowski, T
   Burnett, JC
TI Modulation of functionally active endothelin-converting enzyme by
   chronic neutral endopeptidase inhibition in experimental atherosclerosis
SO CIRCULATION
LA English
DT Article
DE atherosclerosis; endothelin; natriuretic peptides; vasoconstriction
ID ATRIAL-NATRIURETIC-PEPTIDE; SMOOTH-MUSCLE CELLS;
   LOW-DENSITY-LIPOPROTEIN; MESSENGER-RNA; FED RABBITS; EXPRESSION;
   CHOLESTEROL; SUPPRESSION; SECRETION; MACROPHAGES
AB Background-Endothelin-converting enzyme-1 (ECE-1) processes big endothelin-1 (ET-1) to ET-1, a peptide implicated in atheroma formation. ECE-1 exists in 2 isoforms (ECE-1 alpha and ECE-1 beta) the result of alternative splicing of a common gene. Neutral endopeptidase (NEP) is a genetically distinct metallopeptidase that degrades the natriuretic peptides. These peptides mediate antiproliferative and vasodilating actions. We sought to demonstrate the distribution of the 2 ECE-1 isoforms in experimental atherosclerosis, to determine the effects of chronic NEP-I on plasma cGMP concentrations, vascular wall ECE-1 activity, and ET-1 concentration, and to correlate these actions with atheroma formation. Our hypothesis was that chronic NEP-I, in association with augmented cGMP, would inhibit ECE-1 conversion of big ET-1 to active ET-1, thus reducing tissue ET-1 concentrations and associated atheroma formation.
   Methods and Results-Cholesterol-fed New Zealand White rabbits (n=8, 1% cholesterol diet) and NEP-I-treated cholesterol-fed New Zealand White rabbits (n=8; candoxatril, 30 mg/kg per day, Pfizer) were euthanized after 8 weeks of feeding. ECE-1 alpha and ECE-1 beta immunoreactivity was present in the aortas of both groups. Compared with control values, plasma cGMP concentrations were increased (2.8+/-0.6 versus 8.4+/-1.2 pmol/ml, P<0.05), ECE-1 activity was attenuated (68+/-3% versus 32+/-8%, P<0.05), aortic tissue ET-1 concentrations were reduced (4.6+/-0.5 versus 3.2+/-0.3 pg/mg protein, P<0.05), and atheroma formation was attenuated (62+/-6% versus 34+/-5%, P<0.01) by NEP-I.
   Conclusions-These studies suggest that ECE-1 is present and functionally active in the vascular wall in atherosclerosis. Inhibition of ECE-1 by NEP-I represents a novel approach to interruption of the endothelin system in this cardiovascular disease state.
C1 Mayo Clin, Div Cardiovasc Dis, Cardiorenal Res Lab, Rochester, MN 55905 USA.
   BASF Pharma, Ludwigshafen, Germany.
C3 Mayo Clinic; BASF
RP Grantham, JA (corresponding author), Mayo Clin, Div Cardiovasc Dis, Cardiorenal Res Lab, 200 1st St SW, Rochester, MN 55905 USA.
FU NHLBI NIH HHS [HL-07111, HL-36634] Funding Source: Medline
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NR 39
TC 29
Z9 30
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD APR 25
PY 2000
VL 101
IS 16
BP 1976
EP 1981
DI 10.1161/01.CIR.101.16.1976
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA 310EF
UT WOS:000086813000023
PM 10779465
OA Bronze, Green Submitted
DA 2025-04-10
ER

PT J
AU Fukumaru, S
   Horiuchi, M
   Kobayashi, K
   Jalil, MA
   Iijima, M
   Masuda, M
   Begum, L
   Higashi, M
   Wakana, S
   Kanzaki, T
   Saheki, T
AF Fukumaru, S
   Horiuchi, M
   Kobayashi, K
   Jalil, MA
   Iijima, M
   Masuda, M
   Begum, L
   Higashi, M
   Wakana, S
   Kanzaki, T
   Saheki, T
TI Novel mRNA molecules are induced in hypertrophied ventricles of
   carnitine-deficient mice and belong to a family of up-regulated gene in
   cells overexpressing c-erbB-2
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
LA English
DT Article
DE cardiac hypertrophy; carnitine deficiency; c-erbB-2; differential mRNA
   display analysis
ID VISCERAL STEATOSIS MICE; UREA CYCLE ENZYMES; JVS MICE; SUPPRESSED
   EXPRESSION; CARDIAC-HYPERTROPHY; ALTERED EXPRESSION; JUVENILE; MOUSE;
   MUSCLE; LIVER
AB To clarify the pathogenesis of cardiac hypertrophy in carnitine-deficient juvenile visceral steatosis (JVS) mice, we performed differential mRNA display analysis with the ventricles of control and JVS mice. We found a novel up-regulated gene, designated as carnitine deficiency-associated gene expressed in ventricle (CDV)-3. Northern blot analysis with a cDNA probe derived from the novel gene revealed two substantial mRNA species of prominent 4.1- and faint 3.5-kb in examined tissues of control and JVS mice. In spite of their widely expressed features, up-regulation of the gene was found predominantly in the ventricles and slightly in the auricles and skeletal muscles of JVS mice. The up-regulation of CDV-3 gene in the ventricles of JVS mice was significantly relieved by carnitine administration within 6 h. The entire cDNA nucleotide sequences showed that two kinds of cDNA, long and short versions (CDV-3A and -3B), corresponding to the detected mRNAs, are different in a 711 base fragment. Analysis of genomic DNA revealed that the two mRNAs were derived from a single CDV-3 gene with five exons by alternative splicing. The deduced amino acid sequences indicated that the isoforms consist of 236 and 281 residues, differing at regions near the carboxy-terminus but sharing 231 residues of the amino-terminal regions. A BLAST search revealed that they show a high similarity to a human predicted nuclear protein (H41), which has been reported to be up-regulated in breast cancer cells overexpressing cellular-erythroblastosis B-2 (c-erbB-2, a kind of tyrosine kinase).
   We report the identification and characterization of novel transcripts that may be involved in the development of cardiac hypertrophy caused by carnitine deficiency. (C) 2002 Elsevier Science B.V. All rights reserved.
C1 Kagoshima Univ, Fac Med, Dept Biochem, Kagoshima 8908520, Japan.
   Kagoshima Univ, Fac Med, Dept Dermatol, Kagoshima 8908520, Japan.
   Kagoshima Univ, Fac Med, Dept Anesthesiol & Crit Care Med, Kagoshima 8908520, Japan.
   RIKEN, Genom Sci Ctr, Mouse Funct Genom Res Grp, Yokohama, Kanagawa 2440804, Japan.
C3 Kagoshima University; Kagoshima University; Kagoshima University; RIKEN
RP Kagoshima Univ, Fac Med, Dept Biochem, 8-35-1 Sakuragaoka, Kagoshima 8908520, Japan.
EM masakun@m.kufm.kagoshima-u.ac.jp
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NR 33
TC 6
Z9 8
U1 0
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0167-4781
J9 BBA-GENE STRUCT EXPR
JI Biochim. Biophys. Acta-Gene Struct. Expression
PD SEP 27
PY 2002
VL 1577
IS 3
BP 437
EP 444
AR PII S0167-4781(02)00447-5
DI 10.1016/S0167-4781(02)00447-5
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 602TA
UT WOS:000178519500009
PM 12359334
DA 2025-04-10
ER

PT J
AU LeMasters, KE
   Blech-Hermoni, Y
   Stillwagon, SJ
   Vajda, NA
   Ladd, AN
AF LeMasters, Kathryn E.
   Blech-Hermoni, Yotam
   Stillwagon, Samantha J.
   Vajda, Natalie A.
   Ladd, Andrea N.
TI Loss of muscleblind-like 1 promotes invasive mesenchyme formation in
   endocardial cushions by stimulating autocrine TGFβ3
SO BMC DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE Muscleblind-like 1; Alternative splicing; TGF beta; Endocardial
   cushions; Epithelial-mesenchymal transition; Cell invasion
ID GROWTH-FACTOR-BETA; EXTRACELLULAR-MATRIX; TRANSFORMATION; HEART;
   EXPRESSION; TRANSITION; TISSUE; ACTIVATION; INDUCTION; REGULATOR
AB Background: Valvulogenesis and septation in the developing heart depend on the formation and remodeling of endocardial cushions in the atrioventricular canal (AVC) and outflow tract (OFT). These cushions are invaded by a subpopulation of endocardial cells that undergo an epithelial-mesenchymal transition in response to paracrine and autocrine transforming growth factor beta (TGF beta) signals. We previously demonstrated that the RNA binding protein muscleblind-like 1 (MBNL1) is expressed specifically in the cushion endocardium, and knockdown of MBNL1 in stage 14 embryonic chicken AVC explants enhances TGF beta-dependent endocardial cell invasion.
   Results: In this study, we demonstrate that the effect of MBNL1 knockdown on invasion remains dependent on TGF beta 3 after it is no longer required to induce basal levels of invasion. TGF beta 3, but not TGF beta 2, levels are elevated in medium conditioned by MBNL1-depleted AVC explants. TGF beta 3 is elevated even when the myocardium is removed, indicating that MBNL1 modulates autocrine TGF beta 3 production in the endocardium. More TGF beta 3-positive cells are observed in the endocardial monolayer following MBNL1 knockdown. Addition of exogenous TGF beta 3 to AVC explants recapitulates the effects of MBNL1 knockdown. Time course experiments demonstrate that knockdown of MBNL1 induces precocious TGF beta 3 secretion, and early exposure to excess TGF beta 3 induces precocious invasion. MBNL1 expression precedes TGF beta 3 in the AVC endocardium, consistent with a role in preventing precocious autocrine TGF beta 3 signaling. The stimulatory effects of MBNL1 knockdown on invasion are lost in stage 16 AVC explants. Knockdown of MBNL1 in OFT explants similarly enhances cell invasion, but not activation. TGF beta is necessary and sufficient to mediate this effect.
   Conclusions: Taken together, these data support a model in which MBNL1 negatively regulates cell invasion in the endocardial cushions by restricting the magnitude and timing of endocardial-derived TGF beta 3 production.
C1 [LeMasters, Kathryn E.; Blech-Hermoni, Yotam; Stillwagon, Samantha J.; Vajda, Natalie A.; Ladd, Andrea N.] Cleveland Clin, Lerner Res Inst, Dept Cell Biol, Cleveland, OH 44195 USA.
C3 Cleveland Clinic Foundation
RP Ladd, AN (corresponding author), Cleveland Clin, Lerner Res Inst, Dept Cell Biol, 9500 Euclid Ave,Mail Code NC10, Cleveland, OH 44195 USA.
EM ladda@ccf.org
OI Ladd, Andrea/0000-0003-4725-5644; Blech-Hermoni,
   Yotam/0000-0002-3328-8122
FU National Institutes of Health [1R01HL089376, T32GM008056]; Case Western
   Reserve University/Cleveland Clinic CTSA from NIH/National Center for
   Research Resources (NCRR) [UL1 RR024989]
FX We thank Dr. Oliver Wessely and members of his laboratory for technical
   assistance with the in situ hybridization protocol. This work was
   supported by a grant to A.N.L. from the National Institutes of Health
   (1R01HL089376), and by the Case Western Reserve University/Cleveland
   Clinic CTSA (UL1 RR024989) from NIH/National Center for Research
   Resources (NCRR). Y.B-H. is supported by a National Institutes of Health
   training grant (T32GM008056).
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NR 25
TC 17
Z9 20
U1 0
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-213X
J9 BMC DEV BIOL
JI BMC Dev. Biol.
PD AUG 6
PY 2012
VL 12
AR 22
DI 10.1186/1471-213X-12-22
PG 14
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA 029YS
UT WOS:000310534900001
PM 22866814
OA Green Published, hybrid
DA 2025-04-10
ER

PT J
AU Liang, Y
   Song, MM
   Liu, SY
   Ma, LL
AF Liang, Yan
   Song, Meng Meng
   Liu, Shi Yan
   Ma, Liang Liang
TI Relationship between expression of glucocorticoid receptor isoforms and
   glucocorticoid resistance in immune thrombocytopenia
SO HEMATOLOGY
LA English
DT Article
DE Idiopathic thrombocytopenia purpura; Glucocorticoid receptor; Receptor
   isoform; Glucocorticoid resistance
ID MESSENGER-RNAS; CELLS; ALPHA; LEUKEMIA; GAMMA; BETA
AB Background: Glucocorticoids (GCs) play an important role in the treatment of several hematological malignancies, such as immune thrombocytopenia (ITP). The glucocorticoid receptor (GR) mediates the effects of GCs. Five isoforms of GR mRNA were described: GR alpha, GR beta, GR gamma, GRP, and GRA. GR levels are regulated by alternative splicing of GR mRNA. Several studies demonstrated that a lower GR expression was associated with poor GC response.
   Purpose: This study investigated the expression of GR isoforms and the relationship between GC resistance in ITP.
   Methods: This study determined GR alpha/beta/gamma/P mRNA and GR alpha/beta protein expression levels using SYBR Green Real-time PCR and Western blot, respectively, in 49 newly diagnosed ITP patients and 31 controls.
   Results: The expression of GR isoform mRNA in ITP and controls showed the following trend: GR alpha > GRP > GR gamma > GR beta. The expression of GR alpha, beta mRNA and the total frequency of the four GR isoforms in ITP was significantly higher than in controls (P < 0.05). The expression of GR alpha mRNA and protein in the GC-resistant group was significantly lower than that in the GC-sensitive group and controls (P < 0.05). GR beta could not be detected at the protein level in our experimental conditions.
   Conclusion: GR alpha and GRP were the main GR isoforms responsible for the effects of GC, and GR alpha and GRP exhibited synergistic effects. The down-regulation of GR alpha levels may play an important role in GC resistance in ITP. The effects of GCs in ITP were not associated with changes in GR beta and GR gamma.
C1 [Liang, Yan; Song, Meng Meng; Liu, Shi Yan] Taian Hosp Tradit Chinese Med TCM, Dept Hematol Oncol, Tai An 271000, Shandong, Peoples R China.
   [Ma, Liang Liang] Dalian Med Univ, Dept Hematol, Affiliated Hosp 1, Dalian 116011, Liaoning Provin, Peoples R China.
C3 Dalian Medical University
RP Liang, Y (corresponding author), Taian Tradit Chinese Med Hosp, Dept Hematol Oncol, Tai An 271000, Shandong, Peoples R China.
EM qigougoumaitang@163.com
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NR 16
TC 6
Z9 10
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1024-5332
EI 1607-8454
J9 HEMATOLOGY
JI Hematology
PY 2016
VL 21
IS 7
BP 440
EP 446
DI 10.1080/10245332.2015.1102371
PG 7
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA DS2CL
UT WOS:000380527900009
PM 27077774
OA gold
DA 2025-04-10
ER

PT J
AU Amiry-Moghaddam, M
   Lindland, H
   Zelenin, S
   Roberg, BÅ
   Gundersen, BB
   Petersen, P
   Rinvik, E
   Torgner, IA
   Ottersen, OP
AF Amiry-Moghaddam, M
   Lindland, H
   Zelenin, S
   Roberg, BÅ
   Gundersen, BB
   Petersen, P
   Rinvik, E
   Torgner, IA
   Ottersen, OP
TI Brain mitochondria contain aquaporin water channels:: evidence for the
   expression of a short AQP9 isoform in the inner mitochondrial membrane
SO FASEB JOURNAL
LA English
DT Article
DE water channels; mitochondria; Parkinson's disease; astrocytes;
   substantia nigra
ID PHOSPHATE-ACTIVATED GLUTAMINASE; NEUTRAL SOLUTE CHANNEL; RAT-BRAIN;
   ISCHEMIC BRAIN; MOLECULAR CHARACTERIZATION; ASTROCYTE MITOCHONDRIA;
   GLYCEROL FACILITATOR; ENERGY-METABOLISM; ESCHERICHIA-COLI;
   HYPOXIA-ISCHEMIA
AB Aquaporins are a family of water channels found in animals, plants, and microorganisms. A subfamily of aquaporins, the aquaglyceroporins, are permeable for water as well as certain solutes such as glycerol, lactate, and urea. Here we show that the brain contains two isoforms of AQP9 - an aquaglyceroporin with a particularly broad substrate specificity - and that the more prevalent of these isoforms is expressed in brain mitochondria. The mitochondrial AQP9 isoform is detected as an similar to 25 kDa band in immunoblots. This isoform is likely to correspond to a new AQP9 mRNA that is obtained by alternative splicing and has a shorter ORF than the liver isoform. Subfractionation experiments and high-resolution immunogold analyses revealed that this novel AQP9 isoform is enriched in mitochondrial inner membranes. AQP9 immunopositive mitochondria occurred in astrocytes throughout the brain and in a subpopulation of neurons in the substantia nigra, ventral tegmental area, and arcuate nucleus. In the latter structures, the AQP9 immunopositive mitochondria were located in neurons that were also immunopositive for tyrosine hydroxylase, as demonstrated by double labeling immunogold electron microscopy. Our findings suggest that mitochondrial AQP9 is a hallmark of astrocytes and midbrain dopaminergic neurons. In physiological conditions, the flux of lactate and other metabolites through AQP9 may confer an advantage by allowing the mitochondria to adjust to the metabolic status of the extramitochondrial cytoplasm. We hypothesize that the complement of mitochondrial AQP9 in dopaminergic neurons may relate to the vulnerability of these neurons in Parkinson's disease.
C1 Univ Oslo, Ctr Mol Biol & Neurosci, N-0317 Oslo, Norway.
   Univ Oslo, Nord Ctr Water Imbalance Related Disorders, N-0317 Oslo, Norway.
   Univ Oslo, Inst Basic Med Sci, Dept Biochem, N-0317 Oslo, Norway.
   Karolinska Inst, Dept Woman & Child Hlth, Stockholm, Sweden.
C3 University of Oslo; University of Oslo; University of Oslo; Karolinska
   Institutet
RP Univ Oslo, Ctr Mol Biol & Neurosci, POB 1105 Blindern, N-0317 Oslo, Norway.
EM mahmo@medisin.uio.no
RI Roberg, Bjørg/B-4589-2013
OI Amiry-Moghaddam, Mahmood/0000-0003-1071-1247; Gundersen,
   Brigitta/0000-0002-7801-9348
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NR 47
TC 116
Z9 129
U1 0
U2 13
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD SEP
PY 2005
VL 19
IS 11
BP 1459
EP 1467
DI 10.1096/fj.04-3515com
PG 9
WC Biochemistry & Molecular Biology; Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics; Cell Biology
GA 970NA
UT WOS:000232315700039
PM 16126913
DA 2025-04-10
ER

PT J
AU Marietta, M
   Coluccio, V
   Luppi, M
AF Marietta, Marco
   Coluccio, Valeria
   Luppi, Mario
TI Potential mechanisms of vaccine-induced thrombosis
SO EUROPEAN JOURNAL OF INTERNAL MEDICINE
LA English
DT Review
DE COVID-19 vaccines; BNT162b; ChAdOx1 nCoV-19; Ad26.COV2.S; Vaccine;
   induced immune thrombocytopenia; and thrombosis; Autoimmune
   heparin-induced; thrombocytopenia
ID CHADOX1 NCOV-19; IMMUNE THROMBOCYTOPENIA; ANTIBODIES
AB Vaccine-induced immune thrombocytopenia and thrombosis (VITT) is a rare syndrome characterized by hightiter anti-platelet factor 4 (PF4) antibodies, thrombocytopenia and arterial and venous thrombosis in unusual sites, as cerebral venous sinuses and splanchnic veins.
   VITT has been described to occur almost exclusively after administration of ChAdOx1 nCoV-19 and Ad26. COV2.S adenovirus vector- based COVID-19 vaccines.
   Clinical and laboratory features of VITT resemble those of heparin-induced thrombocytopenia (HIT). It has been hypothesized that negatively charged polyadenylated hexone proteins of the AdV vectors could act as heparin to induce the conformational changes of PF4 molecule that lead to the formation of anti-PF4/polyanion antibodies. The anti-PF4 immune response in VITT is fostered by the presence of a proinflammatory milieu, elicited by some impurities found in ChAdOx1 nCoV-19 vaccine, as well as by soluble spike protein resulting from alternative splice events.
   Anti-PF4 antibodies bind PF4, forming immune complexes which activate platelets, monocytes and granulocytes, resulting in the VITT's immunothrombosis.
   The reason why only a tiny minority of patents receiving AdV-based COVID-19 vaccines develop VITT is still unknown. It has been hypothesized that individual intrinsic factors, either acquired (i.e., pre-priming of B cells to produce anti-PF4 antibodies by previous contacts with bacteria or viruses) or inherited (i.e., differences in platelet T-cell ubiquitin ligand-2 [TULA-2] expression) can predispose a few subjects to develop VITT.
   A better knowledge of the mechanistic basis of VITT is essential to improve the safety and the effectiveness of future vaccines and gene therapies using adenovirus vectors.
C1 [Marietta, Marco; Coluccio, Valeria; Luppi, Mario] Azienda Ospedaliero Univ, Hematol Unit, Modena, Italy.
   [Luppi, Mario] Univ Modena & Reggio Emilia, Sect Hematol, Dept Med & Surg Sci, Modena, Italy.
C3 Universita di Modena e Reggio Emilia
RP Marietta, M (corresponding author), Azienda Ospedaliero Univ, Hematol Unit, Modena, Italy.
EM marco.marietta@unimore.it
CR Andrews NJ, 2022, LANCET REG HEALTH-EU, V13, DOI 10.1016/j.lanepe.2021.100260
   [Anonymous], COVID Data Tracker: COVID-19 Vaccinations in the United States
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NR 60
TC 14
Z9 15
U1 1
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0953-6205
EI 1879-0828
J9 EUR J INTERN MED
JI Eur. J. Intern. Med.
PD NOV
PY 2022
VL 105
BP 1
EP 7
DI 10.1016/j.ejim.2022.08.002
EA OCT 2022
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA D9BY7
UT WOS:000971619700001
PM 35953336
OA Green Published, Bronze
DA 2025-04-10
ER

PT J
AU Caselli, A
   Taddei, ML
   Bini, C
   Paoli, P
   Camici, G
   Manao, G
   Cirri, P
   Ramponi, G
AF Caselli, Anna
   Taddei, Maria Letizia
   Bini, Chiara
   Paoli, Paolo
   Camici, Guido
   Manao, Giampaolo
   Cirri, Paolo
   Ramponi, Giampietro
TI Low molecular weight protein tyrosine phosphatase and caveolin-1:
   Interaction and isoenzyme-dependent regulation
SO BIOCHEMISTRY
LA English
DT Article
ID NITRIC-OXIDE SYNTHASE; LMW-PTP; SCAFFOLDING DOMAIN; KINASE;
   PHOSPHORYLATION; PURIFICATION; SRC; IDENTIFICATION; INACTIVATION;
   ACTIVATION
AB Low molecular weight protein tyrosine phosphatases (LMW-PTPs) are small enzymes that are ubiquitous in many organisms. They are important in biological processes such as cell proliferation, adhesion, migration, and invasiveness. LMW-PTP is expressed in mammalian cells as two isoforms (IF1 and IF2) originating through alternative splicing. We have previously shown that IF2 targets lipid rafts called caveolae and interacts with caveolin-1, their major structural protein. Caveolae are cholesterol- and sphingolipid-rich membrane microdomains that have been implicated in a variety of cellular functions, including signal transduction events. Caveolin-1 contains a scaffolding region that contributes to the binding of the protein to the plasma membrane and mediates protein omo- and etero-oligomerization. Interaction of many signaling molecules with the scaffolding domain sequesters them into caveolae and inhibits or suppresses their activities. Caveolin-interacting proteins usually have a typical sequence motif, also present in all the LMW-PTPs, which is characterized by aromatic or large hydrophobic residues in specific positions. We have examined here the interaction of the LMW-PTP isoforms with caveolin-1 and its molecular mechanism, together with the consequences for their tyrosine phosphatase activities. We found that IF1 and IF2 are both capable of interacting with defined regions of caveolin-1 and that their putative caveolin binding sequence motif is not responsible for the association. The formation of LMW-PTP/caveolin-1 complexes is accompanied by modulation of the enzyme activities, and the inhibitory effect elicited against IF1 is stronger than that against IF2. The caveolin scaffolding domain is directly involved in the observed phenomena.
C1 Univ Florence, Dept Biochem Sci, I-50121 Florence, Italy.
   Univ Florence, Ctr Res, High Educ DENOTHE, I-50121 Florence, Italy.
C3 University of Florence; University of Florence
RP Caselli, A (corresponding author), Univ Florence, Dept Biochem Sci, I-50121 Florence, Italy.
EM anna.caselli@unifi.it
RI Camici, Giovanni/H-1631-2018; Caselli, Anna/O-7512-2014; Paoli,
   Paolo/A-2040-2014
OI Camici, Giovanni/0000-0002-0523-0695; Caselli, Anna/0000-0001-8140-3415;
   Paoli, Paolo/0000-0001-6448-7266
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NR 52
TC 12
Z9 14
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD MAY 29
PY 2007
VL 46
IS 21
BP 6383
EP 6392
DI 10.1021/bi0620858
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 170ER
UT WOS:000246645700023
PM 17469800
DA 2025-04-10
ER

PT J
AU Zhang, XY
   Clark, AF
   Yorio, T
AF Zhang, XY
   Clark, AF
   Yorio, T
TI Regulation of glucocorticoid responsiveness in glaucomatous trabecular
   meshwork cells by glucocorticoid receptor-β
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID INTRAOCULAR-PRESSURE RESPONSE; MESSENGER-RNA; SQUIRREL-MONKEY;
   EXPRESSION; ISOFORM; GENE; DEXAMETHASONE; IDENTIFICATION; RESISTANCE;
   MYOC
AB PURPOSE. Glucocorticoid administration can lead to increased intraocular pressure in greater than 90% of patients with primary open-angle glaucoma (POAG), compared with 30% to 40% of the general population. The molecular mechanisms for increased steroid responsiveness among patients with glaucoma are unknown. An alternative splicing variant of the human glucocorticoid receptor GR beta has dominant negative activity and has been implicated in a variety of steroid-resistant diseases. GR beta also may play a role in glucocorticoid hyperresponsiveness in glaucoma.
   METHODS. Western blot analysis was performed to detect the expression of GR alpha and GR beta in TM cells and its regulation by dexamethasone (DEX). Immunocytochemistry was used to compare the subcellular expression of GR beta between normal and glaucomatous TM cell lines. DEX transgene induction in a luciferase reporter was performed to investigate the differential glucocorticoid responsiveness between multiple normal and glaucomatous TM cell lines. Overexpression of GR beta was conducted in glaucomatous TM cell lines, and the regulation of GR beta in the Dex-induced reporter gene luciferase or endogenous myocilin and fibronectin expression were determined.
   RESULTS. Trabecular meshwork (TM) cell lines derived from normal individuals expressed higher levels of GR beta than did glaucomatous TM cells. Glaucomatous TM cells were more susceptible to DEX induction of a luciferase reporter gene than were TM cells derived from normal donors. Overexpression of GR beta in glaucomatous TM cells inhibited DEX induction of a luciferase reporter gene as well as the endogenous genes MYOC and fibronectin.
   CONCLUSIONS. The decreased amount of GR beta in glaucomatous TM cells could result in enhanced glucocorticoid responsiveness and ocular hypertension.
C1 Univ N Texas, Hlth Sci Ctr, Dept Pharmacol & Neurosci, Ft Worth, TX 76107 USA.
   Alcon Res Ltd, Ft Worth, TX USA.
C3 University of North Texas System; University of North Texas Health
   Science Center; Novartis; Alcon
RP Univ N Texas, Hlth Sci Ctr, Dept Pharmacol & Neurosci, 3500 Camp Bowie Blvd, Ft Worth, TX 76107 USA.
EM yoriot@hsc.unt.edu
FU NEI NIH HHS [EY11979, EY016242] Funding Source: Medline
CR *APPL BIOS INC, US B, V2
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NR 55
TC 54
Z9 61
U1 0
U2 3
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD DEC
PY 2005
VL 46
IS 12
BP 4607
EP 4616
DI 10.1167/iovs.05-0571
PG 10
WC Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Ophthalmology
GA 988FV
UT WOS:000233578600038
PM 16303956
DA 2025-04-10
ER

PT J
AU Kiage, J
   Venkatanarayan, A
   Roth, M
   Elam, M
AF Kiage, James
   Venkatanarayan, Ajay
   Roth, Mendel
   Elam, Marshall
TI Atorvastatin-associated rhabdomyolysis in a patient with a novel variant
   of the SLCO1B1 gene: A case report
SO JOURNAL OF CLINICAL LIPIDOLOGY
LA English
DT Article
DE Rhabdomyolysis; SLCO1B1; Genetic risk; HMG-CoA reductase inhibitors
   (statins); Lipoprotein(a)
AB We report the case of an individual with severe hypercholesterolemia who experienced rhabdomyolysis with high dose atorvastatin. Genetic testing was undertaken to evaluate for suspected familial hypercholesterolemia (FH) and for the presence of gene variants associated with susceptibility to statin associated muscle disease. Genetic testing identified the presence of a potentially damaging variant of the hepatic xenobiotic transporter pump SLCO1B1, a single nucleotide variant (SNV) (rs77271279, c.481+1G>T) that disrupts the canonical donor splice motif. Although this variant has not previously been reported as associated with rhabdomyolysis and thus requires validation in population studies, it likely played a role in this patient's susceptibility to rhabdomyolysis based on functional assessment of the effect of this variant on SLCO1B1 protein function and given the known role of this transporter in statin uptake by the liver. The presence of this gene variant reinforced our decision to treat the patient's hypercholesterolemia with non-statin alternatives (PCSK9 inhibitor and ezetimibe). Genetic testing also identified the presence of a second SLCO1B1 gene variant, c.1200C>G (p.Phe400Leu, rs59113707) and homozygosity for an intron variant of the apolipoprotein(a) (LPA) gene (c.2604.138G>A intron variant, rs9457951) associated with increased Lp(a), a risk factor for atherosclerotic cardiovascular disease. Notably, all three variants are rare in persons of European descent but more frequent in African-Americans. These findings underscore the role of disabling mutations of the SLCO1B1 gene in statin myopathy and the need to validate these and other gene variants associated with statin myopathy in a population of patients with statin-associated muscle disease. Published by Elsevier Inc. on behalf of National Lipid Association.
C1 Vet Affairs Med Ctr, Memphis, TN 38104 USA.
   Univ Tennessee, Hlth Sci Ctr, Memphis, TN USA.
   GB Healthwatch, San Diego, CA USA.
C3 US Department of Veterans Affairs; Veterans Health Administration (VHA);
   Memphis VA Medical Center; University of Tennessee System; University of
   Tennessee Health Science Center
RP Elam, M (corresponding author), Vet Affairs Med Ctr, Hypertens Lipid Res Clin 151, 1030 Jefferson, Memphis, TN 38104 USA.
EM melam@uthsc.edu
OI Roth, Mendel/0000-0001-8651-3832
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NR 24
TC 4
Z9 4
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1933-2874
EI 1876-4789
J9 J CLIN LIPIDOL
JI J. Clin. Lipidol.
PD JAN-FEB
PY 2022
VL 16
IS 1
BP 23
EP 27
DI 10.1016/j.jacl.2021.11.007
PG 5
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YY0WX
UT WOS:000754515200005
PM 34887219
DA 2025-04-10
ER

PT J
AU Lorincz, T
   Szarka, A
AF Lorincz, Tamas
   Szarka, Andras
TI In silico Analysis on the Possible Role of Mitochondria in
   Ferroptosis
SO PERIODICA POLYTECHNICA-CHEMICAL ENGINEERING
LA English
DT Article
DE mitochondria; ferroptosis; GPX4; glutathione; in silico; subcellular
   localization
ID HYDROPEROXIDE GLUTATHIONE-PEROXIDASE; CELL-DEATH;
   SUBCELLULAR-LOCALIZATION; 2-OXOGLUTARATE CARRIER; MECHANISMS; TRANSPORT;
   PROTEINS; CANCER; IDENTIFICATION; CHOLESTEROL
AB The lipid peroxide scavenger enzyme glutathione peroxidase 4 (GPX4) and its cofactor glutathione play a crucial role in the recently described programmed cell death, ferroptosis. Since mitochondria are the major sources of reactive oxygen species in mammalian cells the linkage between mitochondria, mitochondrial ROS generation and ferroptosis emerged quite early. As a result of alternative splicing human GPX4 has three different isoforms: long form (IGPX4), short form (sGPX4) and nuclear form (nGPX4) of which sGPX4 was found essential. To clarify the potential role of mitochondria in ferroptosis the localization of both the long and short versions of GPX4 and the only verified glutathione transport protein SLC25A11 was investigated by different in silica tools. Targeting of IGPX4 and sGPX4 to multiple organelles is possible as a number of rule- and neural network-based algorithms showed concordant results to specific pathways. Hence the mitochondrial localization of both isoforms on the base of in silica prediction is possible. Since sGPX4 was found in multiple organelles and non-canonical import pathways are presumable we also evaluated the previously used in silica methods in predicting the localization of a chimeric signal containing peptide CYP2B1 as well as a solely mitochondrial targeted CYP27A1. Our in silica results showed that only the CELLO prediction tool ranked mitochondrial import with meaningful possibility based on neighboring sequence composition. Summarily the possible mitochondrial localization of both long and short isoforms of GPX4 and the glutathione transporter SLC25A11 support the assumption that mitochondria play an important role in the pathways leading to ferroptosis.
C1 [Lorincz, Tamas; Szarka, Andras] Budapest Univ Technol & Econ, Fac Chem Technol & Biotechnol, Dept Appl Biotechnol & Food Sci, POB 91, H-1521 Budapest, Hungary.
C3 Budapest University of Technology & Economics
RP Szarka, A (corresponding author), Budapest Univ Technol & Econ, Fac Chem Technol & Biotechnol, Dept Appl Biotechnol & Food Sci, POB 91, H-1521 Budapest, Hungary.
EM szarka@mail.bme.hu
RI Lőrincz, Tamás/AAA-3847-2022; Szarka, Andras/H-8130-2012
OI Lorincz, Tamas/0000-0003-1762-4007; Szarka, Andras/0000-0001-6594-254X
FU National Scientific Research Fund grant [OTKA 123752]; BME-Biotechnology
   FIKP grant of EMMI; New National Excellence Program of the Ministry of
   Human Capacities [UNKP-17-3-III]; MedinProt Protein Excellence
   foundation
FX This work was financially supported by the National Scientific Research
   Fund grant (OTKA 123752), by the BME-Biotechnology FIKP grant of EMMI,
   by UNKP-17-3-III New National Excellence Program of the Ministry of
   Human Capacities and MedinProt Protein Excellence foundation.
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NR 46
TC 0
Z9 0
U1 1
U2 23
PU BUDAPEST UNIV TECHNOLOGY ECONOMICS
PI BUDAPEST
PA PERIODICA POLYTECHNICA CIVIL ENGINEERING, BUDAPEST, 1521, HUNGARY
SN 0324-5853
EI 1587-3765
J9 PERIOD POLYTECH-CHEM
JI Period. Polytech.-Chem. Eng.
PY 2018
VL 62
IS 4
BP 370
EP 378
DI 10.3311/PPch.12571
PG 9
WC Engineering, Chemical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering
GA HA9PT
UT WOS:000450637800002
OA gold
DA 2025-04-10
ER

PT J
AU White, AJ
   Northcutt, MJ
   Rohrback, SE
   Carpenter, RO
   Niehaus-Sauter, MM
   Gao, YP
   Wheatly, MG
   Gillen, CM
AF White, Alexandra J.
   Northcutt, Michael J.
   Rohrback, Suzanne E.
   Carpenter, Robert O.
   Niehaus-Sauter, Margaret M.
   Gao, Yongping
   Wheatly, Michele G.
   Gillen, Christopher M.
TI Characterization of sarcoplasmic calcium binding protein (SCP) variants
   from freshwater crayfish Procambarus clarkii
SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR
   BIOLOGY
LA English
DT Article
DE Alternative splicing; Cold; RNAi; Muscle
ID ABDOMINAL FLEXOR MUSCLES; AMINO-ACID-SEQUENCE; K-CL COTRANSPORTER;
   SHRIMP TAIL MUSCLE; CARDIAC TROPONIN-C; LITOPENAEUS-VANNAMEI; SWIMMING
   MUSCLE; SKELETAL-MUSCLE; RELAXATION RATE; REFLEX CONTROL
AB Sarcoplasmic calcium binding protein (SCP) is an invertebrate EF-hand calcium buffering protein that has been proposed to fulfill a similar function in muscle relaxation as vertebrate parvalbumin. We have identified three SCP variants in the freshwater crayfish Procambarus clarkii. The variants (pcSCP1a, pcSCP1b, and pcSCP1c) differ across a 37 amino acid region that lies mainly between the second and third EF-hand calcium binding domains. We evaluated tissue distribution and response of the variants to cold exposure, a stress known to affect expression of parvalbumin. Expression patterns of the variants were not different and therefore do not provide a functional rationale for the polymorphism of pcSCP1. Compared to hepatopancreas, expression of pcSCP1 variants was 100,000-fold greater in axial abdominal muscle and 10-fold greater in cardiac muscle. Expression was 10-100 greater in fast-twitch deep flexor and extensor muscles compared to slow-twitch superficial flexor and extensors. In axial muscle, no significant changes of pcSCP1, calmodulin (CaM), or sarcoplasmic/endoplasmic reticulum Ca-ATPase (SERCA) expression were measured after one week of 4 degrees C exposure. In contrast, large decreases of pcSCP1 were measured in cardiac Muscle, with no changes in CaM or SERCA. Knockdown of pcSCP1 by dsRNA led to reduced muscle activity and decreased expression of SERCA. In summary, the pattern of pcSCP1 tissue expression is similar to parvalbumin, supporting a role in muscle contraction. However, the response of pcSCP1 to cold exposure differs from parvalbumin, suggesting possible functional divergence between the two proteins. (C) 2011 Elsevier Inc. All rights reserved.
C1 [White, Alexandra J.; Northcutt, Michael J.; Rohrback, Suzanne E.; Carpenter, Robert O.; Niehaus-Sauter, Margaret M.; Gillen, Christopher M.] Kenyon Coll, Dept Biol, Gambier, OH 43022 USA.
   [Gao, Yongping; Wheatly, Michele G.] Wright State Univ, Dept Biol Sci, Dayton, OH 45435 USA.
C3 University System of Ohio; Kenyon College; University System of Ohio;
   Wright State University Dayton
RP Gillen, CM (corresponding author), Kenyon Coll, Dept Biol, Gambier, OH 43022 USA.
EM gillenc@kenyon.edu
RI White, Alexandra/D-9687-2019; Wheatly, Michele/AGH-5197-2022
OI White, Alexandra/0000-0003-2455-2945; Wheatly,
   Michele/0000-0001-8025-1050
FU National Science Foundation [IBN 0445202]; Kenyon College
FX The authors thank Dr. Kathy M. Gillen and Dr. Wade H. Powell for
   comments on the manuscript. Support for this research was provided by
   National Science Foundation grant IBN 0445202 to MGW, YG, and CMG and by
   the Kenyon College Summer Science Scholars program.
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NR 51
TC 31
Z9 34
U1 22
U2 272
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1096-4959
J9 COMP BIOCHEM PHYS B
JI Comp. Biochem. Physiol. B-Biochem. Mol. Biol.
PD SEP
PY 2011
VL 160
IS 1
BP 8
EP 14
DI 10.1016/j.cbpb.2011.04.003
PG 7
WC Biochemistry & Molecular Biology; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Zoology
GA 799WV
UT WOS:000293317800002
PM 21530674
DA 2025-04-10
ER

PT J
AU Graham, IR
   Beattie, SG
   Hill, VJ
   Dickson, G
AF Graham, IR
   Beattie, SG
   Hill, VJ
   Dickson, G
TI Oligonucleotide-based gene correction strategies: Applications to
   neuromuscular and cardiovascular diseases
SO CROATIAN MEDICAL JOURNAL
LA English
DT Article
DE apolipoproteins; cardiovascular diseases; dystrophin; gene engineering;
   gene targeting; gene therapy; hyperlipidemia; muscular dystrophies;
   neuromuscular diseases; point mutation; risk factors; RNA, antisense;
   RNA splicing
ID CHIMERIC RNA/DNA OLIGONUCLEOTIDES; RNA-DNA OLIGONUCLEOTIDE;
   SITE-DIRECTED MUTAGENESIS; DYSTROPHIN GENE; ANTISENSE OLIGONUCLEOTIDES;
   NUCLEOTIDE EXCHANGE; MAMMALIAN-CELLS; MESSENGER-RNA; MUTATION; REPAIR
AB Gene augmentation is an attractive and viable approach in treatment of inherited diseases, despite its limitations, ie, the amount of viral genome in replication-defective viral vectors is often too small for larger copy DNAs to be inserted. in addition, most viral vectors, when assessed in vivo, can elicit a host immune response, especially in cases of introduction of a gene copy where protein is completely absent, may have potential mutagenic effect on the host genome, or may be down-regulated. Therefore, alternative therapeutic approaches are being investigated, such as chimeraplasty, in which a mutated allele that already exists in an affected individual can be corrected. Although the only gene defects that can be corrected by chimeraplasty are point mutations, and the correction frequncies are variable, it has been observed that intracellular delivery of oligonucleotides is likely to be more efficient than that of plasmid DNA or viral vectors, because corrected genes are expressed from their autologous promoters, ensuring thus correct spatial and temporal expression, and host immune response is not elicited. Another strategy in the therapy of inherited diseases, such as Duchenne muscular dystrophy, is the application of antisense RNA oligonucleotides, or splicomers, to the exclusion of exons whose mutation leads to production of deficient essential proteins. Here we report the recent progress made and problems encountered in each of these fields, and discuss the potential of nucleotide-based gene correction strategies in treatment of neuromuscular and cardiovascular diseases.
C1 Univ London Royal Holloway & Bedford New Coll, Sch Biol Sci, Ctr Biomed Res, Egham TW20 0EX, Surrey, England.
C3 University of London; Royal Holloway University London
RP Univ London Royal Holloway & Bedford New Coll, Sch Biol Sci, Ctr Biomed Res, Egham TW20 0EX, Surrey, England.
EM g.dickson@rhul.ac.uk
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NR 26
TC 2
Z9 2
U1 0
U2 1
PU MEDICINSKA NAKLADA
PI ZAGREB
PA VLASKA 69, HR-10000 ZAGREB, CROATIA
SN 0353-9504
EI 1332-8166
J9 CROAT MED J
JI Croat. Med. J.
PD AUG
PY 2001
VL 42
IS 4
BP 467
EP 472
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 466GW
UT WOS:000170637900018
PM 11471201
DA 2025-04-10
ER

PT J
AU Vawter, MP
AF Vawter, MP
TI Dysregulation of the neural cell adhesion molecule and neuropsychiatric
   disorders
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Review
DE schizophrenia; bipolar disorder; depression; memory; synaptic
   plasticity; ventricle enlargement; neurocognitive impairment
ID LONG-TERM POTENTIATION; MONOZYGOTIC TWINS DISCORDANT; DEPENDENT NEURITE
   OUTGROWTH; PASSIVE-AVOIDANCE RESPONSE; FIRST-EPISODE PATIENTS; N-CAM;
   BIPOLAR DISORDER; VASE EXON; MEMORY FORMATION; NERVOUS-SYSTEM
AB Cell adhesion molecule proteins play a diverse role in neural development, signal transduction, structural Linkages to extracellular and intracellular proteins, synaptic stabilization, neurogenesis, and learning. Three basic mRNA isoforms and potent posttranslational modifications differentially regulate these neurobiological properties of the neural cell adhesion molecule (N-CAM). Abnormal concentrations of N-CAM 105-115 kDa (cN-CAM), N-CAM variable alternative spliced exon (VASE), and N-CAM secreted exon (SEC) are related to schizophrenia and bipolar neuropsychiatric disorders. These N-CAM isoforms provide potential mechanisms for expression of multiple neurobiological alterations between controls and individuals with schizophrenia or bipolar illness. Multiple processes can trigger the dysregulation of N-CAM isoforms. Differences in neuropil volume, neuronal diameter, gray matter thickness, and ventricular size can be related to N-CAM neurobiological properties in neuropsychiatric disorders. Potential test of the N-CAM dysregulation hypothesis of neuropsychiatric disorder is whether ongoing dysregulation of N-CAM would cause cognitive impairments, increased lateral ventricle volume, and decreased hippocampal volume observed in schizophrenia and to a lesser extent in bipolar disorder. An indirect test of this theory conducted in animal experiments lend support to this N-CAM hypothesis. N-CAM dysregulation is consistent with a synaptic abnormality that could underlie the disconnection between brain regions consistent with neuroimaging reports. Synapse stability and plasticity may be put of the molecular neuropathology of these disorders. (C) 2000 Elsevier Science B.V. All rights reserved.
C1 NIDA, Addict Res Ctr, IRP, Sect Dev & Plast, Baltimore, MD 21224 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute on
   Drug Abuse (NIDA)
RP NIDA, Addict Res Ctr, IRP, Sect Dev & Plast, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM mvawter@intra.nida.nih.gov
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NR 140
TC 88
Z9 100
U1 1
U2 7
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD SEP 29
PY 2000
VL 405
IS 1-3
BP 385
EP 395
DI 10.1016/S0014-2999(00)00568-9
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Pharmacology & Pharmacy
GA 360PQ
UT WOS:000089676800036
PM 11033343
DA 2025-04-10
ER

PT J
AU Del Galdo, F
   Maul, GG
   Jiménez, SA
   Artlett, CM
AF Del Galdo, Francesco
   Maul, Gerd G.
   Jimenez, Sergio A.
   Artlett, Carol M.
TI Expression of allograft inflammatory factor 1 in tissues from patients
   with systemic sclerosis and in vitro differential expression of its
   isoforms in response to transforming growth factor β
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID SMOOTH-MUSCLE-CELLS; AU-RICH ELEMENTS; MESSENGER-RNA;
   POSTTRANSCRIPTIONAL REGULATION; PERIPHERAL-BLOOD; GENE-EXPRESSION;
   ACTIVATION; PROTEIN; PROLIFERATION; CLONING
AB Objective. Allograft inflammatory factor 1 (AIF-1), a protein initially identified in chronically rejected rat cardiac allografts, is involved in the immune response and proliferative vasculopathy that occurs during allograft rejection. Three well-characterized isoforms of AIF-1 result from alternative messenger RNA (mRNA) splicing. We previously identified a strong association of systemic sclerosis (SSc) with a polymorphism in AIF-1 isoform 2. The purpose of this study was to investigate AIF-1 expression in affected tissues from patients with SSc and to examine the regulation of its isoforms by transforming growth factor beta (TGF beta).
   Methods. AIF-1 in the skin and lung tissues of patients with SSc was analyzed by immunochemistry. AIF-1 isoform expression in response to TGF beta and interferon-gamma stimulation was examined by quantitative polymerase chain reaction (PCR).
   Results. AIF-1 protein was present in affected vessels of the lung and skin lesions of patients with SSc. Quantitative PCR showed an average of 14-fold higher mRNA levels in affected SSc skin than in normal skin. Double-label immunofluorescence staining demonstrated that T cells, macrophages, and endothelial cells in affected tissues expressed AIF-1. Stimulation of peripheral blood mononuclear cells with TGF beta caused a specific and significant increase in the expression of AIF-1 isoform 2 transcripts (P < 0.005), which was due to stabilization of AIF-1 isoform 2 mRNA.
   Conclusion. These data suggest that AIF-1 plays an important role in the pathogenesis of SSc owing to its increased expression in affected tissues and to the specific stimulation of AIF-1 isoform 2 by TGF beta.
C1 Thomas Jefferson Univ, Div Rheumatol, Philadelphia, PA 19107 USA.
   Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
C3 Thomas Jefferson University; The Wistar Institute
RP Artlett, CM (corresponding author), Thomas Jefferson Univ, Div Rheumatol, 233 S 10th St,Room 509, Philadelphia, PA 19107 USA.
EM Carol.Artlett@jefferson.edu
RI Jimenez-Perez, Salvio/H-5824-2015; Del+Galdo, Francesco/ABD-9872-2021
OI Jimenez, Sergio/0000-0001-5213-1203
FU NIAMS NIH HHS [R01-AR-19616] Funding Source: Medline
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NR 33
TC 53
Z9 61
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD AUG
PY 2006
VL 54
IS 8
BP 2616
EP 2625
DI 10.1002/art.22010
PG 10
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA 071ZC
UT WOS:000239641400032
PM 16868985
DA 2025-04-10
ER

PT J
AU Schennink, A
   Trott, JF
   Manjarin, R
   Lemay, DG
   Freking, BA
   Hovey, RC
AF Schennink, Anke
   Trott, Josephine F.
   Manjarin, Rodrigo
   Lemay, Danielle G.
   Freking, Bradley A.
   Hovey, Russell C.
TI Comparative genomics reveals tissue-specific regulation of prolactin
   receptor gene expression
SO JOURNAL OF MOLECULAR ENDOCRINOLOGY
LA English
DT Article
DE prolactin; receptor; kidney; transcription factors; gene regulation
ID MULTIPLE 1ST EXONS; PORCINE PROLACTIN; PERIPARTUM CARDIOMYOPATHY;
   CARDIOVASCULAR CHANGES; CALCIUM-TRANSPORT; CHOROID-PLEXUS;
   MAMMARY-GLAND; MESSENGER-RNA; SHORT-FORM; LACTATION
AB Prolactin (PRL), acting via the PRL receptor (PRLR), controls hundreds of biological processes across a range of species. Endocrine PRL elicits well-documented effects on target tissues such as the mammary glands and reproductive organs in addition to coordinating whole-body homeostasis during states such as lactation or adaptive responses to the environment. While changes in PRLR expression likely facilitates these tissue-specific responses to circulating PRL, the mechanisms regulating this regulation in non-rodent species has received limited attention. We performed a wide-scale analysis of PRLR 50 transcriptional regulation in pig tissues. Apart from the abundantly expressed and widely conserved exon 1, we identified alternative splicing of transcripts from an additional nine first exons of the porcine PRLR (pPRLR) gene. Notably, exon 1.5 transcripts were expressed most abundantly in the heart, while expression of exon 1.3-containing transcripts was greatest in the kidneys and small intestine. Expression of exon 1.3 mRNAs within the kidneys was most abundant in the renal cortex, and increased during gestation. A comparative analysis revealed a human homologue to exon 1.3, hE1(N2), which was also principally transcribed in the kidneys and small intestines, and an exon hE1(N3) was only expressed in the kidneys of humans. Promoter alignment revealed conserved motifs within the proximal promoter upstream of exon 1.3, including putative binding sites for hepatocyte nuclear factor-1 and Sp1. Together, these results highlight the diverse, conserved and tissue-specific regulation of PRLR expression in the targets for PRL, which may function to coordinate complex physiological states such as lactation and osmoregulation.
C1 [Schennink, Anke; Trott, Josephine F.; Hovey, Russell C.] Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA.
   [Lemay, Danielle G.] Univ Calif Davis, Genome Ctr, Davis, CA 95616 USA.
   [Manjarin, Rodrigo] USDA ARS, Childrens Nutr Res Ctr, Baylor Coll Med, Houston, TX USA.
   [Freking, Bradley A.] ARS, USDA, US Meat Anim Res Ctr, Clay Ctr, NE 68933 USA.
C3 University of California System; University of California Davis;
   University of California System; University of California Davis; United
   States Department of Agriculture (USDA); Baylor College of Medicine;
   United States Department of Agriculture (USDA)
RP Trott, JF (corresponding author), Univ Calif Davis, Dept Anim Sci, 2335 Meyer Hall,One Shields Ave, Davis, CA 95616 USA.
EM jftrott@ucdavis.edu
RI Freking, Brad/M-1938-2019
OI Freking, Brad/0000-0001-5385-5692; Manjarin,
   Rodrigo/0000-0001-5691-1549; Lemay, Danielle/0000-0003-3318-0485
FU National Research Initiative Competitive from the USDA National
   Institute for Food and Agriculture [2008-35206-18895]; ARS [ARS-0422291,
   813242] Funding Source: Federal RePORTER
FX This project was supported by National Research Initiative Competitive
   grant number 2008-35206-18895 from the USDA National Institute for Food
   and Agriculture.
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NR 55
TC 6
Z9 9
U1 0
U2 22
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
   ENGLAND
SN 0952-5041
J9 J MOL ENDOCRINOL
JI J. Mol. Endocrinol.
PD FEB
PY 2015
VL 54
IS 1
BP 1
EP 15
DI 10.1530/JME-14-0212
PG 15
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA CI3EE
UT WOS:000354629600003
PM 25358647
OA Bronze
DA 2025-04-10
ER

PT J
AU Van Esch, H
   Agarwal, AK
   Debeer, P
   Fryns, JP
   Garg, A
AF Van Esch, H
   Agarwal, AK
   Debeer, P
   Fryns, JP
   Garg, A
TI A homozygous mutation in the lamin A/C gene associated with a novel
   syndrome of arthropathy, tendinous calcinosis, and progeroid features
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID HUTCHINSON-GILFORD-PROGERIA; FAMILIAL PARTIAL LIPODYSTROPHY;
   MANDIBULOACRAL DYSPLASIA; PHENOTYPIC HETEROGENEITY; DISEASE; LMNA;
   LAMINOPATHIES; ZMPSTE24; ACTIN
AB Context: Mutations in the lamin A/C (LMNA) gene have been reported in a wide variety of disorders, including lipodystrophies, cardiomyopathy, muscular dystrophies, neuropathy, mandibuloacral dysplasia, restrictive dermopathy, and progeria.
   Objective: The objective of this study was to carry out mutational analysis of LMNA in a patient with a novel syndrome of arthropathy, tendinous calcinosis, and progeroid features.
   Design: The study design was a descriptive case report.
   Setting: The study was performed at a referral center.
   Patient: A 44-yr-old male of European descent with an autosomal recessive arthropathy syndrome affecting predominantly the distal femora and proximal tibia in the knee with tendinous calcifications was studied. He also had progeroid features, such as pinched nose and micrognathia, cataract, alopecia, generalized lipodystrophy, and sclerodermatous skin.
   Main Outcome Measures: The main outcome measures were mutational analysis of lamin A/C (LMNA) and its processing enzyme, zinc metalloproteinase (ZMPSTE24), as candidate genes.
   Results: We found a homozygous nucleotide substitution, 1718C > T, in exon 11 of the LMNA gene, resulting in substitution of a well-conserved residue serine at position 573 with leucine (S573L). This missense mutation only affects lamin A, not lamin C, because the alternative splicing site is located in exon 10. Immunofluorescence staining of the nuclei from his skin fibroblasts showed occasional misshapen morphology.
   Conclusions: The S573L homozygous LMNA mutation is associated with a novel phenotype of arthropathy, tendinous calcifications, and progeroid features distinct from the acroosteolysis previously reported in patients with mandibuloacral dysplasia caused by LMNA or ZMPSTE24 mutations. Thus, arthropathy with tendinous calcifications can be added to the growing list of disorders associated with LMNA mutations.
C1 Univ Texas, SW Med Ctr, Dept Internal Med, Div Nutr & Metab Dis, Dallas, TX 75390 USA.
   Univ Texas, SW Med Ctr, Ctr Human Nutr, Dallas, TX 75390 USA.
   Univ Hosp Leuven, Ctr Human Genet, B-3000 Louvain, Belgium.
   Univ Hosp Leuven, Dept Orthoped, B-3000 Louvain, Belgium.
C3 University of Texas System; University of Texas Dallas; University of
   Texas Southwestern Medical Center Dallas; University of Texas System;
   University of Texas Southwestern Medical Center Dallas; University of
   Texas Dallas; KU Leuven; University Hospital Leuven; KU Leuven;
   University Hospital Leuven
RP Garg, A (corresponding author), Univ Texas, SW Med Ctr, Dept Internal Med, Div Nutr & Metab Dis, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM Abhimanyu.garg@utsouthwestern.edu
RI Van+Esch, Hilde/AAU-5688-2020
OI Van Esch, Hilde/0000-0002-9604-5726
FU NIDDK NIH HHS [R01 DK 54387] Funding Source: Medline
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NR 20
TC 34
Z9 36
U1 1
U2 3
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD FEB
PY 2006
VL 91
IS 2
BP 517
EP 521
DI 10.1210/jc.2005-1297
PG 5
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 010CC
UT WOS:000235161200026
PM 16278265
OA Bronze
DA 2025-04-10
ER

PT J
AU Hori, Y
   Wada, H
   Mori, Y
   Shimura, M
   Hiyoyama, K
   Nakasaki, T
   Nishii, K
   Tamaki, S
   Nishikawa, M
   Deguchi, K
   Minami, N
   Shiku, H
AF Hori, Y
   Wada, H
   Mori, Y
   Shimura, M
   Hiyoyama, K
   Nakasaki, T
   Nishii, K
   Tamaki, S
   Nishikawa, M
   Deguchi, K
   Minami, N
   Shiku, H
TI Plasma sFas and sFas ligand levels in patients with thrombotic
   thrombocytopenic purpura and in those with disseminated intravascular
   coagulation
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
DE sFas; sFas-ligand; DIC; TTP; apoptosis
ID SOLUBLE FAS; ENDOTHELIAL-CELLS; APOPTOSIS; SERUM; DISEASES; APO-1; CD95
AB Fas, a member of the tumor necrosis receptor superfamily, is 36 kD surface protein containing a single transmembrane region and induces apoptosis by Fas-Fas ligand binding. Soluble Fas (sFas) is produced as the form lacking 21 amino acid residues containing the transmembrane domain by alternative splicing. We found that the plasma sFas levels of 33 patients with thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS), 19 patients with disseminated intravascular coagulation (DIC), and 10 non-DIG patients with multiple organ failure (MOF) were significantly higher than those of 21 non-DIG patients without organ failure and those of 25 healthy volunteers. The plasma sFas ligand levels of the TTP/HUS patients, the DIC patients, and the non-DIG patients with MOF were significantly higher than those of the non-DIG patients without organ failure and those of the healthy volunteers. The plasma sFas levels were significantly correlated with the plasma sFas ligand levels in all subjects. The plasma thrombomodulin (TM) levels were increased significantly in the TTP/HUS patients, the DIG patients, and the non-DIG patients with MOF compared with the levels of the non-DIG patients without organ failure and the healthy volunteers, The plasma sFas antigen levels were correlated significantly with the plasma TM levels in all subjects. These findings suggest that the increases of sFas and sFas ligand that cause apoptosis might be related to the vascular endothelial cell injuries in TTP and DIG with organ failure. (C) 1999 Wiley-Liss, Inc.
C1 Mie Univ, Sch Med, Dept Internal Med 2, Tsu, Mie 514, Japan.
   Mie Univ, Sch Med, Dept Blood Transfus, Tsu, Mie 514, Japan.
C3 Mie University; Mie University
RP Wada, H (corresponding author), Mie Univ, Sch Med, Dept Internal Med 2, 2-174 Edobashi, Tsu, Mie 514, Japan.
RI Shiku, Hiroshi/U-7321-2019
OI Shiku, Hiroshi/0000-0002-0362-755X; Hori, Yasuhide/0000-0002-0053-995X
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NR 27
TC 10
Z9 12
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD MAY
PY 1999
VL 61
IS 1
BP 21
EP 25
PG 5
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA 193CX
UT WOS:000080119200005
PM 10331507
DA 2025-04-10
ER

PT J
AU Nilsson, SC
   Karpman, D
   Vaziri-Sani, F
   Kristoffersson, AC
   Salomon, R
   Provot, F
   Fremeaux-Bacchi, V
   Trouw, LA
   Blom, AM
AF Nilsson, Sara C.
   Karpman, Diana
   Vaziri-Sani, Fariba
   Kristoffersson, Ann-Charlotte
   Salomon, Remi
   Provot, Francois
   Fremeaux-Bacchi, Veronique
   Trouw, Leendert A.
   Blom, Anna M.
TI A mutation in factor I that is associated with atypical hemolytic uremic
   syndrome does not affect the function of factor I in complement
   regulation
SO MOLECULAR IMMUNOLOGY
LA English
DT Article
DE complement; kidney; aHUS; factor I; regulation
ID MEMBRANE COFACTOR PROTEIN; FACTOR-H MUTATIONS; C4B-BINDING PROTEIN;
   ENDOTHELIAL-CELLS; DEFICIENCY; GENE; GLOMERULONEPHRITIS; SUSCEPTIBILITY;
   C3B; PURIFICATION
AB Factor I (FI) is the major complement inhibitor that degrades Ob and C4b in the presence of cofactors such as factor H (FH) and membrane cofactor protein (MCP). Recently, mutations and polymorphisms in complement regulator molecules FH and MCP but also in FI have been associated with atypical hemolytic uremic syndrome (aHUS). HUS is a disorder characterized by hemolytic anemia, thrombocytopenia and acute renal failure. In this study, we report three unrelated patients with an identical heterozygous mutation, G261D, in the FI heavy chain who developed severe aHUS at different time points in their lives. Two of the patients also have polymorphisms in FH previously associated with risk of developing aHUS. Testing in particular one patient and control serum samples we did not observe major differences in complement hemolytic activity, FI plasma levels or the capability to degrade C4b or Ob. A recombinant protein was produced in order to analyze the functional consequences of the mutation. Mutant FI had a slightly different migration pattern during electrophoresis under reducing conditions. An alteration due to alternative splicing or glycosylation was ruled out, thus the altered migration may be due to proximity of the mutation to a cysteine residue. The recombinant mutant FI degraded Ob and C4b in a manner comparable to wild-type protein. In conclusion, despite the association between the heterozygous mutation in FI and aHUS we did not observe any abnormalities in the function of FI regarding complement regulation. (c) 2006 Elsevier Ltd. All rights reserved.
C1 Lund Univ, Univ Hosp Malmo, Dept Lab Med, S-20502 Malmo, Sweden.
   Lund Univ, Dept Pediat, Lund, Sweden.
   Hop Necker Enfants Malad, AP HP, Serv Nephrol Pediat, Paris, France.
   Hop Calmette, Serv Nephrol, Lille, France.
   Hop Europeen Georges Pompidou, Serv Immunol Biol, Paris, France.
C3 Lund University; Skane University Hospital; Lund University; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Necker-Enfants Malades - APHP; Universite de Lille; CHU
   Lille; Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP
RP Blom, AM (corresponding author), Lund Univ, Univ Hosp Malmo, Dept Lab Med, S-20502 Malmo, Sweden.
EM Anna.Blom@med.lu.se
RI Trouw, Leendert/AGK-5202-2022; Vaziri-Sani, Fariba/J-6390-2014; Blom,
   Anna/B-9607-2009
OI Trouw, Leendert/0000-0001-5186-2290; Karpman, Diana/0000-0001-7220-7658;
   Blom, Anna/0000-0002-1348-1734
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NR 35
TC 78
Z9 79
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD MAR
PY 2007
VL 44
IS 8
BP 1835
EP 1844
DI 10.1016/j.molimm.2006.10.005
PG 10
WC Biochemistry & Molecular Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Immunology
GA 138GQ
UT WOS:000244351500003
PM 17084897
DA 2025-04-10
ER

PT J
AU Kato, N
   Sugiyama, T
   Morita, H
   Kurihara, H
   Yamori, Y
   Yazaki, Y
AF Kato, N
   Sugiyama, T
   Morita, H
   Kurihara, H
   Yamori, Y
   Yazaki, Y
TI G protein β3 subunit variant and essential hypertension in Japanese
SO HYPERTENSION
LA English
DT Article
DE hypertension, essential; association; case-control studies; G proteins;
   genetics
ID SODIUM-PROTON EXCHANGE; ANGIOTENSINOGEN GENE; ASSOCIATION; DISEASE
AB Enhanced G protein activation has been implicated to underlie the increased sodium-proton transport in blood cells, an impaired characteristic observed in 30% to 50% of patients with essential hypertension. Recently, significant association between a C825T polymorphism of the gene encoding the G protein beta 3 subunit and hypertension was demonstrated in a white population, together with the finding that the T825 variant might be related to alternative splicing through unidentified mechanisms. We therefore investigated the disease relevance of this candidate gene by conducting an association study in a relatively large Japanese population. Participants comprised 718 hypertensive case subjects (without diabetes mellitus), 515 normotensive control subjects, and 191 hypertensive subjects with borderline or established diabetes mellitus; all individuals were recruited at a single institution. Genotype distribution of the C825T polymorphism was compared between hypertensive subjects, with or without diabetes, and the control group with chi(2) statistics. No significant association was observed in the present study. Results were still not significant when the case group was subdivided according to more stringent classification criteria. Allele frequencies of T825 proved to be almost concordant among the 3 study groups and higher in Japanese (49.0% to 49.6%) compared with a reported prevalence of 25% to 31% in whites. Our data suggest that the T825 variant of the G protein beta 3 subunit gene is unlikely to constitute major susceptibility for essential hypertension in the Japanese population studied. However, further investigation is required to answer the question of whether the lack of association reflects ethnic differences in the nature of genetic susceptibility loci.
C1 Kyoto Univ, Otsuka Dept Intl Prevent Nutr Med, Grad Sch Human & Environm Studies, Sakyo Ku, Kyoto 606, Japan.
   Asahi Life Fdn, Inst Adult Dis, Tokyo, Japan.
   Univ Tokyo, Grad Sch Med, Dept Cardiovasc Med, Tokyo, Japan.
C3 Kyoto University; Asahi Life Foundation; University of Tokyo
RP Kato, N (corresponding author), Kyoto Univ, Otsuka Dept Intl Prevent Nutr Med, Grad Sch Human & Environm Studies, Sakyo Ku, Yoshida Nihonmatsu Cho, Kyoto 606, Japan.
OI Kurihara, Hiroki/0000-0002-6476-5593
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NR 21
TC 97
Z9 110
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD NOV
PY 1998
VL 32
IS 5
BP 935
EP 938
DI 10.1161/01.HYP.32.5.935
PG 4
WC Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA 141RB
UT WOS:000077156300021
PM 9822456
OA Bronze
DA 2025-04-10
ER

PT J
AU Liu, L
   Fu, JP
   Tang, QY
   Wang, H
   Lin, CG
   Wei, LL
AF Liu, Lin
   Fu, Jianping
   Tang, Qiongying
   Wang, Hui
   Lin, Changgao
   Wei, Lili
TI Combined transcriptomics and metabolomics analysis reveals lipid
   metabolic disruption in swamp eel (Monopterus albus) under
   chronic waterborne copper exposure
SO AQUATIC TOXICOLOGY
LA English
DT Article
DE Copper; Monopterus albus; Liver; Lipid metabolism
ID HEPATIC STEATOSIS; FATTY-ACIDS; EXPRESSION; RECEPTORS; DIVERSITY;
   POLLUTION; MECHANISM; BIOMARKER; PATHWAY; OBESITY
AB Excessive copper can induce many adverse effects although it's an essential trace element in organisms. The effects of copper on the lipid metabolism have aroused increasing attention. This study investigated the liver lipid metabolism in swamp eel (Monopterus albus, M. albus) chronically exposed to 0, 10, 50, and 100 mu g/L Cu2+ for 56 days. The results showed that copper increased the contents of triglyceride (TG), total cholesterol (T-CHO), non-esterified fatty acids (NEFA), and lipid droplets. Transcriptomic analysis found 1901 differentially expressed genes (DEGs) and 140 differential alternative splicing (DAS) genes in the 50 mu g/L Cu2+ group, and 1787 DEGs and 184 DAS genes in the 100 mu g/L Cu2+ group, respectively, which were enriched in peroxisome proliferator-activated receptor (PPAR), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK), and other signaling pathways. The expression levels of key genes related to PPAR and AMPK signaling pathways were significantly down-regulated after chronic exposure to Cu2+. Meanwhile, metabolomics analysis showed that 52 and 110 differentially expressed metabolites (DEMs) were identified, which were mainly enriched in glycer-ophospholipids metabolism and steroid synthesis. Moreover, combined analysis of transcriptome and metab-olome showed that glycerophospholipid metabolism co-enriched 19 down-regulated DEGs and 4 down-regulated DEMs. Taken together, our results suggested that chronic waterborne copper exposure promoted lipid synthesis, disrupted the metabolic homeostasis of glycerophospholipid, and led to excessive hepatic lipid deposition in M. albus. The combined omics approach enhanced our understanding of copper pollution to lipid metabolism.
C1 [Liu, Lin; Wang, Hui; Lin, Changgao; Wei, Lili] Jiangxi Agr Univ, Coll Anim Sci & Technol, Nanchang 330045, Jiangxi, Peoples R China.
   [Fu, Jianping] Jiangxi Normal Univ, Coll life Sci, Nanchang 330045, Jiangxi, Peoples R China.
   [Tang, Qiongying] Huzhou Univ, Coll Life Sci, Zhejiang Prov Key Lab Aquat Resources Conservat &, Huzhou 313000, Zhejiang, Peoples R China.
C3 Jiangxi Agricultural University; Jiangxi Normal University; Huzhou
   University
RP Wei, LL (corresponding author), Jiangxi Agr Univ, Coll Anim Sci & Technol, Nanchang 330045, Jiangxi, Peoples R China.
EM liliweifish@jxau.edu.cn
FU National Natural Science Founda-tion of China [31960729, 31760764]
FX Acknowledgments This research was funded by the National Natural Science
   Founda-tion of China (project no. 31960729 and 31760764) .
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NR 66
TC 4
Z9 4
U1 4
U2 49
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0166-445X
EI 1879-1514
J9 AQUAT TOXICOL
JI Aquat. Toxicol.
PD JUN
PY 2023
VL 259
AR 106520
DI 10.1016/j.aquatox.2023.106520
EA MAY 2023
PG 15
WC Marine & Freshwater Biology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Marine & Freshwater Biology; Toxicology
GA I1TE7
UT WOS:001000670200001
PM 37061419
DA 2025-04-10
ER

PT J
AU Prüss, H
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AF Pruess, Harald
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TI Inducible nitric oxide synthase does not mediate brain damage after
   transient focal cerebral ischemia in mice
SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
LA English
DT Article
DE bone marrow transplantation; gene expression; inflammation; iNOS;
   knockout mouse; middle cerebral artery occlusion
ID GENE-EXPRESSION; INDUCTION; CELLS; LACKING; TOLERANCE; STROKE; INJURY;
   ALPHA
AB Nitric oxide produced by the inducible nitric oxide synthase (iNOS) is believed to participate in the pathogenic events after cerebral ischemia. In this study, we examined the expression of iNOS in the brain after transient focal cerebral ischemia in mice. We detected differential expression of exons 2 and 3 of iNOS mRNA (16-fold upregulation at 24 to 72 h after middle cerebral artery occlusion, MCAO) compared with exons 6 to 8, 12 to 14, 21 to 22, and 26 to 27 (2- to 5-fold upregulation after 72 and 96 h), which would be compatible with alternative splicing. Expression levels of iNOS mRNA were too low for detection by the Northern blot analysis. Using specific antibodies, we did not detect any iNOS immunoreactivity in the mouse brain 1 to 5 days after MCAO, although we detected iNOS immunoreactivity in the lungs of mice with stroke-associated pneumonia, and in mouse and rat dura mater after lipopolysaccharide administration. In chimeric iNOS-deficient mice transplanted with wild-type bone marrow (BM) cells expressing the green fluorescent protein (GFP) or in wild-type mice transplanted with GFP(+) iNOS-deficient BM cells, no expression of iNOS was detected in GFP+ leukocytes invading the ischemic brain or in resident brain cells. Moreover, both experimental groups did not show any differences in infarct size. Analysis of three different strains of iNOS-deficient mice and wild-type controls confirmed that infarct size was independent of iNOS deletion, but strongly confounded by the genetic background of mouse strains. In conclusion, our data suggest that iNOS is not a universal mediator of brain damage after cerebral ischemia.
C1 [Pruess, Harald; Baeva, Nevena; Priller, Josef] Charite Univ Med Berlin, Lab Mol Psychiat, D-10117 Berlin, Germany.
   [Pruess, Harald; Prass, Konstantin; Ghaeni, Leyli; Milosevic, Milan; Muselmann, Claudia; Freyer, Dorette; Royl, Georg; Reuter, Uwe; Baeva, Nevena; Dirnagl, Ulrich; Meisel, Andreas; Priller, Josef] Charite Univ Med Berlin, Ctr Stroke Res, Dept Expt Neurol, D-10117 Berlin, Germany.
   [Prass, Konstantin] Landesklinikum Waldviertel, Horn, Austria.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Berlin
   Institute of Health; Free University of Berlin; Humboldt University of
   Berlin; Charite Universitatsmedizin Berlin
RP Priller, J (corresponding author), Charite Univ Med Berlin, Lab Mol Psychiat, D-10117 Berlin, Germany.
EM josef.priller@charite.de
RI Dirnagl, Ulrich/D-8633-2013; Priller, Josef/ABW-3835-2022; Meisel,
   Andreas/AFL-0385-2022; Reuter, Uwe/HLG-6096-2023
OI Dirnagl, Ulrich/0000-0003-0755-6119; Meisel,
   Andreas/0000-0001-7233-5342; Priller, Josef/0000-0001-7596-0979; Reuter,
   Uwe/0000-0002-8527-0725
CR Alderton WK, 2001, BIOCHEM J, V357, P593, DOI 10.1042/0264-6021:3570593
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NR 37
TC 21
Z9 23
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0271-678X
EI 1559-7016
J9 J CEREBR BLOOD F MET
JI J. Cereb. Blood Flow Metab.
PD MAR
PY 2008
VL 28
IS 3
BP 526
EP 539
DI 10.1038/sj.jcbfm.9600550
PG 14
WC Endocrinology & Metabolism; Hematology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology
GA 266DA
UT WOS:000253410400010
PM 17851454
DA 2025-04-10
ER

PT J
AU Li, XY
   Li, N
   Han, YN
   Rao, KF
   Ji, XY
   Ma, M
AF Li, Xinyan
   Li, Na
   Han, Yingnan
   Rao, Kaifeng
   Ji, Xiaoya
   Ma, Mei
TI 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced suppression of
   immunity in THP-1-derived macrophages and the possible mechanisms
SO ENVIRONMENTAL POLLUTION
LA English
DT Article
DE TCDD; Macrophage; Immunotoxicity; Transcriptome; WGCNA
ID ARYL-HYDROCARBON RECEPTOR; HUMAN BLOOD MONOCYTES;
   CARDIOVASCULAR-DISEASE; CYTOCHROME-P450 1B1; POLYCHLORINATED-BIPHENYLS;
   INDUCED APOPTOSIS; EXPOSURE; TCDD; EXPRESSION; DIOXIN
AB 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a well-known immunotoxic environmental pollutant. However, most immunotoxicology studies of TCDD were based on the animal models and the inner mechanisms have just focused on a few genes/proteins. In this study, the immune functions of THP-1-derived macrophages was measured with in-vitro bioassays after 24-h exposure of TCDD including environmentally relevant concentrations. RNA-seq and Weighted Gene Co-expression Network Analysis were used to characterize the immunotoxicity molecular mechanisms. Our study is the first report on the TCDD-induced effects of cell adhesion, morphology, and multiple cytokines/chemokines production on THP-1 macrophages. After TCDD treatment, we observed an inhibited cell adherence, probably attributed to the suppressed mRNA levels of adhesion molecules ICAM-1, VCAM-1 and CD11b, and a decrease in cell pseudopodia and expression of F-actin. The inflammatory cytokines TNF-alpha, IL-10 and other 8 cytokines/chemokines regulating granulocytes/T cells and angiogenesis were disrupted by TCDD. Alternative splicing event was found to be a sensitive target for TCDD. Using WGCNA, we identified 10 hub genes (TNF, SRC, FGF2, PTGS2, CDH2, GNG11, BDNF, WNT5A, CXCR5 and RUNX2) highly relevant to these observed phenotypes, suggesting AhR less important in the effects TCDD have on THP-1 macrophages than in other cells. Our findings broaden the understanding of TCDD immunotoxicity on macrophages and provide new potential targets for clarifying the molecular mechanisms.
C1 [Li, Xinyan; Li, Na; Han, Yingnan; Rao, Kaifeng; Ji, Xiaoya; Ma, Mei] Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Shuangqing Rd 18, Beijing 100085, Peoples R China.
   [Li, Xinyan; Li, Na; Ji, Xiaoya; Ma, Mei] Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
C3 Chinese Academy of Sciences; Research Center for Eco-Environmental
   Sciences (RCEES); Chinese Academy of Sciences; University of Chinese
   Academy of Sciences, CAS
RP Ma, M (corresponding author), Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Shuangqing Rd 18, Beijing 100085, Peoples R China.
EM mamei@rcees.ac.cn
RI ma, mei/AAG-2415-2019; li, na/MIK-8798-2025
OI Li, Xinyan/0000-0001-6217-1030
FU National Natural Science Foundation of China [52030003, 41977208,
   42007227]; Excellent Innovation Project of Research Center for
   Eco-Environmental Sciences, CAS (RCEES-EEI-2019); National Key Research
   and Development Program of China [2019YFC1804601]
FX This work is supported by the National Natural Science Foundation of
   China (41977208) ; National Natural Science Foundation of China
   (42007227) ; National Natural Science Foundation of China (52030003) ;
   Excellent Innovation Project of Research Center for Eco-Environmental
   Sciences, CAS (RCEES-EEI-2019) ; and The National Key Research and
   Development Program of China (2019YFC1804601) .
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NR 88
TC 15
Z9 18
U1 6
U2 45
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0269-7491
EI 1873-6424
J9 ENVIRON POLLUT
JI Environ. Pollut.
PD OCT 15
PY 2021
VL 287
AR 117302
DI 10.1016/j.envpol.2021.117302
EA MAY 2021
PG 10
WC Environmental Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology
GA UR8KC
UT WOS:000696990100002
PM 34020259
DA 2025-04-10
ER

PT J
AU Huang, X
   Gong, R
   Li, XY
   Virtue, A
   Yang, F
   Yang, IH
   Tran, AH
   Yang, XF
   Wang, H
AF Huang, Xiao
   Gong, Ren
   Li, Xinyuan
   Virtue, Anthony
   Yang, Fan
   Yang, Irene H.
   Tran, Anh H.
   Yang, Xiao-Feng
   Wang, Hong
TI Identification of Novel Pretranslational Regulatory Mechanisms for NF-κB
   Activation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MICRORNAS; PATHWAY
AB NF-kappa B-controlled transcriptional regulation plays a central role in inflammatory and immune responses. Currently, understanding about NF-kappa B activation mechanism emphasizes I kappa B-tethered complex inactivation in the cytoplasm. In the case of NF-kappa B activation, I kappa B phosphorylation leads to its degradation, followed by NF-kappa B relocation to the nucleus and trans-activation of NF-kappa B-targeted genes. Pretranslational mechanism mediated NF-kappa B activation remains poorly understood. In this study, we investigated NF-kappa B pretranslational regulation by performing a series of database mining analyses and using six large national experimental databases (National Center of Biotechnology Information UniGene expressed sequence tag profile database, Gene Expression Omnibus database, Transcription Element Search System database, AceView database, and Epigenomics database) and TargetScan software. We reported the following findings: 1) NF-kappa B-signaling genes are differentially expressed in human and mouse tissues; 2) heart and vessels are the inflammation-privileged tissues and less easy to be inflamed because lacking in key NF-kappa B-signaling molecular expression; 3) NF-kappa B-signaling genes are induced by cardiovascular disease risk factors oxidized phospholipids and proinflammatory cytokines in endothelial cells; 4) transcription factors CCAAT/enhancer-binding proteins and NF-kappa B have higher binding site frequencies in the promoters of proinflammatory cyto-kine-induced NF-kappa B genes; 5) most NF-kappa B-signaling genes have multiple alternative promoters and alternatively spliced isoforms; 6) NF-kappa B family genes can be regulated by DNA methylation; and 7) 27 of 38 NF-kappa B-signaling genes can be regulated by microRNAs. Our findings provide important insight into the mechanism of NF-kappa B activation, which may contribute to cardiovascular disease, inflammatory diseases, and immunological disorders.
C1 [Huang, Xiao; Gong, Ren; Li, Xinyuan; Virtue, Anthony; Tran, Anh H.; Yang, Xiao-Feng; Wang, Hong] Temple Univ, Sch Med, Cardiovasc Res Ctr, Thrombosis Res Ctr,Dept Pharmacol, Philadelphia, PA 19140 USA.
   [Huang, Xiao] Nanchang Univ, Affiliated Hosp 2, Dept Cardiol, Nanchang 330006, Jiangxi, Peoples R China.
   [Gong, Ren] Jiangxi Prov Peoples Hosp, Dept Cardiol, Nanchang 330006, Jiangxi, Peoples R China.
   [Yang, Fan] Griffin Hosp, Dept Med, Derby, CT 06418 USA.
   [Yang, Irene H.] Yale Univ, New Haven Hosp, Dept Neurol, New Haven, CT 06510 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); Temple
   University; Nanchang University; Yale University
RP Yang, XF (corresponding author), Temple Univ, Sch Med, Cardiovasc Res Ctr, 3500 N Broad St,MERB 1059, Philadelphia, PA 19140 USA.
EM xfyang@temple.edu; hongw@temple.edu
RI Li, Xinyuan/Z-6299-2019; HUANG, XIAO/ABB-9211-2020; Li,
   Xinyuan/B-1139-2015
OI , xiao/0000-0003-0686-6318; Li, Xinyuan/0000-0002-6746-8367
FU National Institutes of Health [HL67033, HL77288, HL82774, HL110764,
   HL117654, HL094451, HL108910]
FX This work was supported, in whole or in part, by National Institutes of
   Health Grants HL67033, HL77288 HL82774, HL110764, and HL117654 (to H.
   W.) and HL094451 and HL108910 (to X. F. Y.).
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NR 29
TC 17
Z9 21
U1 0
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 31
PY 2013
VL 288
IS 22
BP 15628
EP 15640
DI 10.1074/jbc.M113.460626
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 156LA
UT WOS:000319822300020
PM 23515310
OA Green Published
DA 2025-04-10
ER

PT J
AU Glasgow, JN
   Qiu, JX
   Rassin, D
   Grafe, M
   Wood, T
   Perez-Polo, JR
AF Glasgow, JN
   Qiu, JX
   Rassin, D
   Grafe, M
   Wood, T
   Perez-Polo, JR
TI Transcriptional regulation of the BCL-X gene by NF-κB is an element of
   hypoxic responses in the rat brain
SO NEUROCHEMICAL RESEARCH
LA English
DT Review
DE hypoxia; NF-kappa B; bcl-x; c-Rel; p50; apoptosis
ID PROGRAMMED CELL-DEATH; TRANSIENT FOREBRAIN ISCHEMIA; CYTOCHROME-C
   RELEASE; PERMEABILITY TRANSITION PORE; CEREBRAL-ARTERY OCCLUSION;
   GLOBAL-ISCHEMIA; IN-VIVO; DNA-BINDING; HIPPOCAMPAL-NEURONS;
   ALZHEIMERS-DISEASE
AB Signal transduction pathways that mediate neuronal commitment to apoptosis involve the nuclear factor kappa B (NF-kappaB) transcription factor. The bcl-x gene is a member of the bcl-2 family of genes that regulate apoptosis, and gives rise to two proteins, Bcl-X-L and Bcl-X-S, via alternative mRNA splicing. Bcl-X-L protein, like Bcl-2, is a dominant inhibitor of apoptotic cell death, whereas Bcl-X-S promotes apoptosis. While there is high expression of Bcl-X-L in the developing and adult brain, few transcriptional control elements have been identified in the bcl-x promoter. There are two functional nuclear factor-kappa B (NF-kappaB) DNA binding sites clustered upstream of the brain-specific transcription start site in the upstream promoter region of murine bcl-x. Recombinant NF-kappaB proteins bind to these sites. Also NF-kappaB overexpression, coupled with bcl-x promoter/reporter assays using a series of murine bcl-x promoter and deletion mutants, has identified the downstream 1.1kb of the bcl-x promoter as necessary for basal promoter activity and induction by NF-kappaB in support of the hypothesis that NF-kappaB can act to enhance Bcl-X-L expression via highly selective interactions with the bcl-x promoter, where NF-kappaB binding and promoter activation are dependent on specific DNA binding site sequences and NF-kappaB protein dinner composition. Hypoxia induces apoptosis in the hippocampus where the NF-kappaB dimers c-Rel/p50 and p50/p50 bind to the bcl-x promoter NF-kappaB site.
C1 Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA.
C3 University of Texas System; University of Texas Medical Branch Galveston
RP Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA.
EM regino.perez-polo@utmb.edu
RI Perez-Polo, Jose/B-6250-2009; Wood, Thomas/B-6172-2012; Grafe,
   Markus/LTZ-6194-2024
OI Glasgow, Joel/0000-0002-2842-7917
FU NINDS NIH HHS [NS33288] Funding Source: Medline
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NR 210
TC 58
Z9 62
U1 0
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-3190
EI 1573-6903
J9 NEUROCHEM RES
JI Neurochem. Res.
PD JUN
PY 2001
VL 26
IS 6
BP 647
EP 659
DI 10.1023/A:1010987220034
PG 13
WC Biochemistry & Molecular Biology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 463VX
UT WOS:000170498900011
PM 11519724
DA 2025-04-10
ER

PT J
AU Ponomarenko, I
   Reshetnikov, E
   Dvornyk, V
   Churnosov, M
AF Ponomarenko, Irina
   Reshetnikov, Evgeny
   Dvornyk, Volodymyr
   Churnosov, Mikhail
TI Functionally significant polymorphisms of the MMP9 gene are
   associated with primary open-angle glaucoma in the population of Russia
SO EUROPEAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
DE Primary open-angle glaucoma; MMP9; MMP1; SNPs; association
ID SINGLE NUCLEOTIDE POLYMORPHISMS; PHOSPHOLIPID TRANSFER PROTEIN; MATRIX
   METALLOPROTEINASES; EXFOLIATION SYNDROME; CANDIDATE GENES;
   AQUEOUS-HUMOR; RISK; VARIANTS; SUSCEPTIBILITY; HYPERTENSION
AB Purpose The aim of this study was to investigate the role of functionally significant loci of the matrix metalloproteinases genes 1, 3, 9 (MMP1, MMP3, and MMP9) in the development of primary open-angle glaucoma (POAG) in Caucasians of the Central region of Russia. Methods In total 604 participants were recruited for the study, including 208 patients with POAG and 396 healthy controls. They were genotyped at eight single nucleotide polymorphisms (SNPs) of the three MMP genes. The association was analyzed using logistic and log-linear regression. POAG-associated loci and their proxies were in silico assessed for their functional prediction. Results Variant allele G*rs2250889 of MMP9 was significantly associated with higher risk of POAG (ORcov = 1.57-1.71). Haplotype CCA [rs3918242-rs3918249-rs17576] of the MMP9 gene was associated with lower risk of POAG (ORcov = 0.33). Allele A*rs3787268 of MMP9 was associated with the low intraocular pressure in the POAG patients (beta(cov) = -0.176 - -0.272), and so were haplotypes AA [rs17576-rs3787268] (beta(cov) = -0.577) and AAC [rs17576-rs3787268- rs2250889] (beta(cov) = -0.742) of the same gene, whereas allele 2G*rs1799750 of MMP1 was associated with the earlier onset of the disease (beta(cov) = -0.112 - -0.218). In silico analysis of the polymorphisms suggested the functionality of POAG-associated SNPs and their proxies (epigenetic potential, expression and alternative splicing effects for several genes). Conclusions The MMP9 gene polymorphisms are associated with POAG and intraocular pressure in POAG patients; rs1799750 of MMP1 was associated with the earlier age of manifestation of the disease symptoms.
C1 [Ponomarenko, Irina; Reshetnikov, Evgeny; Churnosov, Mikhail] Belgorod State Univ, Dept Med Biol Disciplines, 85 Pobedy St, Belgorod 308015, Russia.
   [Dvornyk, Volodymyr] Alfaisal Univ, Coll Sci & Gen Studies, Dept Life Sci, Riyadh, Saudi Arabia.
C3 Belgorod State University; Alfaisal University
RP Reshetnikov, E (corresponding author), Belgorod State Univ, Dept Med Biol Disciplines, 85 Pobedy St, Belgorod 308015, Russia.
EM reshetnikov@bsu.edu.ru
RI Dvornyk, Volodymyr/C-6031-2008; Reshetnikov, Evgeny/O-9133-2017;
   Ponomarenko, Irina/R-3358-2017; churnosov, mikhail/W-1313-2017
OI Reshetnikov, Evgeny/0000-0002-5429-6666; churnosov,
   mikhail/0000-0003-1254-6134
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NR 75
TC 4
Z9 4
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1120-6721
EI 1724-6016
J9 EUR J OPHTHALMOL
JI Eur. J. Ophthalmol.
PD NOV
PY 2022
VL 32
IS 6
BP 3208
EP 3219
AR 11206721221083722
DI 10.1177/11206721221083722
EA MAR 2022
PG 12
WC Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Ophthalmology
GA 4Z0VS
UT WOS:000768407000001
PM 35254145
OA Green Published
DA 2025-04-10
ER

PT J
AU Al-Shaer, AE
   Pal, A
   Shaikh, SR
AF Al-Shaer, Abrar E.
   Pal, Anandita
   Shaikh, Saame Raza
TI Resolvin E1-ChemR23 Axis Regulates the Hepatic Metabolic and
   Inflammatory Transcriptional Landscape in Obesity at the Whole Genome
   and Exon Level
SO FRONTIERS IN NUTRITION
LA English
DT Article
DE resolvin E1; ChemR23; ERV1; exon level analysis; hepatic transcriptome;
   eicosapentaenoic acid; obesity
ID INSULIN-RESISTANCE; MICE; FAT; E1; HOMEOSTASIS; EXPRESSION; MEDIATORS;
   CHEMERIN; RECEPTOR; CHEMR23
AB Resolvin E1 (RvE1) is an immunoresolvent that is synthesized from eicosapentaenoic acid and can bind the receptor ERV1/ChemR23. We previously showed activation of the RvE1-ChemR23 axis improves hyperglycemia and hyperinsulinemia of obese mice; however, it remains unclear how RvE1 controls glucose homeostasis. Here we investigated hepatic metabolic and inflammatory transcriptional targets of the RvE1-ChemR23 axis using lean and obese wild type (VVT) and ChemR23 knockout (KO) mice. We conducted an in-depth transcriptional study by preforming whole gene-level and exon-level analyses, which provide insight into alternative splicing variants and miRNA regulation. Compared to controls, WT and KO obese mice in the absence of RvE1 displayed similar gene-level profiles, which entailed dysregulated pathways related to glucose homeostasis. Notably, obese WT mice relative to lean controls showed a robust decrease in pathways related to the biosynthesis of unsaturated fatty acids. At the exon-level, obese ChemR23 KOs compared to obese WT mice displayed changes in pathways related to hepatic lipid transport, cholesterol metabolism, and immunological functions such as complement cascades and platelet activation. Importantly, upon RvE1 administration to WT obese mice, we discovered upregulated genes in pathways relating to insulin sensitivity and downregulated genes related to regulators of TGF-beta signaling. This transcriptional profile was generally not recapitulated with obese ChemR23 KO mice administered RvE1. Collectively, gene and exon-level analyses suggest RvE1 controls the hepatic transcriptional profile related to glucose homeostasis, insulin sensitivity, and inflammation in a manner that is largely dependent on ChemR23. These studies will drive future mechanistic experiments on the RvE1-ChemR23 axis.
C1 [Shaikh, Saame Raza] Univ N Carolina, Dept Nutr, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27515 USA.
   Univ N Carolina, Sch Med, Chapel Hill, NC 27515 USA.
C3 University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina School of Medicine
RP Shaikh, SR (corresponding author), Univ N Carolina, Dept Nutr, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27515 USA.
EM shaikhsa@email.unc.edu
FU University Cancer Research Fund, Comprehensive Cancer Center Core
   Support grant [P30-CA016086]; UNC Center for Mental Health and
   Susceptibility grant [P30-ES010126]; NIH [R01AT008375, P30DK05635];
   National Science Foundation Graduate Research Fellowship Program
   [1650116]; Division Of Graduate Education; Direct For Education and
   Human Resources [1650116] Funding Source: National Science Foundation
FX We gratefully acknowledge the technical support from the UNC High
   Throughput Sequencing Facility. This facility was supported by the
   University Cancer Research Fund, Comprehensive Cancer Center Core
   Support grant (P30-CA016086), and UNC Center for Mental Health and
   Susceptibility grant (P30-ES010126). This work was supported by NIH
   R01AT008375 (SRS) and P30DK05635 (SRS). This material was also based
   upon work supported by the National Science Foundation Graduate Research
   Fellowship Program under (Grant No. 1650116 to AA-S).
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NR 72
TC 11
Z9 11
U1 1
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-861X
J9 FRONT NUTR
JI Front. Nutr.
PD DEC 24
PY 2021
VL 8
AR 799492
DI 10.3389/fnut.2021.799492
PG 15
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA 6Z6UC
UT WOS:000897908100001
PM 35004828
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Delmaghani, S
   Aghaie, A
   Michalski, N
   Bonnet, C
   Weil, D
   Petit, C
AF Delmaghani, Sedigheh
   Aghaie, Asadollah
   Michalski, Nicolas
   Bonnet, Crystel
   Weil, Dominique
   Petit, Christine
TI Defect in the gene encoding the EAR/EPTP domain-containing protein
   TSPEAR causes DFNB98 profound deafness
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID JUVENILE AUDIOGENIC-SEIZURES; ANKLE-LINK COMPLEX; SYNAPTIC-TRANSMISSION;
   RECESSIVE DEAFNESS; PARTIAL EPILEPSY; CANDIDATE GENE; HAIR-CELLS; MICE;
   LGI1; MUTATIONS
AB We report a consanguineous Iranian family affected by congenital profound sensorineural deafness segregating in an autosomal recessive mode. Auditory tests implicated at least a cochlear defect in these patients. We mapped the deafness, autosomal recessive (DFNB) locus involved by linkage analysis to a 4.8 Mb region at chromosome 21q22.3-qter. Exclusion of the DFNB8/10 gene TMPRSS3, located in this chromosomal interval, led us to identify a new deafness locus, DFNB98. Whole exome sequencing allowed us to identify a homozygous frame-shifting mutation (c.1726GTc.1728delC) in the gene TSPEAR (thrombospondin-type laminin G domain and EAR repeats). This truncating mutation (p.V576LfsX37) impeded the secretion of the encoded protein by cells transfected with the mutated gene. Alternative splicing of TSPEAR transcripts predict two protein isoforms, 522 and 669 amino acids in length, both of which would be affected by the mutation. These isoforms are composed of a thrombospondin-type laminin G (TSP) domain followed by seven tandemly organized epilepsy-associated repeats (EARs), probably forming a -propeller domain. Tspear is expressed in a variety of murine tissues. Only the larger Tspear transcript was found in the cochlea, and the protein was detected by immunofluorescence at the surface of the hair bundles of sensory cells. The mammalian EAR protein family includes six known members. Defects in four of them, i.e. Lgi1, Lgi2, Vlgr1 and, we show here, TSPEAR, cause disorders with auditory features: epilepsy, which can include auditory features in humans; audiogenic seizures in animals; and/or hearing impairments in humans and mice. These observations demonstrate that EAR-containing proteins are essential for the development and function of the auditory system.
C1 [Delmaghani, Sedigheh; Michalski, Nicolas; Weil, Dominique; Petit, Christine] Inst Pasteur, Unite Genet & Physiol Audit, F-75724 Paris 15, France.
   [Delmaghani, Sedigheh; Aghaie, Asadollah; Michalski, Nicolas; Bonnet, Crystel; Weil, Dominique; Petit, Christine] INSERM, UMRS 587, Paris, France.
   [Delmaghani, Sedigheh; Aghaie, Asadollah; Michalski, Nicolas; Bonnet, Crystel; Weil, Dominique; Petit, Christine] Univ Paris 06, Paris, France.
   [Aghaie, Asadollah; Bonnet, Crystel; Petit, Christine] Inst Vis, Paris, France.
   [Petit, Christine] Coll France, F-75231 Paris, France.
C3 Pasteur Network; Universite Paris Cite; Institut Pasteur Paris; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Universite de
   Bordeaux; Sorbonne Universite; Sorbonne Universite; Institut National de
   la Sante et de la Recherche Medicale (Inserm); Universite PSL; College
   de France
RP Petit, C (corresponding author), Inst Pasteur, Unite Genet & Physiol Audit, 25 Rue Dr Roux, F-75724 Paris 15, France.
EM christine.petit@pasteur.fr
RI WEIL, Dominique/AAE-4214-2020; Bonnet, Crystel/AAN-5950-2021
OI Petit, Christine/0000-0002-9069-002X; Aghaie, Asadollah
   Alain/0000-0002-3247-7087; michalski, nicolas/0000-0002-1287-2709;
   Bonnet, Crystel/0000-0002-1916-9119; Delmaghani,
   Sedigheh/0000-0003-2092-5097
FU French Foundation 'Voir et Entendre'; Foundation Louis-Jeantet for
   Medicine; French National Research Agency [ANR-10-LABX-65]; "Groupe de
   Protection Sociale" Reunica Prevoyance
FX A.A. and C. B. were supported by the French Foundation 'Voir et
   Entendre'. This work was supported by grants from Foundation
   Louis-Jeantet for Medicine (Prize to C. P.), the French National
   Research Agency (ANR-10-LABX-65), and the "Groupe de Protection Sociale"
   Reunica Prevoyance.
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NR 36
TC 53
Z9 64
U1 0
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD SEP 1
PY 2012
VL 21
IS 17
BP 3835
EP 3844
DI 10.1093/hmg/dds212
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 988PX
UT WOS:000307504100010
PM 22678063
DA 2025-04-10
ER

PT J
AU Peterson, JA
   Gupta, S
   Martinez, ND
   Hardesty, B
   Maroney, SA
   Mast, AE
AF Peterson, Julie A.
   Gupta, Sweta
   Martinez, Nicholas D.
   Hardesty, Brandon
   Maroney, Susan A.
   Mast, Alan E.
TI Factor V east Texas variant causes bleeding in a three-generation family
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE bleeding; factor V; tissue factor pathway inhibitor
ID FACTOR PATHWAY INHIBITOR; TFPI; PROTHROMBINASE; INITIATION; DISORDER;
   PLASMA; FXA
AB Background The factor V east Texas bleeding disorder (FVETBD) is caused by increased plasma tissue factor pathway inhibitor-alpha (TFPI alpha) concentration. The underlying cause is a variant in F5 causing alternative splicing within exon 13 and producing FV-short, which tightly binds the C-terminus of TFPI alpha, prolonging its circulatory half-life. Objectives To diagnose a family presenting with variable bleeding and laboratory phenotypes. Patients/Methods Samples were obtained from 17 family members for F5 exon 13 sequencing. Plasma/platelet TFPI and platelet FV were measured by ELISA and/or western blot. Plasma thrombin generation potential was evaluated using calibrated automated thrombography. Results The FVET variant was identified in all family members with bleeding symptoms and associated with elevated plasma TFPI alpha (4.5- to 13.4-fold) and total TFPI (2- to 3-fold). However, TFPI alpha and FV-short were not elevated in platelets. TF-initiated thrombin generation in patient plasma was diminished but was restored by a monoclonal anti-TFPI antibody or factor VIIa. TFPI alpha localized within vascular extracellular matrix in an oral lesion biopsy from an affected family member. Conclusions Factor V east Texas bleeding disorder was diagnosed in an extended family. The variant was autosomal dominant and highly penetrant. Elevated plasma TFPI alpha, rather than platelet TFPI alpha, was likely the primary cause of bleeding. Plasma FV-short did not deplete TFPI alpha from extracellular matrix. In vitro thrombin generation was restored with an anti-TFPI antibody or factor VIIa suggesting effective therapies may be available. Increased awareness of, and testing for, bleeding disorders associated with F5 exon 13 variants and elevated plasma TFPI are needed.
C1 [Peterson, Julie A.; Martinez, Nicholas D.; Maroney, Susan A.; Mast, Alan E.] Versiti Blood Res Inst, POB 2178, Milwaukee, WI 53201 USA.
   [Gupta, Sweta; Hardesty, Brandon] Indiana Hemophilia & Thrombosis Ctr, Indianapolis, IN USA.
   [Mast, Alan E.] Med Coll Wisconsin, Dept Cell Biol Neurobiol & Anat, Milwaukee, WI 53226 USA.
C3 Indiana Hemophilia & Thrombosis Center; Medical College of Wisconsin
RP Mast, AE (corresponding author), Versiti Blood Res Inst, POB 2178, Milwaukee, WI 53201 USA.
EM aemast@versiti.org
RI Hardesty, Brandon/Q-7070-2018
OI Hardesty, Brandon/0000-0001-6819-3898; Maroney,
   Susan/0000-0002-8021-0694; Peterson, Julie/0000-0002-5450-0321
FU National Heart, Lung, and Blood Institute [HL068835]; National Heart
   Lung and Blood Institute [R01HL068835] Funding Source: NIH RePORTER
FX National Heart, Lung, and Blood Institute, Grant/Award Number: HL068835
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NR 29
TC 10
Z9 10
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
EI 1538-7836
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD MAR
PY 2022
VL 20
IS 3
BP 565
EP 573
DI 10.1111/jth.15612
EA DEC 2021
PG 9
WC Hematology; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Cardiovascular System & Cardiology
GA ZI0QZ
UT WOS:000727812200001
PM 34847292
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Wade, JB
   Fang, L
   Liu, J
   Li, DM
   Yang, CL
   Subramanya, AR
   Maouyo, D
   Mason, A
   Ellison, DH
   Welling, PA
AF Wade, James B.
   Fang, Liang
   Liu, Jie
   Li, Dimin
   Yang, Chao-Ling
   Subramanya, Arohan R.
   Maouyo, Djikolngar
   Mason, Amanda
   Ellison, David H.
   Welling, Paul A.
TI WNK1 kinase isoform switch regulates renal potassium excretion
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE Gordon's syndrome; hypertension; Kir1.1; renal outer-medullary K+
   channel; WNK kinase
ID CORTICAL COLLECTING TUBULE; K-CHANNEL; APICAL-K; EXPRESSION; KIDNEY;
   ALDOSTERONE; ROMK; SECRETION; HYPERKALEMIA; HYPERTENSION
AB Members of the WNK family of serine/threonine kinases have been implicated as important modulators of salt homeostasis, regulating the balance between renal sodium reabsorption and potassium excretion. Gain-of-expression mutations in the WNK1 gene uncouple Na+ and K+ balance and cause a familial disorder of diminished renal potassium excretion, excessive sodium retention, and hypertension (pseudohypoaldosteronism type II or Gordon's syndrome). Alternative splicing of the WNK1 gene produces a kidney-specific short form of WNK1 (KS-WNK1) and a more ubiquitous long form (L-WNK1), but it is not clear how either of these isoforms influence renal potassium excretion. Here we demonstrate that KS-WNK1 and L-WNK1 converge in a pathway to regulate the renal outer-medullary K+ channel, Kir1.1. Reconstitution studies in Xenopus oocytes reveal that L-WNK1 significantly inhibits Kir1.1 by reducing cell surface localization of the channel. A catalytically inactive L-WNK1 mutant has no inhibitory effect on Kir1.1, indicating that channel inhibition depends on kinase activity. KS-WNK1, lacking an intact kinase domain, does not directly alter Kirl.l. Instead, KS-WNK1 negatively regulates L-WNK1 to release Kir1.1 from inhibition. Acute dietary potassium loading increases the relative abundance of KS-WNK1 to L-WNK1 transcript and protein in the kidney, indicating that physiologic up-regulation of Kir1.1 activity involves a WNK1 isoform switch and KS-WNK1-mediated release from L-WNK1 inhibition. Thus, these observations provide evidence for the physiological regulation of Na+ and K+ balance by a kinase isoform switch mechanism.
C1 Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
   Oregon Hlth & Sci Univ, Div Nephrol & Hypertens, Portland, OR 97239 USA.
C3 University System of Maryland; University of Maryland Baltimore; Oregon
   Health & Science University
RP Wade, JB (corresponding author), Univ Maryland, Sch Med, Dept Physiol, 655 W Baltimore St, Baltimore, MD 21201 USA.
EM jwade@umaryland.edu; pwelling@umaryland.edu
RI Davis, Fred/JAC-3636-2023; Subramanya, Arohan/AAN-5217-2020
OI Subramanya, Arohan/0000-0002-2609-7643; Ellison,
   David/0000-0003-2915-265X
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NR 34
TC 112
Z9 121
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 30
PY 2006
VL 103
IS 22
BP 8558
EP 8563
DI 10.1073/pnas.0603109103
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 052BX
UT WOS:000238206800047
PM 16709664
OA Green Published
DA 2025-04-10
ER

PT J
AU DiPolo, R
   Beaugé, L
AF DiPolo, R
   Beaugé, L
TI Ionic ligand interactions with the intracellular loop of the
   sodium-calcium exchanger.: Modulation by ATP
SO PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY
LA English
DT Review
DE Na+/Ca2+ exchanger; ionic and ATP regulation; calcium regulatory site
ID CARDIAC NA+-CA2+ EXCHANGER; NA-CA EXCHANGE; PROTEIN-KINASE-C; NA+/CA2+
   EXCHANGER; GUINEA-PIG; SARCOLEMMAL VESICLES; DEPENDENT REGULATION;
   STEADY-STATE; CYTOPLASMIC PROTONS; CA2+-BINDING DOMAIN
AB In the last decade, there has been a large increase in the study of the Na+/Ca2+ exchanger due to its implications in physiological and pathophysiological processes at the cell and organ levels. Key areas of these studies have been molecular biology, regulation and physiology-pathophysiology of the exchanger. There are three main types of regulation that take place at the large intracellular loop of the Na+/Ca2+ exchanger: (i) ionic (sodium inactivation, calcium regulation and proton inhibition), (ii) metabolic (ATP as phosphoryl group donor), and (iii) genetic (alternative splicing). This review analyzes the most recent data on the mutual interactions of regulatory ionic ligands (Ca2+, Na+, H+) and how they are secondarily modulated by MgATP, emphasizing the importance of the binding of Ca2+ to its regulatory site as an essential requirement for the exchange function. Intracellular protons and sodium inhibit the Na+/Ca2+ exchanger by reducing the apparent affinity of the Ca-i-regulatory site for Ca2+. Although the metabolic pathways are different in the mammalian heart (membrane lipids) and squid nerve cells (soluble cytosolic regulatory protein), the final mechanism for the protective effect of MgATP is the same: a reduction of Na-i(+)-H-i(+) binding affinities facilitating the attachment of Ca2+ to its regulatory site. Kinetic models, which partially analyzed some of these ionic and metabolic interactions, can be integrated into a single scheme where the Ca-i-regulatory site plays a central role. (C) 2002 Elsevier Science Ltd. All rights reserved.
C1 Inst Venezolano Invest Cient, Ctr Biofis & Bioquim, Lab Permeabilidad Ion, Caracas 1020A, Venezuela.
   Inst Invest Med M&M Ferreyra, Lab Biofis, RA-5000 Cordoba, Argentina.
C3 Venezuelan Institute Science Research
RP Inst Venezolano Invest Cient, Ctr Biofis & Bioquim, Lab Permeabilidad Ion, Apartado 21287, Caracas 1020A, Venezuela.
EM rdipolo@ivic.ve; lbeauge@immf.uncor.edu
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NR 74
TC 14
Z9 15
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0079-6107
J9 PROG BIOPHYS MOL BIO
JI Prog. Biophys. Mol. Biol.
PD JUL-AUG
PY 2002
VL 80
IS 1-2
BP 43
EP 67
AR PII S0079-6107(02)00014-7
DI 10.1016/S0079-6107(02)00014-7
PG 25
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 605ND
UT WOS:000178683200004
PM 12231222
OA Bronze
DA 2025-04-10
ER

PT J
AU Ostergaard, JA
   Thiel, S
   Hoffmann-Petersen, IT
   Hovind, P
   Parving, HH
   Tarnow, L
   Rossing, P
   Hansen, TK
AF Ostergaard, J. A.
   Thiel, S.
   Hoffmann-Petersen, I. T.
   Hovind, P.
   Parving, H. -H.
   Tarnow, L.
   Rossing, P.
   Hansen, T. K.
TI Incident microalbuminuria and complement factor mannan-binding
   lectin-associated protein 19 in people with newly diagnosed type 1
   diabetes
SO DIABETES-METABOLISM RESEARCH AND REVIEWS
LA English
DT Article
DE complement; diabetes; kidney; lectin; microalbuminuria; nephropathy
ID URINARY ALBUMIN; ACTIVATION; PATHWAY
AB Background: Evidence links the lectin pathway of complement activation to diabetic kidney disease. Upon carbohydrate-recognition by pattern-recognition molecules, eg, mannan-binding lectin (MBL), the MBL-associated serine protease (MASP-2) is activated and initiates the complement cascade. The MASP2 gene encodes MASP-2 and the alternative splice product MBL-associated protein 19 (MAp19). Both MAp19 and MASP-2 circulate in complex with MBL. We tested the hypothesis that MAp19 and MASP-2 concentrations predict the risk of incident microalbuminuria.
   Methods: Baseline MAp19 and MASP-2 were measured in 270 persons with newly diagnosed type 1 diabetes tracked for incidence of persistent microalbuminuria in a prospective observational 18-year-follow-up study.
   Results: Seventy-five participants (28%) developed microalbuminuria during follow-up. MBL-associated protein 19 concentrations were higher in participants that later progressed to microalbuminuria as compared with those with persistent normoalbuminuria (268 ng/mL [95% CI, 243-293] vs 236 ng/mL [95% CI, 223-250], P = .02). Participants with MAp19 concentration within the highest quartile of the cohort had an increased risk of microalbuminuria as compared with participants with MAp19 concentration within the combined lower 3 quartiles in unadjusted Cox analysis, hazard ratio 1.86 ([95% CI, 1.17-2.96], P = .009). This remained significant in adjusted models, eg, adjusting for age, sex, HbA(1c), systolic blood pressure, urinary albumin excretion, smoking, serum creatinine, and serum cholesterol. MBL-associated serine protease concentration was not associated with incidence of microalbuminuria.
   Conclusions: In conclusion, the results show an association between baseline MAp19 concentration and the incidence of microalbuminuria in an 18-year-follow-up study on persons with newly diagnosed type 1 diabetes.
C1 [Ostergaard, J. A.; Hoffmann-Petersen, I. T.; Hansen, T. K.] Aarhus Univ Hosp, Dept Endocrinol & Internal Med, Bldg 2,Norrebrogade 44, DK-8000 Aarhus C, Denmark.
   [Ostergaard, J. A.; Hoffmann-Petersen, I. T.; Hansen, T. K.] Aarhus Univ, Fac Hlth, Dept Clin Med, Bldg 2,Norrebrogade 44, DK-8000 Aarhus C, Denmark.
   [Ostergaard, J. A.] Danish Diabet Acad, Odense, Denmark.
   [Thiel, S.] Aarhus Univ, Fac Hlth, Dept Biomed, Aarhus, Denmark.
   [Hovind, P.] Univ Copenhagen, Rigshosp, Dept Clin Physiol Nucl Med & PET, Copenhagen, Denmark.
   [Tarnow, L.; Rossing, P.] Steno Diabet Ctr, Gentofte, Denmark.
   [Parving, H. -H.] Univ Copenhagen, Rigshosp, Dept Endocrinol, Copenhagen, Denmark.
   [Tarnow, L.] Nordsjaellands Hosp, Hillerod, Denmark.
   [Tarnow, L.; Rossing, P.] Aarhus Univ, Fac Hlth, Aarhus, Denmark.
   [Rossing, P.] Univ Copenhagen, Dept Clin Med, Copenhagen, Denmark.
C3 Aarhus University; Aarhus University; Aarhus University; Rigshospitalet;
   University of Copenhagen; Copenhagen University Hospital; Steno Diabetes
   Center; Rigshospitalet; University of Copenhagen; Copenhagen University
   Hospital; Aarhus University; University of Copenhagen
RP Ostergaard, JA (corresponding author), Aarhus Univ Hosp, Dept Endocrinol & Internal Med, Bldg 2,Norrebrogade 44, DK-8000 Aarhus C, Denmark.; Ostergaard, JA (corresponding author), Aarhus Univ, Fac Hlth, Dept Clin Med, Bldg 2,Norrebrogade 44, DK-8000 Aarhus C, Denmark.
EM jakob.oestergaard@clin.au.dk
RI rossing, peter/AAH-7879-2021
OI rossing, peter/0000-0002-1531-4294; Ostergaard,
   Jakob/0000-0002-9877-5327; Thiel, Steffen/0000-0002-4817-155X; Tarnow,
   Lise/0000-0002-8735-966X; Hovind, Peter/0009-0006-3272-4494; Hansen,
   Troels Krarup/0000-0002-0708-2868
FU Danish Diabetes Association; Danish Diabetes Academy; Novo Nordisk
   Foundation
FX Danish Diabetes Association; Danish Diabetes Academy; Novo Nordisk
   Foundation
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NR 30
TC 6
Z9 7
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1520-7552
EI 1520-7560
J9 DIABETES-METAB RES
JI Diabetes-Metab. Res. Rev.
PD JUL
PY 2017
VL 33
IS 5
AR e2895
DI 10.1002/dmrr.2895
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA EZ5BZ
UT WOS:000404728100013
PM 28303635
DA 2025-04-10
ER

PT J
AU Gegelashvili, G
   Schousboe, A
AF Gegelashvili, G
   Schousboe, A
TI High affinity glutamate transporters: Regulation of expression and
   activity
SO MOLECULAR PHARMACOLOGY
LA English
DT Review
ID AMINO-ACID TRANSPORTER; GAMMA-AMINOBUTYRIC-ACID; LONG-TERM POTENTIATION;
   CELL LINE NBL-1; RAT-BRAIN; ARACHIDONIC-ACID; NITRIC-OXIDE;
   MOLECULAR-CLONING; MOUSE-BRAIN; DIFFERENTIAL EXPRESSION
AB L-Glutamic acid is a major excitatory neurotransmitter in the mammalian central nervous system. The termination of the glutamatergic transmission and the clearance of the excessive, neurotoxic concentrations of glutamate is ensured by a high affinity glutamate uptake system. Four homologous types of Na/K-dependent high affinity glutamate transporters, glutamate/aspartate transporter, glutamate transporter 1, excitatory amino acid carrier 1, and excitatory amino acid transporter 4, have recently been cloned and were assigned to a separate gene family, together with two neutral amino acid carriers, alanine/serine/cysteine transporter 1/serine/alanine/threonine transporter and adipocyte amino acid transporter. The genomic organization of these transporters is still under investigation. Very little is known about the nature of the factors and molecular mechanisms that regulate developmental, regional, and cell type-specific expression of the glutamate transporters and their aberrant functioning in neurodegenerative diseases (e.g., amyotrophic lateral sclerosis and Alzheimer's disease). Some experimental conditions (e.g., ischemia, corticostriatal lesions, hyperosmolarity, culturing conditions) and several naturally occurring and synthetic compounds (e.g., glutamate receptor agonists, dopamine, alpha(1)- and beta-adrenergic agonists, cAMP, phorbol esters, arachidonic acid, nitric oxide, oxygen free radicals, amyloid beta-peptide, tumor necrosis factor-alpha, glucocorticosteroids, unidentified neuronal factors) affect the molecular expression and activity of glutamate transporters. Further elucidation of the molecular events that link epigenetic signals with transcriptional and post-transcriptional mechanisms (e.g., alternative splicing, translation and post-translational modifications) is crucial for the development of selective pharmacological tools and strategies interfering with the expression of the individual glutamate transporters.
C1 ROYAL DANISH SCH PHARM,PHARMABIOTEC RES CTR,NEUROBIOL UNIT,DEPT BIOL SCI,DK-2100 COPENHAGEN,DENMARK.
C3 University of Copenhagen
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NR 98
TC 346
Z9 382
U1 0
U2 15
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD JUL
PY 1997
VL 52
IS 1
BP 6
EP 15
DI 10.1124/mol.52.1.6
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XK169
UT WOS:A1997XK16900002
PM 9224806
DA 2025-04-10
ER

PT J
AU Ashton, AW
AF Ashton, Anthony W.
TI Preparing to strike: Acute events in signaling by the serpentine
   receptor for thromboxane A2
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE ThromboxaneA2 receptor; Isoforms; Post-translational modification;
   Protein interactions
ID PROTEIN-COUPLED RECEPTOR; TP-BETA ISOFORMS; ENDOTHELIAL-CELL MIGRATION;
   N-LINKED GLYCOSYLATION; 2ND EXTRACELLULAR LOOP; SMOOTH-MUSCLE-CELLS;
   GTP-BINDING PROTEIN; A(2) RECEPTOR; ALPHA-ISOFORM; LIGAND-BINDING
AB Over the last two decades, awareness of the (patho)physiological roles of thromboxane A2 signaling has been greatly extended. From humble beginnings as a short-lived stimulus that activates platelets and causes vasoconstriction to a dichotomous receptor system involving multiple endogenous ligands capable of modifying tissue homeostasis and disease generation in almost every tissue of the body. Thromboxane A2 receptor (TP) signal transduction is associated with the pathogenesis of cancer, atherosclerosis, heart disease, asthma, and host response to parasitic infection amongst others. The two receptors mediating these cellular responses (TP & alpha; and TP & beta;) are derived from a single gene (TBXA2R) through alternative splicing. Recently, knowledge about the mechanism(s) of signal propagation by the two receptors has undergone a revolution in understanding. Not only have the structural relationships associated with G-protein coupling been established but the modulation of that signaling by post-translational modification to the receptor has come sharply into focus. Moreover, the signaling of the receptor unrelated to G-protein coupling has become a burgeoning field of endeavor with over 70 interacting proteins currently identified. These data are reshaping the concept of TP signaling from a mere guanine nucleotide exchange factors for G & alpha; activation to a nexus for the convergence of diverse and poorly characterized signaling pathways. This review summarizes the advances in understanding in TP signaling, and the potential for new growth in a field that after almost 50 years is finally coming of age. & COPY; 2023 Elsevier Inc. All rights reserved.
C1 [Ashton, Anthony W.] Lankenau Inst Med Res, Div Cardiovasc Med, Rm 128,100 Lancaster Ave, Wynnewood, PA 19096 USA.
   [Ashton, Anthony W.] Univ Sydney, Kolling Inst Med Res, Fac Med & Hlth, Div Perinatal Res, St Leonards, NSW 2065, Australia.
C3 Lankenau Medical Center; Lankenau Institute for Medical Research;
   University of Sydney; Kolling Institute of Medical Research
RP Ashton, AW (corresponding author), Lankenau Inst Med Res, Div Cardiovasc Med, Rm 128,100 Lancaster Ave, Wynnewood, PA 19096 USA.
EM ashtona@mlhs.org
FU Heart Research Australia [2014-02]; Bushell Foundation [G180904,
   G151106]; WW Smith Charitable Trust [C2107]; National Health and Medical
   Research Council of Australia [512154]
FX This work was supported by project grant funding from Heart Research
   Australia (2014-02) , the Bushell Foundation (G180904; G151106) , the WW
   Smith Charitable Trust (C2107) and National Health and Medical Research
   Council of Australia (512154) .
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NR 190
TC 3
Z9 3
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
EI 1879-016X
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD AUG
PY 2023
VL 248
AR 108478
DI 10.1016/j.pharmthera.2023.108478
EA JUN 2023
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA N8DR4
UT WOS:001039261300001
PM 37321373
DA 2025-04-10
ER

PT J
AU Hull, JJ
   Gross, RJ
   Brent, CS
   Christie, AE
AF Hull, J. Joe
   Gross, Roni J.
   Brent, Colin S.
   Christie, Andrew E.
TI Filling in the gaps: A reevaluation of the Lygus hesperus
   peptidome using an expanded de novo assembled transcriptome and
   molecular cloning
SO GENERAL AND COMPARATIVE ENDOCRINOLOGY
LA English
DT Article
DE In silico transcriptome mining; RT-PCR; Western tarnished plant bug;
   Arthropoda; Hexapoda; Insecta; Agatoxin-like peptide
ID FUNNEL-WEB SPIDER; 2 CARDIOACCELERATORY PEPTIDES; INSECT CARDIOACTIVE
   PEPTIDES; MULTIPLE SEQUENCE ALIGNMENT; PROTEIN COUPLED RECEPTORS;
   TARNISHED PLANT BUG; BROWN PLANTHOPPER; NEUROPEPTIDE DISCOVERY;
   APHICIDAL ACTIVITY; SIGNALING SYSTEM
AB Peptides are the largest and most diverse class of molecules modulating physiology and behavior. Previously, we predicted a peptidome for the western tarnished plant bug, Lygus hesperus, using transcriptomic data produced from whole individuals. A potential limitation of that analysis was the masking of underrepresented genes, in particular tissue-specific transcripts. Here, we reassessed the L. hesperus peptidome using a more comprehensive dataset comprised of the previous transcriptomic data as well as tissue-specific reads produced from heads and accessory glands. This augmented assembly significantly improves coverage depth providing confirmatory transcripts for essentially all of the previously identified families and new transcripts encoding a number of new peptide precursors corresponding to 14 peptide families. Several families not targeted in our initial study were identified in the expanded assembly, including agatoxin-like peptide, CNMamide, neuropeptide-like precursor 1, and periviscerokinin. To increase confidence in the in silico data, open reading frames of a subset of the newly identified transcripts were amplified using RT-PCR and sequence validated. Further PCR-based profiling of the putative L. hesperus agatoxin-like peptide precursor revealed evidence of alternative splicing with near ubiquitous expression across L. hesperus development, suggesting the peptide serves functional roles beyond that of a toxin. The peptides predicted here, in combination with those identified in our earlier study, expand the L. hesperus peptidome to 42 family members and provide an improved platform for initiating molecular and physiological investigations into peptidergic functionality in this non-model agricultural pest.
C1 [Hull, J. Joe; Gross, Roni J.; Brent, Colin S.] USDA ARS, Pest Management & Biocontrol Res Unit, Us Arid Land Agr Res Ctr, Maricopa, AZ 85138 USA.
   [Christie, Andrew E.] Univ Hawaii, Bekesy Lab Neurobiol, Pacific Biosci Res Ctr, Sch Ocean & Earth Sci & Technol, 1993 East West Rd, Honolulu, HI 96822 USA.
C3 United States Department of Agriculture (USDA); University of Hawaii
   System
RP Hull, JJ (corresponding author), USDA ARS, Pest Management & Biocontrol Res Unit, Us Arid Land Agr Res Ctr, Maricopa, AZ 85138 USA.
EM joe.hull@usda.gov
FU National Science Foundation [IOS-1856307]; Cades Foundation; US
   Department of Agriculture [2020-22620-022-00D]
FX This work was supported by funds from the National Science Foundation
   (IOS-1856307; AEC), the Cades Foundation (AEC), and base CRIS funding
   from the US Department of Agriculture (2020-22620-022-00D; JJH and CSB).
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NR 125
TC 6
Z9 6
U1 0
U2 13
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0016-6480
EI 1095-6840
J9 GEN COMP ENDOCR
JI Gen. Comp. Endocrinol.
PD MAR 1
PY 2021
VL 303
AR 113708
DI 10.1016/j.ygcen.2020.113708
EA JAN 2021
PG 16
WC Endocrinology & Metabolism; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Zoology
GA QE4GY
UT WOS:000616167000009
PM 33388363
OA Bronze
DA 2025-04-10
ER

PT J
AU Zhai, LY
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AF Zhai, Liuyu
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   Ichikawa-Shindo, Yuka
   Kawate, Hisaka
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   Cui, Nanqi
   Tanimura, Keiya
   Liu, Teng
   Wei, Yangxuan
   Tanaka, Masaaki
   Tomiyama, Haruka
   Yamauchi, Akihiro
   Igarashi, Kyoko
   Shindo, Takayuki
TI Endogenous calcitonin gene-related peptide suppresses ischemic brain
   injuries and progression of cognitive decline
SO JOURNAL OF HYPERTENSION
LA English
DT Article
DE calcitonin gene-related peptide; cerebral blood flow; cerebral ischemia;
   cognitive decline
ID CGRP PROTECTS; STROKE; ADRENOMEDULLIN; ANGIOGENESIS; NEUROPEPTIDE;
   ACTIVATION; PRESSURE; RECEPTOR; SYSTEM; ROLES
AB Background:Calcitonin gene-related peptide (CGRP) is a 37-amino acid peptide and produced by alternative splicing of the transcript of the calcitonin/CGRP gene. Originally identified as a strong vasodilatory and hypotensive peptide, CGRP is now known to be a pleiotropic molecule distributed in various organs, including the brain.Method:In this study, we used CGRP knockout mice (CGRP-/-) to examine the actions of endogenous CGRP during cerebral ischemia. To induce acute and chronic cerebral ischemia, mice were subjected to middle cerebral artery occlusion (MCAO) and bilateral common carotid artery stenosis (BCAS).Results:In the cerebral cortex of wild-type mice, CGRP expression was upregulated after acute infarction. In CGRP-/- subjected to MCAO or BCAS, recovery of cerebral blood flow was slower and exhibited more extensive neuronal cell death. Expression of the inflammatory cytokines was higher in CGRP-/- than wild type in the acute phase of ischemia. Pathological analysis during the chronic phase revealed more extensive neuronal cell loss and demyelination and higher levels of oxidative stress in CGRP-/- than wild-type. CGRP-/- also showed less compensatory capillary growth. In an eight-arm radial maze test, CGRP-/- exhibited poorer reference memory than wild-type. On the other hand, CGRP administration promoted cerebral blood flow recovery after cerebral ischemia. We also found that CGRP directly inhibited the cell death of primary cortical neurons.Conclusion:These results indicate endogenous CGRP is protective against ischemia-induced neuronal cell injury. CGRP could, thus, be a novel candidate for use in the treatment of both cerebral ischemia and progression of cognitive decline.
C1 [Zhai, Liuyu; Sakurai, Takayuki; Kamiyoshi, Akiko; Ichikawa-Shindo, Yuka; Kawate, Hisaka; Tanaka, Megumu; Xian, Xian; Hirabayashi, Kazutaka; Dai, Kun; Cui, Nanqi; Tanimura, Keiya; Liu, Teng; Wei, Yangxuan; Tanaka, Masaaki; Tomiyama, Haruka; Shindo, Takayuki] Shinshu Univ, Grad Sch Med, Dept Cardiovasc Res, Asahi 3-1-1, Matsumoto, Nagano 3908621, Japan.
   [Yamauchi, Akihiro; Igarashi, Kyoko] Japan Bio Prod Co Ltd, Tokyo, Japan.
C3 Shinshu University
RP Zhai, LY (corresponding author), Shinshu Univ, Grad Sch Med, Dept Cardiovasc Res, Asahi 3-1-1, Matsumoto, Nagano 3908621, Japan.
EM tshindo@shinshu-u.ac.jp
RI Xian, Xunde/B-9490-2012
OI Sakurai, Takayuki/0000-0002-7220-5940; Hirabayashi,
   Kazutaka/0000-0002-1342-6700
FU Core Research for Evolutionary Science and Technology (CREST) of Japan
   Science and Technology Agency (JST); Japan Agency for Medical Research
   and Development (AMED); Public Trust Fund For Clinical Cancer Research;
   Mitsui Life Social Welfare Foundation; Takeda Science Foundation
   research grant; Takeda Medical Research Foundation grant; SENSHIN
   Medical Research Foundation; YOKOYAMA Foundation for Clinical
   Pharmacology; Rotary Yoneyama Memorial Foundation; Japanese government;
   National Cardiovascular Center research grant for cardiovascular
   diseases; Grants-in-Aid for Scientific Research [16H06841] Funding
   Source: KAKEN
FX This study was supported by Grants-in-Aid for Scientific Research
   (KAKENHI), Core Research for Evolutionary Science and Technology (CREST)
   of Japan Science and Technology Agency (JST) and the Japan Agency for
   Medical Research and Development (AMED), National Cardiovascular Center
   research grant for cardiovascular diseases, Grants-in aid of The Public
   Trust Fund For Clinical Cancer Research, Mitsui Life Social Welfare
   Foundation, Takeda Science Foundation research grant, Takeda Medical
   Research Foundation grant, SENSHIN Medical Research Foundation and
   YOKOYAMA Foundation for Clinical Pharmacology. L.Z. received a
   scholarship from Rotary Yoneyama Memorial Foundation and X.X. received a
   scholarship from Japanese government.
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NR 44
TC 36
Z9 37
U1 0
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0263-6352
EI 1473-5598
J9 J HYPERTENS
JI J. Hypertens.
PD APR
PY 2018
VL 36
IS 4
BP 876
EP 891
DI 10.1097/HJH.0000000000001649
PG 16
WC Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA GA0HQ
UT WOS:000427994500023
PM 29266061
OA Green Submitted
DA 2025-04-10
ER

PT J
AU Huhle, D
   Hirmer, S
   Göbel, TW
AF Huhle, Daniela
   Hirmer, Sieglinde
   Goebel, Thomas W.
TI Splenic γδ T cell subsets can be separated by a novel mab specific for
   two CD45 isoforms
SO DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
LA English
DT Article
DE Chicken; CD45; gamma delta T cells
ID LEUKOCYTE COMMON ANTIGEN; MONOCLONAL-ANTIBODY; EXTRACELLULAR DOMAIN;
   MOLECULAR-CLONING; MESSENGER-RNA; CHICKEN; EXPRESSION; RECEPTOR;
   IDENTIFICATION; HOMOLOG
AB CD45 isoforms have been identified in a variety of different species and mab against various isoforms have been instrumental to define cellular subsets. In the process of generating novel mab against chicken gamma delta T cells two mab with specificity for CD45 were identified and characterized. The analysis of the chicken CD45 genomic structure suggested three exons being involved in alternative splicing. We cloned and expressed the full length CD45 isoform and three shorter isoforms. While the 7D12 mab reacted with all of these isoforms, the 8B1 mab selectively reacted with two short isoforms lacking either exons 3 and 5 or exons 3, 5 and 6. As expected, the reactivity of 7D12 included all leukocyte subsets, also including thrombocytes. In contrast, the 8B1 mab only reacted with lymphocytes and monocytes. 8B1 expression was found on almost all blood alpha beta T cells, while a gamma delta T cell subset and virtually all B cells lacked 8B1 reactivity. The fraction of 8B1(-) alpha beta and gamma delta cells was larger in splenocytes as compared to PBL and there was also a population of 8B1(+) splenic B cells. CD3 stimulation of splenic T cells resulted in upregulation of the 8B1 antigen on all T cells. Three-color immunofluorescence revealed differences in CD28 expression between the 8B1(+) and 8B1 gamma delta T cell subsets with a higher CD28 expression level on 8B1. cells. The CD28 antigen was upregulated upon stimulation of the cells with IL-2 and IL-12. This novel mab will be a useful tool to further analyze chicken gamma delta T cells in more detail. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Huhle, Daniela; Hirmer, Sieglinde; Goebel, Thomas W.] Univ Munich, Inst Anim Physiol, Dept Vet Sci, Vet Str 13, D-80539 Munich, Germany.
C3 University of Munich
RP Göbel, TW (corresponding author), Univ Munich, Inst Anim Physiol, Dept Vet Sci, Vet Str 13, D-80539 Munich, Germany.
EM goebel@lmu.de
RI Gobel, Thomas/A-9919-2009
FU DFG [GO489/5-2]
FX Supported by DFG Grant GO489/5-2.
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NR 55
TC 9
Z9 9
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0145-305X
EI 1879-0089
J9 DEV COMP IMMUNOL
JI Dev. Comp. Immunol.
PD DEC
PY 2017
VL 77
BP 229
EP 240
DI 10.1016/j.dci.2017.08.013
PG 12
WC Fisheries; Immunology; Veterinary Sciences; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Fisheries; Immunology; Veterinary Sciences; Zoology
GA FK3LR
UT WOS:000413387100025
PM 28842181
DA 2025-04-10
ER

PT J
AU Fava, C
   von Wowern, F
   Berglund, G
   Carlson, J
   Hedblad, B
   Rosberg, L
   Burri, P
   Almgren, P
   Melander, O
AF Fava, C.
   von Wowern, F.
   Berglund, G.
   Carlson, J.
   Hedblad, B.
   Rosberg, L.
   Burri, P.
   Almgren, P.
   Melander, O.
TI 24-h ambulatory blood pressure is linked to chromosome 18q21-22 and
   genetic variation of NEDD4L associates with cross-sectional and
   longitudinal blood pressure in Swedes
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE NEDD4L; genetics; linkage; blood pressure
ID EPITHELIAL NA+ CHANNEL; ESSENTIAL-HYPERTENSION; LINKAGE ANALYSIS;
   INSULIN-RESISTANCE; SODIUM-CHANNEL; C2 DOMAIN; 18Q; PREVALENCE;
   MORTALITY; VARIANCE
AB Numerous linkage studies have indicated chromosome 18q21-22 as a locus of importance for blood pressure regulation. This locus harbors the neural precursor cell expressed developmentally downregulated 4-like (NEDD4L) gene, which is instrumental for the regulation of the amiloride-sensitive epithelial sodium channel (ENaC). In a linkage study of 16 markers (including two single nucleoticle polymorphism markers located within the NEDD4L gene) on chromosome 18 between 70-104cM and ambulatory blood pressure (ABP), in 118 families, the strongest evidence of linkage was found for 24 h and day-time systolic ABP at the NEDD4L locus (82.25 cM) (P = 0.0014). In a large population sample (n = 4001), we subsequently showed that a NEDD4L gene variant (rs4149601), which by alternative splicing leads to varying expression of a functionally crucial C2 domain, was associated with diastolic blood pressure (DBP) (P = 0.03) and DBP progression over time (P = 0.04). A genotype combination of the rs4149601 and an intronic NEDD4L marker (rs2288774) was associated with systolic blood pressure (SBP) (P = 0.01), DBP (P = 0.04), and progression of both SBP (P = 0.03) and DBP (P = 0.05) over time. A quantitative transmission disequilibrium test in the family material of the rs4149601 supported this NEDD4L variant as being at least partially causative of the linkage result. In conclusion, our findings suggest that the chromosome 18 linkage peak at 82.25 cM is explained by genetic NEDD4L variation affecting cross-sectional and longitudinal blood pressure, possibly as a consequence of altered NEDD4L interaction with ENaC.
C1 Univ Hosp MAS, Dept Clin Sci, S-20502 Malmo, Sweden.
   Univ Hosp Verona, Dept Biomed & Surg Sci, Verona, Italy.
C3 Lund University; Skane University Hospital
RP von Wowern, F (corresponding author), Univ Hosp MAS, Dept Clin Sci, S-20502 Malmo, Sweden.
EM fredrik.wowern@med.lu.se
RI FAVA, Cristiano/K-9590-2015
OI FAVA, Cristiano/0000-0002-8910-7378; Melander, Olle/0000-0002-2581-484X
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NR 35
TC 52
Z9 56
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD AUG
PY 2006
VL 70
IS 3
BP 562
EP 569
DI 10.1038/sj.ki.5001590
PG 8
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA 068QT
UT WOS:000239390200023
PM 16788695
OA Bronze
DA 2025-04-10
ER

PT J
AU Lee, LA
   Barrick, SK
   Meller, A
   Walklate, J
   Lotthammer, JM
   Tay, JW
   Stump, WT
   Bowman, G
   Geeves, MA
   Greenberg, MJ
   Leinwand, LA
AF Lee, Lindsey A.
   Barrick, Samantha K.
   Meller, Artur
   Walklate, Jonathan
   Lotthammer, Jeffrey M.
   Tay, Jian Wei
   Stump, W. Tom
   Bowman, Gregory
   Geeves, Michael A.
   Greenberg, Michael J.
   Leinwand, Leslie A.
TI Functional divergence of the sarcomeric myosin, MYH7b, supports
   species-specific biological roles
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BETA-CARDIAC MYOSIN; SKELETAL-MUSCLE MYOSIN; EXTRAOCULAR-MUSCLES;
   STATISTICAL-MODEL; ATP TURNOVER; MOTOR; GENE; ACTIN; EXPRESSION;
   MECHANISM
AB Myosin heavy chain 7b (MYH7b) is an evolutionarily ancient member of the sarcomeric myosin family, which typically supports striated muscle function. However, in mammals, alternative splicing prevents MYH7b protein production in cardiac and most skeletal muscles and limits expression to a subset of specialized muscles and certain nonmuscle environ-ments. In contrast, MYH7b protein is abundant in python cardiac and skeletal muscles. Although the MYH7b expression pattern diverges in mammals versus reptiles, MYH7b shares high sequence identity across species. So, it remains unclear how mammalian MYH7b function may differ from that of other sarcomeric myosins and whether human and python MYH7b motor functions diverge as their expression patterns suggest. Thus, we generated recombinant human and python MYH7b protein and measured their motor properties to investigate any species-specific differences in activity. Our re-sults reveal that despite having similar working strokes, the MYH7b isoforms have slower actin-activated ATPase cycles and actin sliding velocities than human cardiac & beta;-MyHC. Furthermore, python MYH7b is tuned to have slower motor activity than human MYH7b because of slower kinetics of the chemomechanical cycle. We found that the MYH7b isoforms adopt a higher proportion of myosin heads in the ultraslow, super-relaxed state compared with human cardiac & beta;-MyHC. These findings are supported by molecular dynamics simula-tions that predict MYH7b preferentially occupies myosin active site conformations similar to those observed in the structurally inactive state. Together, these results suggest that MYH7b is specialized for slow and energy-conserving motor activity and that differential tuning of MYH7b orthologs contributes to species-specific biological roles.
C1 [Lee, Lindsey A.; Leinwand, Leslie A.] Mol Cellular & Dev Biol Dept, Boulder, CO 80302 USA.
   [Lee, Lindsey A.; Tay, Jian Wei; Leinwand, Leslie A.] Univ Colorado, BioFrontiers Inst, Boulder, CO 80309 USA.
   [Barrick, Samantha K.; Greenberg, Michael J.] Washington Univ, Sch Med, Dept Biochem & Mol Biophys, St Louis, MO USA.
   [Meller, Artur; Lotthammer, Jeffrey M.; Bowman, Gregory] Washington Univ, Ctr Sci & Engn Living Syst, St Louis, MO USA.
   [Walklate, Jonathan; Geeves, Michael A.] Univ Kent, Sch Biosci, Canterbury, England.
   [Bowman, Gregory] Univ Penn, Dept Biochem & Biophys, Philadelphia, PA USA.
C3 University of Colorado System; University of Colorado Boulder;
   Washington University (WUSTL); Washington University (WUSTL); University
   of Kent; University of Pennsylvania
RP Leinwand, LA (corresponding author), Mol Cellular & Dev Biol Dept, Boulder, CO 80302 USA.; Leinwand, LA (corresponding author), Univ Colorado, BioFrontiers Inst, Boulder, CO 80309 USA.
EM leslie.leinwand@colorado.edu
RI L, A/HZI-4043-2023; Tay, Jian/AAK-9854-2021; Geeves, Michael/F-7583-2011
OI Barrick, Samantha/0000-0002-0203-7769; Lotthammer,
   Jeffrey/0000-0002-5022-7006; Meller, Artur/0000-0002-5504-2684;
   Greenberg, Michael/0000-0003-1320-3547
FU National Institutes of Health (NIH) [R01GM029090]; NIH fellowship
   [F31DC017927]; NIH [R01GM124007, RF1AG067194, R01HL141086]; European
   Union [777204 SILICO]; National Science Foundation [DGE-2139839];
   National Science Foundation CAREER Award [MCB-1552471]; Packard
   Fellowship for Science and Engineering from The David amp; Lucile
   Packard Foundation
FX This work was supported by the National Institutes of Health (NIH grant
   R01GM029090; to L. A. Leinwand) , NIH fellowship (grant no.:
   F31DC017927; to L. A. Lee) , and the NIH grant (R01HL141086; to M. G.) .
   M. A. G. was supported by the European Union Horizon 2020 grant (grant
   no.: 777204 SILICO; to F. C. M.) . J. M. L. was supported by the
   National Science Foundation via grant number DGE-2139839. G. R. B. was
   funded by National Science Foundation CAREER Award (MCB-1552471) and NIH
   grants R01GM124007 and RF1AG067194. G. R. B. holds a Packard Fellowship
   for Science and Engineering from The David & Lucile Packard Foundation.
   The content is solely the responsibility of the authors and does not
   necessarily represent the official views of the NIH, the National
   Science Foundation, or the European Commission.
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NR 70
TC 11
Z9 11
U1 1
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JAN
PY 2023
VL 299
IS 1
AR 102657
DI 10.1016/j.jbc.2022.102657
EA DEC 2022
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA J8EO0
UT WOS:001011901600001
PM 36334627
OA Green Published, gold, Green Accepted
DA 2025-04-10
ER

PT J
AU Cai, WX
   Guner, H
   Gregorich, ZR
   Chen, AJ
   Ayaz-Guner, S
   Peng, Y
   Valeja, SG
   Liu, XW
   Ge, Y
AF Cai, Wenxuan
   Guner, Huseyin
   Gregorich, Zachery R.
   Chen, Albert J.
   Ayaz-Guner, Serife
   Peng, Ying
   Valeja, Santosh G.
   Liu, Xiaowen
   Ge, Ying
TI MASH Suite Pro: A Comprehensive Software Tool for Top-Down Proteomics
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID EFFECTIVE PROTEIN SEPARATION; CARDIAC TROPONIN-I; PHASE CHROMATOGRAPHY;
   SPECTROMETRY DATA; PHOSPHORYLATION; SPECTRA; IDENTIFICATION;
   DECONVOLUTION; VISUALIZATION; MYOFILAMENT
AB Top-down mass spectrometry (MS)-based proteomics is arguably a disruptive technology for the comprehensive analysis of all proteoforms arising from genetic variation, alternative splicing, and posttranslational modifications (PTMs). However, the complexity of top-down high-resolution mass spectra presents a significant challenge for data analysis. In contrast to the well-developed software packages available for data analysis in bottom-up proteomics, the data analysis tools in top-down proteomics remain underdeveloped. Moreover, despite recent efforts to develop algorithms and tools for the deconvolution of top-down high-resolution mass spectra and the identification of proteins from complex mixtures, a multifunctional software platform, which allows for the identification, quantitation, and characterization of proteoforms with visual validation, is still lacking. Herein, we have developed MASH Suite Pro, a comprehensive software tool for top-down proteomics with multifaceted functionality. MASH Suite Pro is capable of processing high-resolution MS and tandem MS (MS/MS) data using two deconvolution algorithms to optimize protein identification results. In addition, MASH Suite Pro allows for the characterization of PTMs and sequence variations, as well as the relative quantitation of multiple proteoforms in different experimental conditions. The program also provides visualization components for validation and correction of the computational outputs. Furthermore, MASH Suite Pro facilitates data reporting and presentation via direct output of the graphics. Thus, MASH Suite Pro significantly simplifies and speeds up the interpretation of high-resolution top-down proteomics data by integrating tools for protein identification, quantitation, characterization, and visual validation into a customizable and user-friendly interface. We envision that MASH Suite Pro will play an integral role in advancing the burgeoning field of topdown proteomics.
C1 [Cai, Wenxuan; Guner, Huseyin; Gregorich, Zachery R.; Chen, Albert J.; Ayaz-Guner, Serife; Peng, Ying; Valeja, Santosh G.; Ge, Ying] Univ Wisconsin, Dept Cell & Regenerat Biol, 1300 Univ Ave, Madison, WI 53706 USA.
   [Cai, Wenxuan; Gregorich, Zachery R.] Univ Wisconsin, Mol Pharmacol Training Program, 1300 Univ Ave, Madison, WI 53706 USA.
   [Guner, Huseyin; Ge, Ying] Univ Wisconsin, Human Prote Program, 1300 Univ Ave, Madison, WI 53706 USA.
   [Ge, Ying] Univ Wisconsin, Dept Chem, 1300 Univ Ave, Madison, WI 53706 USA.
   [Ge, Ying] Indiana Univ Purdue Univ, Dept BioHlth Informat, 719 Indiana Ave, Indianapolis, IN 46202 USA.
   [Liu, Xiaowen] Indiana Univ Sch Med, Ctr Computat Biol & Bioinformat, 410 West 10th St, Indianapolis, IN 46202 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison; Purdue
   University System; Purdue University; Indiana University System; Indiana
   University Bloomington
RP Ge, Y (corresponding author), 1300 Univ Ave,SMI 130, Madison, WI 53706 USA.
EM ge2@wisc.edu
RI Ayaz-Guner, Serife/K-4139-2019; Guner, Huseyin/E-3323-2018
OI AYAZ GUNER, SERIFE/0000-0002-1052-0961; Cai,
   Wenxuan/0000-0001-7117-2449; Liu, Xiaowen/0000-0003-4139-1127; Guner,
   Huseyin/0000-0002-0220-5224
FU NIH [R01HL096971, R01HL109810]; American Heart Association Scientist
   Development Grant [0735443Z]; American Heart Association (AHA)
   [0735443Z] Funding Source: American Heart Association (AHA)
FX This work was supported by NIH R01HL096971 and R01HL109810 (to Y.G.). We
   acknowledge American Heart Association Scientist Development Grant
   0735443Z and the Wisconsin Partnership Fund for the establishment of the
   Human Proteomics Program Mass Spectrometry Facility. The content is
   solely the responsibility of the authors and does not necessarily
   represent the official views of the National Institutes of Health.
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NR 53
TC 107
Z9 135
U1 2
U2 31
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD FEB
PY 2016
VL 15
IS 2
BP 703
EP 714
DI 10.1074/mcp.O115.054387
PG 12
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DD0LD
UT WOS:000369610600027
PM 26598644
OA hybrid, Green Published
DA 2025-04-10
ER

PT J
AU Mate, A
   Barfull, A
   Hermosa, AM
   Gómez-Amores, L
   Vázquez, CM
   Planas, JM
AF Mate, Alfonso
   Barfull, Anna
   Hermosa, Angeles M.
   Gomez-Amores, Lucia
   Vazquez, Carmen M.
   Planas, Joana M.
TI Regulation of sodium-glucose cotransporter SGLT1 in the intestine of
   hypertensive rats
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
   PHYSIOLOGY
LA English
DT Article
DE kinetics; Northern blot; spontaneously hypertensive rats; Western blot
ID BRUSH-BORDER MEMBRANE; TRANSPORTER MESSENGER-RNA; HEXOSE-TRANSPORT;
   NA+/GLUCOSE COTRANSPORTER; MONOSACCHARIDE TRANSPORT; BASOLATERAL
   MEMBRANE; INSULIN-RESISTANCE; BLOOD-PRESSURE; ION-TRANSPORT; EXPRESSION
AB Experimental models of hypertension, such as spontaneously hypertensive rats (SHR), show alterations in cellular sodium transport that affects Na+-coupled cotransport processes and has been involved in the pathogenesis of this disease. The objective of the present study was to analyze the kinetic properties of the sodium-dependent glucose transport in the jejunum and ileum of SHR and its genetic control, Wistar-Kyoto (WKY) rats, as well as the regulation of the transporter, SGLT1. In hypertensive rats, the increased systolic blood pressure was accompanied by an enhancement of serum aldosterone levels compared with WKY rats, but no alterations were found in their body weight or serum glucose/insulin levels. The values for D-glucose maximal rate of transport (V-max) were 42 and 60% lower, respectively, in the jejunum and ileum of SHR than those from WKY rats. On the other hand, the values for the Michaelis constant ( Km) were similar in both animal groups, as was the diffusive component of transport (K-d). Immunoblotting and Northern blot analysis revealed the existence of a lower abundance of SGLT1 protein and mRNA in SHR. Moreover, hypertensive rats showed a decrease in the molecular mass of SGLT1 that could not be explained in terms of different glycosylation and/or phosphorylation levels or an alternative splicing in the expression of the protein. These findings demonstrate that SGLT1 is regulated at a transcriptional level in the intestine of hypertensive rats, and suggest that this transporter might participate in the dysregulation of sodium transport observed in hypertension.
C1 Univ Seville, Fac Farm, Dept Fisiol & Zool, E-41012 Seville, Spain.
   Univ Seville, Fac Pharm, Dept Physiol & Zool, Seville, Spain.
   Univ Barcelona, Fac Pharm, Dept Physiol, Barcelona, Spain.
C3 University of Sevilla; University of Sevilla; University of Barcelona
RP Vázquez, CM (corresponding author), Univ Seville, Fac Farm, Dept Fisiol & Zool, E-41012 Seville, Spain.
EM vazquez@us.es
RI Mate, Alfonso/G-7418-2012; Planas, Joana M./M-3446-2014; VAZQUEZ,
   CARMEN/K-7058-2014
OI Mate, Alfonso/0000-0002-2719-8825; Planas, Joana M./0000-0001-7799-5884;
   VAZQUEZ, CARMEN/0000-0002-2999-3582
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NR 60
TC 19
Z9 19
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6119
EI 1522-1490
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD SEP
PY 2006
VL 291
IS 3
BP R760
EP R767
DI 10.1152/ajpregu.00524.2005
PG 8
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 072FH
UT WOS:000239658800035
PM 16690767
DA 2025-04-10
ER

PT J
AU Weiser, DC
   Sikes, S
   Li, S
   Shenolikar, S
AF Weiser, DC
   Sikes, S
   Li, S
   Shenolikar, S
TI The inhibitor-1 C terminus facilitates hormonal regulation of cellular
   protein phosphatase-1 - Functional implications for inhibitor-1 isoforms
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PERFUSED RAT HEMICORPUS; SKELETAL-MUSCLE; TYPE-1 PHOSPHATASE; CATALYTIC
   SUBUNIT; GROWTH ARREST; PHOSPHORYLATION; DARPP-32; EXPRESSION; KINASE;
   PHOSPHOPROTEIN
AB Inhibitor-1 (I-1) is a selective inhibitor of protein phosphatase-1 (PP1) and regulates several PP1-dependent signaling pathways, including cardiac contractility and regulation of learning and memory. The human I-1 gene has been spliced to generate two alternative mRNAs, termed I-1alpha and I-1beta, encoding polypeptides that differ from I-1 in their C-terminal sequences. Reverse transcription-PCR established that I-1alpha and I-1beta mRNAs are expressed in a developmental and tissue-specific manner. Functional analysis of I-1 in a Saccharomyces cerevisiae strain dependent on human I-1 for viability established that a novel domain encompassing amino acids 77-110 is necessary for PP1 inhibition in yeast. Expression of human I-1 in S. cerevisiae with a partial loss-of-function eukaryotic initiation factor-2alpha (eIF2alpha) kinase (Gcn2p) mutation permitted growth during amino acid starvation, consistent with the inhibition of Glc7p/PP1, the yeast eIF2alpha phosphatase. In contrast, human I-1alpha, which lacks amino acids 83-134, and I-1 with C-terminal deletions were significantly less effective in promoting yeast growth under starvation conditions. These data suggest that C-terminal sequences of I-1 enhance regulation of the eukaryotic eIF2alpha phosphatase. In vitro studies established that C-terminal sequences, deleted in both I-1alpha and I-1beta, enhance PP1 binding and inhibition. Expression of full-length and C-terminally truncated I-1 in HEK293T cells established the importance of the I-1 C terminus in transducing cAMP signals that promote eIF2alpha phosphorylation. This study demonstrates that multiple domains in I-1 target cellular PP1 complexes and establishes I-1 as a cellular regulator of eIF2alpha phosphorylation.
C1 Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA.
C3 Duke University
RP Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, LSRC C315,Res Dr, Durham, NC 27710 USA.
EM sheno001@mc.duke.edu
FU NIDDK NIH HHS [R01-DK52054] Funding Source: Medline
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NR 41
TC 17
Z9 22
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 19
PY 2004
VL 279
IS 47
BP 48904
EP 48914
DI 10.1074/jbc.M404416200
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 870ZP
UT WOS:000225098100052
PM 15345721
OA hybrid
DA 2025-04-10
ER

PT J
AU Marshall, JD
   Hinman, EG
   Collin, GB
   Beck, S
   Cerqueira, R
   Maffei, P
   Milan, G
   Zhang, WD
   Wilson, DI
   Hearn, T
   Tavares, P
   Vettor, R
   Veronese, C
   Martin, M
   So, WV
   Nishina, PM
   Naggert, JK
AF Marshall, Jan D.
   Hinman, Elizabeth G.
   Collin, Gayle B.
   Beck, Sebastian
   Cerqueira, Rita
   Maffei, Pietro
   Milan, Gabriella
   Zhang, Weidong
   Wilson, David I.
   Hearn, Tom
   Tavares, Purificao
   Vettor, Roberto
   Veronese, Caterina
   Martin, Mitchell
   So, W. Venus
   Nishina, Patsy M.
   Naggert, Juergen K.
TI Spectrum of ALMS1 variants and evaluation of genotype-phenotype
   correlations in Alstrom syndrome
SO HUMAN MUTATION
LA English
DT Article
DE Alstrom syndrome; ALMS1; genotype-phenotype correlation; SNPs; renal
   disease
ID DILATED CARDIOMYOPATHY; RNA SURVEILLANCE; GENE; MUTATION; OBESITY; SIBS;
   NOMENCLATURE; VARIABILITY
AB Alstrom syndrome is a monogenic recessive disorder featuring an array of clinical manifestations, with systemic fibrosis and multiple organ involvement, including retinal degeneration, hearing loss, childhood obesity, diabetes mellitus, dilated cardiomyopathy (I)CM), urological dysfunction, and pulmonary, hepatic, and renal failure. We evaluated a large cohort of patients with Alstrom syndrome for mutations in the ALMS1 gene. In total, 79 disease,causing variants were identified, of which 55 are novel mutations. The variants are primarily clustered in exons 8, 10, and 16, although we also identified novel mutations in exons 12 and 18. Most alleles were identified only once (45/79), but several were found recurrently. Founder effects are likely in families of English and Turkish descent. We also identified 66 SNPs and assessed the functional significance of these variants based on the conserved identity of the protein and the severity of the resulting amino acid substitution. A genotype-phenotype association study examining 18 phenotypic parameters in a subset of 58 patients found suggestive associations between disease-causing variants in exon 16 and the onset of retinal degeneration before the age of 1 year (P = 0.02), the occurrence of urological dysfunction (P = 0.02), of DCM (P = 0.03), and of diabetes (P = 0.03). A significant association was found between alterations in exon 8 and absent, mild, or delayed renal disease (P = 0.0007). This data may have implications for the understanding of the molecular mechanisms of ALMS1 and provides the basis for further investigation of how alternative splicing of ALMS1 contributes to the severity of the disease.
C1 Jackson Lab, Bar Harbor, ME 04609 USA.
   Ernst Moritz Arndt Univ Greifswald, Dept Neonatol & Pediat Intens Care, Greifswald, Germany.
   Clin Genet Ctr, Oporto, Portugal.
   Univ Padua, Dept Med & Surg Sci, Padua, Italy.
   Univ Southampton, Div Human Genet, Southampton, Hants, England.
   Hoffmann La Roche Inc, Dept Res Informat Genet & Genom, Nutley, NJ 07110 USA.
C3 Jackson Laboratory; Universitat Greifswald; University of Padua;
   University of Southampton; Roche Holding; Roche Holding USA
RP Naggert, JK (corresponding author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
EM juergen.naggert@jax.org
RI Maffei, Pietro/O-1878-2013; VETTOR, ROBERTO/K-7121-2016; Hearn,
   Tom/O-7217-2019; Milan, Gabriella/AAB-6234-2022; Hearn, Tom/G-8846-2013;
   Wilson, David/A-6264-2010
OI Hearn, Tom/0000-0002-8670-6236; Vettor, Roberto/0000-0003-0625-6667;
   Wilson, David/0000-0001-8779-2060; Maffei, Pietro/0000-0002-1717-263X
FU NCI NIH HHS [CA34196] Funding Source: Medline; NICHD NIH HHS [HD36878]
   Funding Source: Medline
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NR 27
TC 120
Z9 133
U1 1
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1059-7794
EI 1098-1004
J9 HUM MUTAT
JI Hum. Mutat.
PD NOV
PY 2007
VL 28
IS 11
BP 1114
EP 1123
DI 10.1002/humu.20577
PG 10
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 226TA
UT WOS:000250610200009
PM 17594715
OA gold
DA 2025-04-10
ER

PT J
AU Wilkins, JT
   Rohatgi, A
AF Wilkins, John T.
   Rohatgi, Anand
TI Resolution of apolipoprotein A1 and A2 proteoforms: their
   cardiometabolic correlates and implications for future research
SO CURRENT OPINION IN LIPIDOLOGY
LA English
DT Review
DE apolipoprotein A1; apolipoprotein A2; cardiometabolic health; proteoform
ID RISK; GLYCOSYLATION; LIPOPROTEINS; EFFLUX; LIPIDS; AII
AB Purpose of review A 'proteoform' is defined as one specific protein structural form that results from the combination of allelic variation, alternative RNA splicing, and/or posttranslational modifications (PTMs) in specific locations on the amino acid backbone. Apolipoproteins A1 and A2 are highly abundant apolipoproteins that mediate HDL structure and function. ApoA1 and apoA2 are known to undergo PTMs, which results in multiple proteoforms. However, the catalogue of apoA1 and apoA2 proteoforms as well as their associations with cardiometabolic health characteristics has not been described until recently. In this brief review, we discuss recent efforts to catalogue the spectrum of apoA1 and apoA2 proteoforms, to understand the relationships between the relative abundance of these proteoforms with cardiometabolic phenotypic characteristics, and we will discuss the implications of these findings to future research. Recent findings A broad spectrum of apoA1 and apoA2 proteoforms has been characterized. Although, the types of apoA1 and A2 proteoforms are consistent across individuals, the relative abundances of proteoforms can vary substantially between individuals. Proteoform-specific associations with cardiometabolic characteristics in humans, independent of absolute apolipoprotein abundance, have been described. These recent findings suggest multiple levels of protein structural variation that arise from known and unknown metabolic pathways may be important markers or mediators of cardiometabolic health. Understanding the associations between apolipoprotein proteoforms and phenotype may lead to enhanced understanding of how apolipoproteins mediate lipid metabolism and affect atherosclerotic cardiovascular disease (ASCVD) risk, which may lead to discovery of novel markers of risk and/or key mechanistic insights that may drive further druggable targets for modifying lipid metabolism and reducing ASCVD risk.
C1 [Wilkins, John T.] Northwestern Univ, Feinberg Sch Med, Div Cardiol, Dept Med, Chicago, IL 60611 USA.
   [Wilkins, John T.] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
   [Rohatgi, Anand] UT Southwestern Med Ctr, Dept Internal Med, Div Cardiol, Dallas, TX USA.
C3 Northwestern University; Feinberg School of Medicine; Northwestern
   University; Feinberg School of Medicine; University of Texas System;
   University of Texas Southwestern Medical Center Dallas
RP Wilkins, JT (corresponding author), Northwestern Univ, Med Cardiol & Prevent Med, Feinberg Sch Med, 680N Lakeshore Dr,Suite 1400, Chicago, IL 60611 USA.
EM j-wilkins@northwestern.edu
FU NHLBI [1RO1HL146844]; NIGMS [5P41GM108569, 1K23HL133601]; National Heart
   Lung and Blood Institute [R01HL136724] Funding Source: NIH RePORTER
FX This work was supported by the following grants: NHLBI: 1RO1HL146844;
   NIGMS: 5P41GM108569; 1K23HL133601.
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NR 35
TC 3
Z9 3
U1 2
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0957-9672
EI 1473-6535
J9 CURR OPIN LIPIDOL
JI Curr. Opin. Lipidology
PD AUG
PY 2022
VL 33
IS 4
BP 264
EP 269
DI 10.1097/MOL.0000000000000840
PG 6
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Peripheral
   Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
   Cardiovascular System & Cardiology
GA 4J9KW
UT WOS:000851582600007
PM 36082946
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Hull, JJ
   Stefanek, MA
   Dickinson, PS
   Christie, AE
AF Hull, J. Joe
   Stefanek, Melissa A.
   Dickinson, Patsy S.
   Christie, Andrew E.
TI Cloning of the first cDNA encoding a putative CCRFamide precursor:
   identification of the brain, eyestalk ganglia, and cardiac ganglion as
   sites of CCRFamide expression in the American lobster, Homarus
   americanus
SO INVERTEBRATE NEUROSCIENCE
LA English
DT Article
DE Decapoda; Homarus americanus; In silico transcriptome mining; RT-PCR;
   Nervous system
ID MULTIPLE SEQUENCE ALIGNMENT; NEUROMUSCULAR SYSTEM; CRAB HEARTBEAT;
   NEUROPEPTIDES; PREDICTION; PEPTIDES; GENERATION; GENES
AB Over the past decade, many new peptide families have been identified via in silico analyses of genomic and transcriptomic datasets. While various molecular and biochemical methods have confirmed the existence of some of these new groups, others remain in silico discoveries of computationally assembled sequences only. An example of the latter are the CCRFamides, named for the predicted presence of two pairs of disulfide bonded cysteine residues and an amidated arginine-phenylalanine carboxyl-terminus in family members, which have been identified from annelid, molluscan, and arthropod genomes/transcriptomes, but for which no precursor protein-encoding cDNAs have been cloned. Using routine transcriptome mining methods, we identified four Homarus americanus (American lobster) CCRFamide transcripts that share high sequence identity across the predicted open reading frames but more limited conservation in their 5 ' terminal ends, suggesting the Homarus gene undergoes alternative splicing. RT-PCR profiling using primers designed to amplify an internal fragment common to all of the transcripts revealed expression in the supraoesophageal ganglion (brain), eyestalk ganglia, and cardiac ganglion. Variant specific profiling revealed a similar profile for variant 1, eyestalk ganglia specific expression of variant 2, and an absence of variant 3 expression in the cDNAs examined. The broad distribution of CCRFamide transcript expression in the H. americanus nervous system suggests a potential role as a locally released and/or circulating neuropeptide. This is the first report of the cloning of a CCRFamide-encoding cDNA from any species, and as such, provides the first non-in silico support for the existence of this invertebrate peptide family.
C1 [Hull, J. Joe; Stefanek, Melissa A.] ARS, Pest Management & Biocontrol Res Unit, US Arid Land Agr Res Ctr, USDA, 21881 North Cardon Lane, Maricopa, AZ 85138 USA.
   [Dickinson, Patsy S.] Bowdoin Coll, Dept Biol, 6500 Coll Stn, Brunswick, ME 04011 USA.
   [Christie, Andrew E.] Univ Hawaii Manoa, Sch Ocean & Earth Sci & Technol, Pacific Biosci Res Ctr, Bekesy Lab Neurobiol, 1993 East West Rd, Honolulu, HI 96822 USA.
C3 United States Department of Agriculture (USDA); Bowdoin College;
   University of Hawaii System; University of Hawaii Manoa
RP Hull, JJ (corresponding author), ARS, Pest Management & Biocontrol Res Unit, US Arid Land Agr Res Ctr, USDA, 21881 North Cardon Lane, Maricopa, AZ 85138 USA.
EM joe.hull@ars.usda.gov
FU National Science Foundation [IOS-1353023, IOS-1354567, IOS-1856307,
   IOS-1856433]; National Institutes of Health (INBRE) [8P20GM103423-12];
   Cades Foundation; base CRIS funding from the US Department of
   Agriculture [2020-22620-022-00D]
FX This work was supported by funds from the National Science Foundation
   (IOS-1353023; IOS-1354567; IOS-1856307; IOS-1856433), the National
   Institutes of Health (INBRE Grant 8P20GM103423-12), the Cades
   Foundation, and base CRIS funding from the US Department of Agriculture
   (2020-22620-022-00D).
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NR 36
TC 2
Z9 2
U1 0
U2 4
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1354-2516
EI 1439-1104
J9 INVERTEBR NEUROSCI
JI Invertebr. Neurosci.
PD DEC
PY 2020
VL 20
IS 4
AR 24
DI 10.1007/s10158-020-00257-z
PG 8
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA OW5ZN
UT WOS:000592964400001
PM 33244646
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Lee, KJ
   Doran, RM
   Mykles, DL
AF Lee, Kara J.
   Doran, Rachelle M.
   Mykles, Donald L.
TI Crustacean hyperglycemic hormone from the tropical land crab,
   Gecarcinus lateralis:: Cloning, isoforms, and tissue expression
SO GENERAL AND COMPARATIVE ENDOCRINOLOGY
LA English
DT Article
DE Crustacea; Arthropoda; neuropeptide; hormone; molting; CHH; isoforms;
   tissue expressions; gene expression; mRNA; DNA sequence; amino acid
   sequence; cloning; cDNA
ID MOLT-INHIBITING HORMONE; PRECURSOR-RELATED PEPTIDES; SINUS GLAND
   COMPLEX; MOLECULAR-CLONING; AMINO-ACID; MACROBRACHIUM-ROSENBERGII;
   CANCER-PAGURUS; MESSENGER-RNAS; SHORE CRAB; EYESTALK
AB Crustacean hyperglycemic hormone (CHIT) regulates carbohydrate metabolism, molting, and ion and water transport. cDNAs encoding four CHH isoforms (designated EG-CHH-A, -B, -C, and -D) were cloned from eyestalk ganglia (EG) from land crab, Gecarcinus lateralis. The isoforms differed in the 3' reaion of the open reading frame and/or the length of the 3' untranslated region. All encoded essentially identical preprohormones containing a 28-amino acid (aa) signal peptide, a 42-aa precursor related peptide and a 72-aa mature CHH. All deduced aa sequences had the six cysteines, two arginines, one aspartate, one phenylalanine, and one arginine originally identified as characteristic of this neuropeptide family. There was a single aa difference between the EG-CHH-D mature hormone and the other three isoforms. The EG-CHH isoforms were expressed in EG, hindgut, and thoracic ganglion. A fifth CHH isoform, designated pericardial organ (PO)-CHH, was similar to the PO-CHH isoform described in green crab, Carcinus maenas. It was expressed in hindaut and testis, but not in eyestalk ganglia; its expression in PO was not determined. The deduced aa sequence of the PO-CHH was identical to that of the EG-CHH isoforms through aa #40 of the mature peptide. The divergent aa sequence between positions #41 and #73 was encoded by an insertion of a 111-bp sequence absent in EG-CHH cDNAs. The data suggest that EG-CHH and PO-CHH isoforms are generated by alternative splicing of at least two CHH genes. (C) 2007 Elsevier Inc. All rights reserved.
C1 Colorado State Univ, Dept Biol, Ft Collins, CO 80523 USA.
C3 Colorado State University System; Colorado State University Fort Collins
RP Mykles, DL (corresponding author), Colorado State Univ, Dept Biol, Ft Collins, CO 80523 USA.
EM don@lamar.colostate.edu
OI Mykles, Donald/0000-0003-4030-2575
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NR 50
TC 27
Z9 33
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0016-6480
EI 1095-6840
J9 GEN COMP ENDOCR
JI Gen. Comp. Endocrinol.
PD OCT-DEC
PY 2007
VL 154
IS 1-3
BP 174
EP 183
DI 10.1016/j.ygcen.2007.05.019
PG 10
WC Endocrinology & Metabolism; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Zoology
GA 213BO
UT WOS:000249641100021
PM 17586505
DA 2025-04-10
ER

PT J
AU Chen, CM
   Wen, ML
   Jin, Y
AF Chen, Changming
   Wen, Meiling
   Jin, Ya
TI 1DE-MS Profiling for Proteoform-Correlated Proteomic Analysis, by
   Combining SDS-PAGE, Whole-Gel Slicing, Quantitative LC-MS/MS, and
   Reconstruction of Gel Distributions of Several Thousands of Proteins
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE 1DE-MS profiling; SDS-PAGE; gel slicing; LC-MS/MS; gel distributions;
   proteoforms; structural information; proteomics; cerebral
   ischemia-reperfusion injury
ID NONDENATURING MICRO 2DE; CELLULAR SOLUBLE-PROTEINS; ONE-DIMENSIONAL
   PAGE; SMOOTH-MUSCLE-CELLS; CATHEPSIN-B; GALECTIN-3-BINDING PROTEIN;
   DENSITY-LIPOPROTEIN; REACTIVE ASTROCYTES; HUMAN PLASMA; TOP-DOWN
AB SDS-PAGE has often been used in proteomic analysis, but generally for sample prefractionation although the technique separates proteins by molecular masses (M(w)s) and the information would contribute to proteoform-level analysis. Here, we report a method that combines SDS-PAGE, whole-gel slicing, and quantitative LC-MS/MS for establishing gel distributions of several thousand proteins in a proteome. A previously obtained data set on rat cerebral cortex with cerebral ischemia-reperfusion injury1 was analyzed, and the gel distributions of 5906 proteins were reconstructed. These distributions, referred to as 1DE-MS profiles, revealed that about 30% of the proteins had more than one proteoform detected in the gels. The profiles were categorized into six types by distribution (narrow, dispersed, or broad) and relative deviations between the abundance-peak apparent M(w)s and calculated M(w)s. Only 56% of the proteins showed narrow distributions and matched M(w)s, while the others had rather complex profiles. Bioinformatic analysis on example profiles showed the resolved proteoforms involved alternative splicing, proteolytic processing, glycosylation and ubiquitination, fragmentation, and probably transmembrane structures. Profile-based differential analysis revealed that many of the disease-caused changes were proteoform dependent. This work provided a proteome-scale view of protein distributions in SDS-PAGE gels, and the method would be useful to obtain proteoform-correlated information for in-depth proteomics.
C1 [Chen, Changming; Wen, Meiling; Jin, Ya] Guangdong Univ Technol, Inst Biomed & Pharmaceut Sci, Guangzhou 510006, Peoples R China.
C3 Guangdong University of Technology
RP Jin, Y (corresponding author), Guangdong Univ Technol, Inst Biomed & Pharmaceut Sci, Guangzhou 510006, Peoples R China.
EM yajin@gdut.edu.cn
RI Jin, Ya/AAW-8523-2020
OI Chen, Changming/0000-0002-5998-322X; wen, meiling/0000-0003-3757-1918;
   Jin, Ya/0000-0001-6095-0882
FU Research Foundation of Guangdong University of Technology [17ZK0048]
FX This work was financially supported by Project 17ZK0048 of the Research
   Foundation of Guangdong University of Technology.
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NR 94
TC 3
Z9 3
U1 3
U2 14
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD OCT 7
PY 2022
VL 21
IS 10
BP 2311
EP 2330
DI 10.1021/acs.jproteome.2c00180
EA AUG 2022
PG 20
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 7N2UH
UT WOS:000874767000001
PM 36018058
DA 2025-04-10
ER

PT J
AU Wigle, JT
   Demchyshyn, L
   Pratt, MAC
   Staines, WA
   Salih, M
   Tuana, BS
AF Wigle, JT
   Demchyshyn, L
   Pratt, MAC
   Staines, WA
   Salih, M
   Tuana, BS
TI Molecular cloning, expression, and chromosomal assignment of
   sarcolemmal-associated proteins -: A family of acidic amphipathic
   α-helical proteins associated with the membrane
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID INSITU HYBRIDIZATION; CALCIUM CHANNELS; LEUCINE ZIPPER; RECEPTOR GENE;
   COILED-COIL; CARCINOMA; MUSCLE; HETERODIMER; MECHANISM; REGIONS
AB Two overlapping cDNAs encoding a novel sarcolemmal associated protein (SLAP) were isolated from a cardiac cDNA expression library by immunoscreening with anti-sarcolemmal antibodies, Further characterization of these clones showed that they belonged to a family of related cDNAs that potentially encode polypeptides of 37, 46, and 74 kDa designated SLAP1, SLAP2, and SLAP3, respectively, The SLAP3 transcript was ubiquitously expressed, whereas SLAP1 and SLAP2 transcripts were predominantly expressed in cardiac, soleus, and smooth muscle, SLAP was encoded by a single gene that mapped to chromosome 3p14.3-21.2, and the various transcripts are likely generated by alternative splicing, The primary structure of SLAP predicted that it would have large regions of coiled-coil structure including an 11-heptad acidic amphipathic alpha-helical segment, The carboxyl-terminal region of the SLAP proteins was predicted to have a transmembrane domain, although there was no discernible signal sequence, SLAPs could only be solubilized from cardiac membrane with detergents suggesting that they were integral membrane proteins, Subcellular distribution studies showed that MYC epitope-tagged SLAP localized to regions of juxtaposition between neighboring cell membranes although an intracellular pool of the protein was also present in cells undergoing apparent cleavage, Immunohistochemical localization of SLAP in cardiac muscle revealed that SLAP associated with the sarcolemma and also displayed a reticular pattern of staining that resembled the transverse tubules and the sarcoplasmic reticulum, The SLAPs define a new family of tail-anchored membrane proteins that exhibit tissue-specific expression and are uniquely situated to serve a variety of roles through their coiled-coil motifs.
C1 Univ Ottawa, Dept Pharmacol, Ottawa, ON K1H 8M5, Canada.
   Univ Ottawa, Dept Anat & Neurobiol, Ottawa, ON K1H 8M5, Canada.
C3 University of Ottawa; University of Ottawa
RP Tuana, BS (corresponding author), Univ Ottawa, Dept Pharmacol, 451 Smyth Rd, Ottawa, ON K1H 8M5, Canada.
RI ; Wigle, Jeffrey/G-2005-2014
OI Staines, Willim/0000-0002-7288-5026; Wigle, Jeffrey/0000-0002-4985-7684
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NR 50
TC 30
Z9 34
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD DEC 19
PY 1997
VL 272
IS 51
BP 32384
EP 32394
DI 10.1074/jbc.272.51.32384
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA YM852
UT WOS:000071108000066
PM 9405447
OA hybrid
DA 2025-04-10
ER

PT J
AU Fan, JJ
   Li, XL
   Issop, L
   Culty, M
   Papadopoulos, V
AF Fan, Jinjiang
   Li, Xinlu
   Issop, Leeyah
   Culty, Martine
   Papadopoulos, Vassilios
TI ACBD2/ECI2-Mediated Peroxisome-Mitochondria Interactions in Leydig Cell
   Steroid Biosynthesis
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID SUBCELLULAR-LOCALIZATION; ENDOPLASMIC-RETICULUM; ACYL-COENZYME; PROTEIN;
   CHOLESTEROL; EXPRESSION; IMPORT; STEROIDOGENESIS; BIOGENESIS;
   DIFFERENTIATION
AB Fatty acid metabolism and steroid biosynthesis are 2 major pathways shared by peroxisomes and mitochondria. Both organelles are in close apposition to the endoplasmic reticulum, with which they communicate via interorganelle membrane contact sites to promote cellular signaling and the exchange of ions and lipids. To date, no convincing evidence of the direct contact between peroxisomes and mitochondria was reported in mammalian cells. Hormone-induced, tightly controlled steroid hormone biosynthesis requires interorganelle interactions. Using immunofluorescent staining and live-cell imaging, we found that dibutyryl-cAMP treatment of MA-10 mouse tumor Leydig cells rapidly induces peroxisomes to approach mitochondria and form peroxisome-mitochondrial contact sites/fusion, revealed by the subcellular distribution of the endogenous acyl-coenzyme A-binding domain (ACBD) 2/ECI2 isoform A generated by alternative splicing, and further validated using a proximity ligation assay. This event occurs likely via a peroxisome-like structure, which is mediated by peroxisomal and mitochondrial matrix protein import complexes: peroxisomal import receptor peroxisomal biogenesis factor 5 (PEX5), and the mitochondrial import receptor subunit translocase of outer mitochondrial membrane 20 homolog (yeast) protein. Similar results were obtained using the mLTC-1 mouse tumor Leydig cells. Ectopic expression of the ACBD2/ECI2 isoform A in MA-10 cells led to increased basal and hormone-stimulated steroid formation, indicating that ACBD2/ECI2-mediated peroxisomes-mitochondria interactions favor in the exchange of metabolites and/or macromolecules between these 2 organelles in support of steroid biosynthesis. Considering the widespread occurrence of the ACBD2/ECI2 protein, we propose that this protein might serve as a tool to assist in understanding the contact between peroxisomes and mitochondria.
C1 [Fan, Jinjiang; Li, Xinlu; Issop, Leeyah; Culty, Martine; Papadopoulos, Vassilios] McGill Univ, Ctr Hlth, Res Inst, Glen Site,1001 Blvd Decarie,Block E,Room E013152, Montreal, PQ H4A 3J1, Canada.
   [Fan, Jinjiang; Issop, Leeyah; Culty, Martine; Papadopoulos, Vassilios] McGill Univ, Dept Med, Montreal, PQ H4A 3J1, Canada.
   [Li, Xinlu; Papadopoulos, Vassilios] McGill Univ, Dept Biochem, Montreal, PQ H4A 3J1, Canada.
   [Culty, Martine; Papadopoulos, Vassilios] McGill Univ, Dept Pharmacol & Therapeut, Montreal, PQ H4A 3J1, Canada.
C3 McGill University; McGill University; McGill University; McGill
   University
RP Papadopoulos, V (corresponding author), McGill Univ, Ctr Hlth, Res Inst, Glen Site,1001 Blvd Decarie,Block E,Room E013152, Montreal, PQ H4A 3J1, Canada.
EM vassilios.papadopoulos@mcgill.ca
RI Papadopoulos, Vassilios/AAI-2613-2019; li, xinlu/HLX-5595-2023; Fan,
   Jinjiang/C-2010-2009
OI Fan, Jinjiang/0000-0003-3102-4833; Papadopoulos,
   Vassilios/0000-0002-1183-8568; ISSOP, LEEYAH/0000-0002-2359-7722
FU Canadian Institutes of Health Research Grant [MOP-102647]; Canada
   Research Chair in Biochemical Pharmacology; Le Fonds de Recherche du
   Quebec-Sante
FX This work was supported by the Canadian Institutes of Health Research
   Grant MOP-102647 and the Canada Research Chair in Biochemical
   Pharmacology (V.P.). The Research Institute of McGill University Health
   Centre was supported by a center grant from Le Fonds de Recherche du
   Quebec-Sante.
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NR 89
TC 68
Z9 77
U1 1
U2 31
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0888-8809
EI 1944-9917
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD JUL
PY 2016
VL 30
IS 7
BP 763
EP 782
DI 10.1210/me.2016-1008
PG 20
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA DQ5DK
UT WOS:000379224600006
PM 27167610
OA Green Published, Bronze
DA 2025-04-10
ER

PT J
AU Harries, LW
AF Harries, Lorna W.
TI RNA Biology Provides New Therapeutic Targets for Human Disease
SO FRONTIERS IN GENETICS
LA English
DT Review
DE mRNA processing; RNA editing; RNA export; RNA therapeutics; ncRNA;
   splicing; RNA epitranscriptomics; therapeutics
ID LONG NONCODING RNAS; CIRCULAR RNA; BINDING PROTEINS; MESSENGER-RNAS;
   CARDIOVASCULAR-DISEASE; ALTERNATIVE CLEAVAGE; GENE-EXPRESSION; NUCLEAR
   EXPORT; EMERGING ROLE; CELL-GROWTH
AB RNA is the messenger molecule that conveys information from the genome and allows the production of biomolecules required for life in a responsive and regulated way. Most genes are able to produce multiple mRNA products in response to different internal or external environmental signals, in different tissues and organs, and at specific times in development or later life. This fine tuning of gene expression is dependent on the coordinated effects of a large and intricate set of regulatory machinery, which together orchestrate the genomic output at each locus and ensure that each gene is expressed at the right amount, at the right time and in the correct location. This complexity of control, and the requirement for both sequence elements and the entities that bind them, results in multiple points at which errors may occur. Errors of RNA biology are common and found in association with both rare, single gene disorders, but also more common, chronic diseases. Fortunately, complexity also brings opportunity. The existence of many regulatory steps also offers multiple levels of potential therapeutic intervention which can be exploited. In this review, I will outline the specific points at which coding RNAs may be regulated, indicate potential means of intervention at each stage, and outline with examples some of the progress that has been made in this area. Finally, I will outline some of the remaining challenges with the delivery of RNA-based therapeutics but indicate why there are reasons for optimism.
C1 [Harries, Lorna W.] Univ Exeter, RNA Mediated Mech Dis Coll, Coll Med & Hlth, Inst Biomed & Clin Sci,Med Sch, Exeter, Devon, England.
C3 University of Exeter
RP Harries, LW (corresponding author), Univ Exeter, RNA Mediated Mech Dis Coll, Coll Med & Hlth, Inst Biomed & Clin Sci,Med Sch, Exeter, Devon, England.
EM l.w.harries@exeter.ac.uk
RI Harries, Lorna/D-2241-2014; Lunnon, Katie/C-4638-2012
OI Harries, Lorna/0000-0001-7791-8061; Lunnon, Katie/0000-0001-7570-6065
FU Dunhill Medical Trust [R386/1114]
FX The Harries lab is funded by the Dunhill Medical Trust (grant number
   R386/1114).
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NR 161
TC 30
Z9 34
U1 0
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD MAR 8
PY 2019
VL 10
AR 205
DI 10.3389/fgene.2019.00205
PG 12
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA HO4FY
UT WOS:000460879100002
PM 30906315
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Gray, AL
   Wappler-Guzzetta, EA
   Wang, J
   Le Cao, H
   Liu, Y
AF Gray, Austin L.
   Wappler-Guzzetta, Edina A.
   Wang, Jun
   Le Cao, Huynh
   Liu, Yan
TI Case report of a patient with chronic myeloid leukemia, BCR::ABL1
   positive presented with isolated thrombocytosis and an uncommon
   JAK2 alteration detected in peripheral blood
SO JOURNAL OF HEMATOPATHOLOGY
LA English
DT Article
DE Leukemia; Myeloid; Chronic; Janus Kinase 2; Fusion proteins; BCR; ABL;
   Myeloproliferative disorders
ID FEATURES
AB Chronic myeloid leukemia (CML) is a common myeloproliferative neoplasm (MPN). However, CML presenting with isolated thrombocytosis and lacking all the typical features of CML is quite rare. The purpose of this report is to demonstrate the importance of BCR::ABL1 testing for correct diagnosis and treatment even when the presenting features are unusual for CML. We report a case of isolated thrombocytosis with subsequently discovered alternative splicing of JAK2 resulting in skipping of exon 15 in the peripheral blood as the initial presentation of CML in a 67-year-old male with metastatic hepatocellular carcinoma, with BCR::ABL1 detected in the bone marrow aspirate. Bone marrow aspirate was collected in EDTA for evaluation and testing. Bone marrow clot and core sections were obtained and the core was decalcified, then each was fixed in neutral-buffered formalin (10%). The clot and core were embedded in formalin and sectioned at 4 microns for evaluation. Bone marrow aspirate and biopsy demonstrated markedly increased megakaryocytes with clustering. The chromosome analysis demonstrated t(9;22) and molecular studies for BCR::ABL1 were positive. JAK2, MPL, and CALR mutations were negative. The patient did not show a response to hydroxyurea (HU) as the initial treatment. His platelet count normalized within 1 month after treatment with Tyrosine kinase inhibitor (TKI) Imatinib. This report highlights the importance of pursuing BCR::ABL1 testing in the workup of patients with isolated thrombocytosis, even in the presence of abnormal JAK2 transcripts and unusual bone marrow features.
C1 [Gray, Austin L.; Wappler-Guzzetta, Edina A.; Wang, Jun; Liu, Yan] Loma Linda Univ Hlth, Dept Pathol & Lab Med, Loma Linda, CA 92354 USA.
   [Le Cao, Huynh] Loma Linda Univ Hlth, Dept Med, Div Hematol & Oncol, Loma Linda, CA 92354 USA.
C3 Loma Linda University; Loma Linda University
RP Liu, Y (corresponding author), Loma Linda Univ Hlth, Dept Pathol & Lab Med, Loma Linda, CA 92354 USA.
EM YANLIU@llu.edu
OI Wappler-Guzzetta, Edina/0000-0002-2195-5960
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NR 14
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1868-9256
EI 1865-5785
J9 J HEMATOP
JI J. Hematop.
PD JUN
PY 2022
VL 15
IS 2
BP 95
EP 99
DI 10.1007/s12308-022-00496-6
EA MAY 2022
PG 5
WC Hematology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Pathology
GA 1U1QY
UT WOS:000793073800001
OA Bronze
DA 2025-04-10
ER

PT J
AU Rose, KWJ
   Taye, N
   Karoulias, SZ
   Hubmacher, D
AF Rose, Keron W. J.
   Taye, Nandaraj
   Karoulias, Stylianos Z.
   Hubmacher, Dirk
TI Regulation of ADAMTS Proteases
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Review
DE extracellular matrix; arthritis; small molecule inhibitor;
   posttranslational modifications; alternative splicing; cartilage;
   aggrecan
ID MATRIX-METALLOPROTEINASE INHIBITORS; EXTRACELLULAR-MATRIX; NONCATALYTIC
   DOMAINS; AGGRECAN DEGRADATION; TRANSCRIPTIONAL REGULATION; PROTEOLYTIC
   ACTIVITIES; FUNCTIONAL DIFFERENCES; CHONDROITIN SULFATE; CANCER-THERAPY;
   MURINE MODEL
AB A disintegrin and metalloprotease with thrombospondin type I motifs (ADAMTS) proteases are secreted metalloproteinases that play key roles in the formation, homeostasis and remodeling of the extracellular matrix (ECM). The substrate spectrum of ADAMTS proteases can range from individual ECM proteins to entire families of ECM proteins, such as the hyalectans. ADAMTS-mediated substrate cleavage is required for the formation, remodeling and physiological adaptation of the ECM to the needs of individual tissues and organ systems. However, ADAMTS proteases can also be involved in the destruction of tissues, resulting in pathologies such as arthritis. Specifically, ADAMTS4 and ADAMTS5 contribute to irreparable cartilage erosion by degrading aggrecan, which is a major constituent of cartilage. Arthritic joint damage is a major contributor to musculoskeletal morbidity and the most frequent clinical indication for total joint arthroplasty. Due to the high sequence homology of ADAMTS proteases in their catalytically active site, it remains a formidable challenge to design ADAMTS isotype-specific inhibitors that selectively inhibit ADAMTS proteases responsible for tissue destruction without affecting the beneficial functions of other ADAMTS proteases. In vivo, proteolytic activity of ADAMTS proteases is regulated on the transcriptional and posttranslational level. Here, we review the current knowledge of mechanisms that regulate ADAMTS protease activity in tissues including factors that induce ADAMTS gene expression, consequences of posttranslational modifications such as furin processing, the role of endogenous inhibitors and pharmacological approaches to limit ADAMTS protease activity in tissues, which almost exclusively focus on inhibiting the aggrecanase activity of ADAMTS4 and ADAMTS5.
C1 [Rose, Keron W. J.; Taye, Nandaraj; Karoulias, Stylianos Z.; Hubmacher, Dirk] Icahn Sch Med Mt Sinai, Orthopaed Res Labs, Leni & Peter W May Dept Orthopaed, New York, NY 10029 USA.
C3 Icahn School of Medicine at Mount Sinai
RP Hubmacher, D (corresponding author), Icahn Sch Med Mt Sinai, Orthopaed Res Labs, Leni & Peter W May Dept Orthopaed, New York, NY 10029 USA.
EM dirk.hubmacher@mssm.edu
RI Hubmacher, Dirk/AAE-1875-2020; taye, nandaraj/AGW-0870-2022
OI Karoulias, Stylianos/0000-0002-4177-1114; taye,
   nandaraj/0000-0003-3259-1020
FU NIH/NIAMS [R01AR070748]; Ines Mandl Research Foundation; Leni and Peter
   W. May Department for Orthopedics at the Icahn School of Medicine at
   Mount Sinai
FX Research in the Hubmacher laboratory is currently supported by the
   NIH/NIAMS (R01AR070748), the Ines Mandl Research Foundation and seed
   funding from the Leni and Peter W. May Department for Orthopedics at the
   Icahn School of Medicine at Mount Sinai.
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NR 159
TC 46
Z9 46
U1 3
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-889X
J9 FRONT MOL BIOSCI
JI Front. Mol. Biosci.
PD JUN 29
PY 2021
VL 8
AR 701959
DI 10.3389/fmolb.2021.701959
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA TH5RY
UT WOS:000672148300001
PM 34268335
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Peterson, NA
   Anderson, TK
   Yoshino, TP
AF Peterson, Nathan A.
   Anderson, Tavis K.
   Yoshino, Timothy P.
TI In Silico Analysis of the Fucosylation-Associated Genome of the
   Human Blood Fluke Schistosoma mansoni: Cloning and
   Characterization of the Fucosyltransferase Multigene Family
SO PLOS ONE
LA English
DT Article
ID CAENORHABDITIS-ELEGANS; MOLECULAR-CLONING; BIOMPHALARIA-GLABRATA;
   PROTEIN O-FUCOSYL-TRANSFERASE-1; SUBSTRATE-SPECIFICITY;
   ENDOPLASMIC-RETICULUM; CERCARIAL GLYCOCALYX; MEMBRANE-PROTEINS;
   GENE-EXPRESSION; MIXED MODELS
AB Fucosylated glycans of the parasitic flatworm Schistosoma mansoni play key roles in its development and immunobiology. In the present study we used a genome-wide homology-based bioinformatics approach to search for genes that contribute to fucosylated glycan expression in S. mansoni, specifically the alpha 2-, alpha 3-, and alpha 6-fucosyltransferases (FucTs), which transfer L-fucose from a GDP-L-fucose donor to an oligosaccharide acceptor. We identified and in silico characterized several novel schistosome FucT homologs, including six alpha 3-FucTs and six alpha 6-FucTs, as well as two protein O-FucTs that catalyze the unrelated transfer of L-fucose to serine and threonine residues of epidermal growth factor- and thrombospondin-type repeats. No alpha 2-FucTs were observed. Primary sequence analyses identified key conserved FucT motifs as well as characteristic transmembrane domains, consistent with their putative roles as fucosyltransferases. Most genes exhibit alternative splicing, with multiple transcript variants generated. A phylogenetic analysis demonstrated that schistosome alpha 3- and alpha 6-FucTs form monophyletic clades within their respective gene families, suggesting multiple gene duplications following the separation of the schistosome lineage from the main evolutionary tree. Quantitative decreases in steady-state transcript levels of some FucTs during early larval development suggest a possible mechanism for differential expression of fucosylated glycans in schistosomes. This study systematically identifies the complete repertoire of FucT homologs in S. mansoni and provides fundamental information regarding their genomic organization, genetic variation, developmental expression, and evolutionary history.
C1 [Yoshino, Timothy P.] Univ Wisconsin, Dept Pathobiol Sci, Madison, WI 53706 USA.
   [Peterson, Nathan A.] Univ Wisconsin, Dept Entomol, Madison, WI 53706 USA.
   [Anderson, Tavis K.] ARS, Virus & Prion Res Unit, Natl Anim Dis Ctr, USDA, Ames, IA USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison; United
   States Department of Agriculture (USDA); USDA Agricultural Research
   Service
RP Yoshino, TP (corresponding author), Univ Wisconsin, Dept Pathobiol Sci, Madison, WI 53706 USA.
EM yoshinot@vetmed.wisc.edu
OI Anderson, Tavis/0000-0002-3138-5535
FU National Institutes of Health [AI015503, AI061436]; NIH-NIAID
   [HHSN272201000005I]; NRSA predoctoral fellowship through the Cellular
   and Molecular Parasitology Training Grant [NIH T32 AI007414]
FX This work was supported by the National Institutes of Health grants
   AI015503 and AI061436 to TPY and NIH-NIAID schistosome supply contract
   no. HHSN272201000005I. NAP was supported by a NRSA predoctoral
   fellowship through the Cellular and Molecular Parasitology Training
   Grant NIH T32 AI007414. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 86
TC 6
Z9 9
U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 16
PY 2013
VL 8
IS 5
AR e63299
DI 10.1371/journal.pone.0063299
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 146HW
UT WOS:000319081900024
PM 23696810
OA Green Submitted, gold, Green Published
DA 2025-04-10
ER

PT J
AU Millot, GA
   Feger, F
   Garcon, L
   Vainchenker, W
   Dumenil, D
   Svinarchuk, F
AF Millot, GA
   Feger, F
   Garcon, L
   Vainchenker, W
   Dumenil, D
   Svinarchuk, F
TI MplK, a natural variant of the thrombopoietin receptor with a truncated
   cytoplasmic domain, binds thrombopoietin but does not interfere with
   thrombopoietin-mediated cell growth
SO EXPERIMENTAL HEMATOLOGY
LA English
DT Article
ID C-MPL; ERYTHROPOIETIN RECEPTOR; MEGAKARYOCYTIC DIFFERENTIATION;
   ESSENTIAL THROMBOCYTHEMIA; EXTRACELLULAR DOMAIN; IN-VIVO; EXPRESSION;
   ACTIVATION; LIGAND; SUPERFAMILY
AB Objective. Interaction of thrombopoietin (TPO) with its receptor c-Mpl is responsible for the formation of megakaryocytes and platelets. In humans, there are two major c-mpl molecules, MplP and MplK, which are generated by alternative splicing. In contrast to MplP, MplK has none of the intracellular sequences required for typical signal transduction but instead has a unique 27 amino acid sequence that is coded by intron 10. We tested to determine if MplK exerts a negative effect on TPO MpI signal transduction by interfering with the normal homodimerization of MplP.
   Matetials and Methods. A cassette coding for MplK cDNA was introduced into parental and MplP-expressing BaF3 cells and TPO-mediated cell growth studied.
   Results. Cells expressing MplK alone did not respond to TPO compared to cells that expressed MplP. When MplK was coexpressed with MplP on the cell surface of BaF3, no modification in cell growth was observed when compared to those expressing MplP alone. To determine if the normal homodimerization process was negatively influenced, two genetically engineered variants of c-Mpl, one lacking the box I sequence and the other containing only the first nine amino acids of the intracellular domain, were introduced into MplP-expressing cells. In contrast to MplK, these mutants had a dominant negative effect on TPO-mediated cell growth.
   Conclusions. MplK does not influence TPO-mediated growth of Mpl-expressing cells. Our data suggest that the absence of a dominant negative effect of MplK most probably is due to the inability of MplK to dimerize with the MplP receptor. (C) 2002 International Society for Experimental Hematology. Published by Elsevier Science Inc.
C1 Inst Gustave Roussy, INSERM, U362, F-94805 Villejuif, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
   UNICANCER; Gustave Roussy
RP Dumenil, D (corresponding author), Inst Gustave Roussy, INSERM, U362, 39 Rue Camille Desmoulins, F-94805 Villejuif, France.
RI Millot, Gael/AAO-7115-2020
OI Vainchenker, William/0000-0003-4705-202X
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TC 11
Z9 12
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-472X
J9 EXP HEMATOL
JI Exp. Hematol.
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BP 166
EP 175
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DI 10.1016/S0301-472X(01)00776-7
PG 10
WC Hematology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Research & Experimental Medicine
GA 526KJ
UT WOS:000174129400009
PM 11823052
DA 2025-04-10
ER

PT J
AU Wang, J
   Jin, JP
AF Wang, J
   Jin, JP
TI Conformational modulation of troponin T by configuration of the
   NH2-terminal variable region and functional effects
SO BIOCHEMISTRY
LA English
DT Article
ID COMPLETE NUCLEOTIDE-SEQUENCE; RABBIT SKELETAL-MUSCLE; METAL-BINDING
   CLUSTER; CA2+ SENSITIVITY; F-ACTIN; NONPOLYMERIZABLE TROPOMYOSIN;
   HYPERTROPHIC CARDIOMYOPATHY; MONOCLONAL-ANTIBODIES; ALPHA-TROPOMYOSIN;
   ADULT ISOFORMS
AB Troponin T (TnT) is an essential element in the thin filament-based regulatory system of striated muscle. Alternative mRNA splicing generates multiple TnT isoforms with primary structural differences in the NH2-terminal region. The functional significance of this hypervariable NH2-terminal domain and the developmental or muscle type-specific TnT isoforms is not fully understood. We have analyzed chicken breast muscle TnT containing a metal-binding cluster [H(E/A)EAH](4-7) (Tx) in the NH2-terminal region to demonstrate potential effects of the NH2-terminal structure on the conformation of TnT [Ogut, O., and Jin, J.-P. (1996) Biochemistry 35, 16581-16590]. Using specific antibody epitope analysis on this metal-binding TnT model, this study revealed that the binding of Zn2+ to the NH2-terminal region of chicken breast muscle TnT induces extensive conformational changes in the whole protein as demonstrated by a significant decrease in binding avidity of a polyclonal anti-TnT serum which recognizes multiple epitopes on the TnT molecule. This NH2-terminal configuration-based effect is not restricted to the metal ion interaction, whereas the binding of anti-NH2 terminus monoclonal antibodies to TnT induced similar changes. Protein-binding assays have shown that the NH2-terninal variability-induced conformational changes can alter TnT's binding affinity for tropomyosin and troponin I. The results suggest a functional modulation of TnT through the configuration of the NH2-terminal domain, and this novel mechanism may mediate the physiological significance of the TnT isoform regulation.
C1 Case Western Reserve Univ, Sch Med, Dept Physiol & Biophys, Cleveland, OH 44106 USA.
C3 University System of Ohio; Case Western Reserve University
RP Jin, JP (corresponding author), Case Western Reserve Univ, Sch Med, Dept Physiol & Biophys, 10900 Euclid Ave, Cleveland, OH 44106 USA.
RI Jin, Jian-Ping/AAD-1149-2020
OI Jin, JP/0000-0001-9932-1063
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NR 43
TC 75
Z9 87
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD OCT 13
PY 1998
VL 37
IS 41
BP 14519
EP 14528
DI 10.1021/bi9812322
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 129VP
UT WOS:000076485000022
PM 9772180
DA 2025-04-10
ER

PT J
AU Blanchard, H
   Legrand, P
   Pédrono, F
AF Blanchard, H.
   Legrand, P.
   Pedrono, F.
TI Fatty Acid Desaturase 3 (Fads3) is a singular member of the
   Fads cluster
SO BIOCHIMIE
LA English
DT Review
DE Fatty Acid Desaturase 3 (Fads3); The Fads cluster; Polyunsaturated fatty
   acids; Gene expression; Single nucleotide polymorphism
ID SQUAMOUS-CELL CARCINOMA; GENE-EXPRESSION; IDENTIFICATION; VARIANTS;
   DISEASE; FAMILY; HEAD; NECK
AB Since its identification in 2000, no function has been attributed to the Fatty Acid Desaturase 3 (Fads3) gene. This gene is located within the Fads cluster, which also contains Fads1 and Fads2, coding respectively for the Delta 5- and Delta 6- desaturases. Based on the sequence homology between these three genes. Fads3 may be a new fatty acid desaturase. It is thus essential to understand its involvement in Polyunsaturated Fatty Acid (PUFA) biosynthesis in order to improve our knowledge on lipid metabolism.
   Gene expression studies provided evidences on the specificity of Fads3 compared to Fads1 and Fads2, concerning the tissue distribution, alternative splicing and regulation. These works also identified possible physiological functions in which Fads3 could be involved. Thus, the Fads3 gene was transcripted in many tissues, and displayed a weak expression in the liver compared to other organs such as the lung or spleen. Fads3 was also showed to be a target gene for NK-kappa B, MYCN or p63 transcription factors and could consequently be involved in cell survival mechanisms. Polymorphism analysis underlined the possible implication of Fads3 in lipid homeostasis, particularly by modulating cholesterol and triglyceride plasma levels.
   In terms of proteins, FADS3 has been recently described in rodents. One of the identified isoforms may display the classical structure of a fatty acid desaturase but no enzymatic activity has been observed yet. Therefore, it is essential to consider the desaturase diversity in terms of catalysis and substrates to elucidate the FADS3 function. (c) 2010 Elsevier Masson SAS. All rights reserved.
C1 [Blanchard, H.; Legrand, P.; Pedrono, F.] Agrocampus Ouest, INRA, USC 2012, Lab Biochim & Nutr Humaine, F-35042 Rennes, France.
C3 INRAE; Universite de Rennes; Institut Agro; Agrocampus Ouest
RP Blanchard, H (corresponding author), Agrocampus Ouest, INRA, USC 2012, Lab Biochim & Nutr Humaine, 65 Rue St Brieuc,CS 84215, F-35042 Rennes, France.
EM helene.blanchard@agrocampus-ouest.fr
RI Pedrono, Frederique/KYQ-3788-2024; Legrand, Philippe/AAM-6060-2020; ,
   AGROCAMPUS OUEST/O-6651-2016
OI Legrand, Philippe/0000-0001-5763-4854; , AGROCAMPUS
   OUEST/0000-0002-1800-4558; Pedrono, Frederique/0000-0002-4973-7738
FU Valorex (Combourtille, France)
FX The authors thank Valorex (Combourtille, France) for financial support.
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NR 27
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U1 0
U2 22
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0300-9084
J9 BIOCHIMIE
JI Biochimie
PD JAN
PY 2011
VL 93
IS 1
SI SI
BP 87
EP 90
DI 10.1016/j.biochi.2010.03.002
PG 4
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 710TG
UT WOS:000286539300014
PM 20226833
DA 2025-04-10
ER

PT J
AU Yao, CC
   Ziober, BL
   Sutherland, AE
   Mendrick, DL
   Kramer, RH
AF Yao, CC
   Ziober, BL
   Sutherland, AE
   Mendrick, DL
   Kramer, RH
TI Laminins promote the locomotion of skeletal myoblasts via the alpha 7
   integrin receptor
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE alpha 7 integrin; laminin; myoblast; adhesion; motility
ID DYSTROPHIN-GLYCOPROTEIN COMPLEX; CYTOPLASMIC DOMAINS; MUSCLE
   DEVELOPMENT; ALPHA-6-BETA-1 INTEGRIN; DIFFERENTIALLY MODULATE;
   EXTRACELLULAR-MATRIX; CARDIAC-MUSCLE; GROWTH-FACTOR; CELL-LINES;
   EXPRESSION
AB The alpha 7 beta 1 integrin is specifically expressed by skeletal and cardiac muscles, and its expression and alternative mRNA splicing at the cytoplasmic domain are developmentally regulated, We analyzed the role of alpha 7 integrin in mediating myoblast adhesion and motility on different laminin isoforms. Mouse C2C12 and MM14 myoblast cell lines were found by flow cytometry and immunoprecipitation to express high levels of the alpha 7 integrin. Overall expression of alpha 7 increased as the C2C12 myoblasts differentiated; myoblasts expressed only the alpha 7B cytoplasmic variant whereas in differentiating myotubes alpha 7A increased markedly. Function-perturbing monoclonal antibodies generated to alpha 7 integrin efficiently blocked both adhesion and migration of MM14 and C2C12 mouse myoblasts on laminin I, Other studies with MM14 myoblasts showed that alpha 7 is also a receptor for laminin 2/4 (human placental merosins) but not for epithelial-cell-specific laminin 5. Blocking antibody to alpha 7 only partially inhibited adhesion to laminin 2/4 but almost completely blocked motility on this substrate. Finally, to assess the potential role of the alpha 7 cytoplasmic domain, CHO cells were stably transfected to express chimeric alpha 5 cDNA constructs containing the wild-type alpha 5 or the alpha 7A or alpha 7B cytoplasmic domain; all forms of the integrin showed identical activities for adhesion, migration, proliferation, and matrix assembly on fibronectin substrates. These results established that alpha 7 beta 1 receptor can promote myoblast adhesion and motility on a restricted number of laminin isoforms and may be important in myogenic precursor recruitment during regeneration and differentiation.
C1 UNIV CALIF SAN FRANCISCO,SCH DENT,DEPT STOMATOL,SAN FRANCISCO,CA 94143.
   UNIV CALIF SAN FRANCISCO,SCH MED,DEPT ANAT,SAN FRANCISCO,CA 94143.
   HUMAN GENOME SCI,ROCKVILLE,MD 20850.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   GlaxoSmithKline; Glaxosmithkline USA; Human Genome Sciences Inc
RI Yao, Chung-Chen/D-1470-2018
OI YAO, CHUNG-CHEN JANE/0000-0002-2293-7000; Sutherland,
   Ann/0000-0003-1925-2825
FU NCI NIH HHS [R01 CA 33834] Funding Source: Medline; NIDCR NIH HHS [DE
   10564, R01 DE 10306] Funding Source: Medline
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NR 67
TC 113
Z9 130
U1 0
U2 3
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS,
   ENGLAND CB4 4DL
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD DEC
PY 1996
VL 109
BP 3139
EP 3150
PN 13
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA WB438
UT WOS:A1996WB43800018
PM 9004048
DA 2025-04-10
ER

PT J
AU Laurin, NN
   Wang, SP
   Mitchell, GA
AF Laurin, NN
   Wang, SP
   Mitchell, GA
TI The hormone-sensitive lipase gene is transcribed from at least five
   alternative first exons in mouse adipose tissue
SO MAMMALIAN GENOME
LA English
DT Article
ID CHOLESTEROL ESTER HYDROLASE; MESSENGER-RNA; TRANSCRIPTIONAL REGULATION;
   LIPE GENE; EXPRESSION; PROMOTER; IDENTIFICATION; ADIPOCYTES; LIPOLYSIS;
   SEQUENCE
AB Hormone-sensitive lipase (HSL) mediates triglyceride hydrolysis in adipocytes, in which its expression varies with physiological stress and is controlled posttranslationally and transcriptionally. We sequenced the mouse HSL gene for 8.2 kb upstream of the translation start codon and studied the steady-state HSL mRNA levels in mouse adipose tissue. In 50 clones derived from primer extension and PCR of mouse adipose cDNA, we found five distinct 5' extremities that correspond to distinct exons in genomic DNA. Exon A is located similar to7 kb 5' to the HSL translation start site. Exons B, C, and D are clustered 1.5-2 kb upstream, and the previously described exon 1 is immediately upstream and contiguous with the previously described HSL translation start site. Exon A is located similar to7 kb upstream and contains an in-frame methionine codon that could potentially generate another HSL isoform with 43 additional N-terminal residues. cDNA clones containing the newly described exons suggested that each exon has several transcription start sites but that all splice to an acceptor site located 20 nt upstream of the translation initiation codon in exon 1. HSL transcription in mouse adipose tissue originates from multiple sites in the 7-kb region between exon A and exon 1, with peaks at exon C (50-70% of HSL transcripts), exon 1 (5-30%), and exon A (similar to 10%). There are multiple potential transcription factor-binding elements upstream of each exon, suggesting the possibility of differential transcriptional regulation of HSL in different tissues and under various physiologic conditions.
C1 Hop St Justine, Med Genet Serv, Res Ctr, Montreal, PQ H3T 1C5, Canada.
C3 Universite de Montreal
RP Mitchell, GA (corresponding author), Hop St Justine, Med Genet Serv, Res Ctr, 3175 Cote St Catherine, Montreal, PQ H3T 1C5, Canada.
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NR 61
TC 24
Z9 26
U1 0
U2 3
PU SPRINGER-VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010 USA
SN 0938-8990
J9 MAMM GENOME
JI Mamm. Genome
PD NOV
PY 2000
VL 11
IS 11
BP 972
EP 978
DI 10.1007/s003350010185
PG 7
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
GA 367HU
UT WOS:000090056300025
PM 11063252
DA 2025-04-10
ER

PT J
AU Li, JZ
   Sabath, DF
   Kuter, DJ
AF Li, JZ
   Sabath, DF
   Kuter, DJ
TI Cloning and functional characterization of a novel c-mpl variant
   expressed in human CD34 cells and platelets
SO CYTOKINE
LA English
DT Article
DE CD34 cells; c-mpl; megakaryocyte; platelet; thrombopoietin
ID HUMAN BLOOD-PLATELETS; IMMORTALIZES HEMATOPOIETIC PROGENITORS;
   PROTEIN-TYROSINE PHOSPHORYLATION; TRUNCATED CYTOKINE RECEPTOR;
   THROMBOPOIETIN RECEPTOR; MEGAKARYOCYTE GROWTH; V-MPL; LIGAND; MICE;
   PROLIFERATION
AB The thrombopoietin receptor, c-mpl, is a crucial element not only in thrombopoietin (TPO)-initiated signaling pathways but also in the regulation of the circulating amount of TPO, We have identified a new c-mpl isoform, called c-mpl-del, that lacks 72 bp (24 amino acids) in the extracellular region of c-mpl and arises as a consequence of alternative RNA splicing between exons 8 and 9, c-mpl-del is expressed along with c-mpl-wt in blood mononuclear cells, CD34(+) cells, megakaryocytes, and platelets prepared from either normal donors or ET patients, although its relative expression appears to increase with megakaryocyte differentiation. The c-mpl-del-transfected cells expressed greater amounts of c-mpl-del RNA and protein than the comparable c-mpl-wt-transfected cells, however flow cytometry analysis could not detect any c-mpl receptor on the surface of the c-mpl-del-transfected cells. Further evidence for the absence of surface c-mpl-del was that in contrast to cells transfected with c-mpl-wt, those transfected with c-mpl-del did not grow in response to TPO, failed to undergo tyrosine phosphorylation of TPO-specific signal molecules, and did not bind I-125-rHuTPO. Taken together, these results demonstrate that c-mpl-del, a naturally occurring variant of c-mpl, fails to be incorporated into the cell membrane but might serve as a mechanism to decrease the overall expression of functional c-mpl late in megakaryocyte differentiation. (C) 2000 Academic Press.
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Hematol Oncol Unit, Boston, MA 02114 USA.
   Univ Washington, Dept Med, Seattle, WA USA.
C3 Harvard University; Harvard University Medical Affiliates; Massachusetts
   General Hospital; Harvard Medical School; University of Washington;
   University of Washington Seattle
RP Kuter, DJ (corresponding author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Hematol Oncol Unit, 100 Blossom St, Boston, MA 02114 USA.
RI Kuter, David/AAS-1123-2020
FU NHLBI NIH HHS [HL61222, HL54838] Funding Source: Medline; NIDDK NIH HHS
   [DK02448] Funding Source: Medline
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NR 41
TC 21
Z9 22
U1 0
U2 18
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399 USA
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD JUL
PY 2000
VL 12
IS 7
BP 835
EP 844
DI 10.1006/cyto.1999.0654
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 335AY
UT WOS:000088220900001
PM 10880227
DA 2025-04-10
ER

PT J
AU Yang, Z
   Yu, GL
   Zhu, X
   Peng, TH
   Lv, YC
AF Yang, Zhou
   Yu, Guang-li
   Zhu, Xiao
   Peng, Tian-hong
   Lv, Yun-cheng
TI Critical roles of FTO-mediated mRNA m6A demethylation in regulating
   adipogenesis and lipid metabolism: Implications in lipid metabolic
   disorders
SO GENES & DISEASES
LA English
DT Review
DE Adipose tissue; FTO; Lipid disorder diseases; Lipid metabolism; Liver;
   Skeletal muscle
ID FAT MASS; ALLEVIATES ATHEROSCLEROSIS; CHOLESTEROL EFFLUX;
   INSULIN-RESISTANCE; FOAM CELLS; ER STRESS; OBESITY; GENE; PROTEIN;
   EXPRESSION
AB The goal this review is to clarify the effects of the fat mass and obesity-associated protein (FTO) in lipid metabolism regulation and related underlying mechanisms through the FTO-mediated demethylation of m(6)A modification. FTO catalyzes the demethylation of m(6)A to alter the processing, maturation and translation of the mRNAs of lipid-related genes. FTO overexpression in the liver promotes lipogenesis and lipid droplet (LD) enlargement and suppresses CPT-1-mediated fatty acid oxidation via the SREBP1c pathway, promoting excessive lipid storage and nonalcoholic fatty liver diseases (NAFLD). FTO enhances preadipocyte differentiation through the C/EBP beta pathway, and facilitates adipogenesis and fat deposition by altering the alternative splicing of RUNX1T1, the expression of PPAR gamma and ANGPTL4, and the phosphorylation of PLIN1, whereas it inhibits lipolysis by inhibiting IRX3 expression and the leptin pathway, causing the occurrence and development of obesity. Suppression of the PPAR beta/delta and AMPK pathways by FTO-mediated m(6)A demethylation damages lipid utilization in skeletal muscles, leading to the occurrence of diabetic hyperlipidemia. m(6)A demethylation by FTO inhibits macrophage lipid influx by downregulating PPAR gamma protein expression and accelerates cholesterol efflux by phosphorylating AMPK, thereby impeding foam cell formation and atherosclerosis development. In summary, FTO-mediated m(6)A demethylation modulates the expression of lipid-related genes to regulate lipid metabolism and lipid disorder diseases. Copyright (C) 2021, Chongqing Medical University. Production and hosting by Elsevier B.V.
C1 [Yang, Zhou; Yu, Guang-li; Peng, Tian-hong; Lv, Yun-cheng] Univ South China, Hengyang Med Coll, Clin Anat & Reprod Med Applicat Inst, Hengyang 421001, Hunan, Peoples R China.
   [Zhu, Xiao; Lv, Yun-cheng] Guilin Med Univ, Guangxi Key Lab Diabet Syst Med, Guilin 541199, Guangxi, Peoples R China.
C3 University of South China; Guilin Medical University
RP Peng, TH (corresponding author), Univ South China, Hengyang Med Coll, Clin Anat & Reprod Med Applicat Inst, Hengyang 421001, Hunan, Peoples R China.; Lv, YC (corresponding author), Guilin Med Univ, Guangxi Key Lab Diabet Syst Med, Guilin 541199, Guangxi, Peoples R China.
EM thpeng67@163.com; anthony0723@163.com
RI 陈, 凌燕/HLQ-3324-2023
FU National Natural Science Foundation of China [81770460]; Natural Science
   Foundation of Guangxi Zhuang Autonomous Region, China [2019JJA140728];
   Natural Science Foundation of Hunan Province, China [2020JJ4532];
   Scientific Research Foundation for the Excellent Youth of the Education
   Department of Hunan province, China [18B264]; Aid Program from the
   Science and Technology Bureau of Hengyang City, China [2017KJ268]; Key
   Lab for Clinical Anatomy & Reproductive Medicine, China from the Science
   and Technology Bureau of Hengyang City, China [2017KJ182]
FX The authors gratefully acknowledge the financial supports from the
   National Natural Science Foundation of China (No. 81770460); the Natural
   Science Foundation of Guangxi Zhuang Autonomous Region, China (No.
   2019JJA140728): the Natural Science Foundation of Hunan Province, China
   (No. 2020JJ4532); Scientific Research Foundation for the Excellent Youth
   of the Education Department of Hunan province, China (No. 18B264); Aid
   Program (No. 2017KJ268) and Key Lab for Clinical Anatomy & Reproductive
   Medicine, China (No. 2017KJ182) from the Science and Technology Bureau
   of Hengyang City, China.
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U2 88
PU KEAI PUBLISHING LTD
PI BEIJING
PA 16 DONGHUANGCHENGGEN NORTH ST, Building 5, Room 411, BEIJING, DONGCHENG
   DISTRICT 100009, PEOPLES R CHINA
SN 2352-4820
EI 2352-3042
J9 GENES DIS
JI Genes Dis.
PD JAN
PY 2022
VL 9
IS 1
BP 51
EP 61
DI 10.1016/j.gendis.2021.01.005
EA DEC 2021
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA XW9EE
UT WOS:000735912200007
PM 35005107
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Lu, C
   Shao, ZR
   Zhang, PY
   Duan, DL
AF Lu, Chang
   Shao, Zhanru
   Zhang, Pengyan
   Duan, Delin
TI Genome-wide analysis of the Saccharina japonica sulfotransferase
   genes and their transcriptional profiles during whole developmental
   periods and under abiotic stresses
SO BMC PLANT BIOLOGY
LA English
DT Article
DE Saccharina japonica; Sulfotransferase; Fucoidan; Transcriptome; Genome
ID BROWN ALGA; CLADOSIPHON-OKAMURANUS; MYOCARDIAL-INFARCTION;
   EXTRACELLULAR-MATRIX; SULFATED FUCAN; FUCOIDAN; ANTICOAGULANT;
   EVOLUTION; PROTEIN; POLYSACCHARIDES
AB Background As a unique sulfated polysaccharide, fucoidan is an important component of cell wall in brown seaweeds. Its biochemical properties are determined by the positions and quantity of sulfate groups. Sulfotransferases (STs) catalyze the sulfation process, which transfer the sulfuryl groups to carbohydrate backbones and are crucial for fucoidan biosynthesis. Nevertheless, the structures and functions ofSTsin brown seaweeds are rarely investigated. Results There are a total of 44 STgenes identified from our genome and transcriptome analysis ofSaccharina japonica, which were located in the 17 scaffolds and 11 contigs. TheS. japonica STgenes have abundant introns and alternative splicing sites, and five tandem duplicated gene clusters were identified. Generally, theSTgenes could be classified into five groups (Group I similar to V) based on phylogenetic analysis. Accordingly, the ST proteins, which were encoded by genes within the same group, contained similar conserved motifs. Members of theS. japonica STgene family show various expression patterns in different tissues and developmental stages. Transcriptional profiles indicate that the transcriptional levels of more than half of theSTgenes are higher in kelp basal blades than in distal blades. Except forST5andST28,mostSTgenes are down-regulated with the kelp development stages. The expression levels of nineST geneswere detected by real-time quantitative PCR, which demonstrates that they responded to low salinity and drought stresses. Conclusions Various characteristics of theSTsallow the feasibilities ofS. japonicato synthesize fucoidans with different sulfate groups. This enables the kelp the potential to adapt to the costal environments and meet the needs ofS. japonica growth.
C1 [Lu, Chang; Shao, Zhanru; Duan, Delin] Chinese Acad Sci, Ctr Ocean Megasci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao 266071, Peoples R China.
   [Lu, Chang; Shao, Zhanru; Zhang, Pengyan; Duan, Delin] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266237, Peoples R China.
   [Lu, Chang] Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
   [Zhang, Pengyan] Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, Div Mariculture Ecol & Technol, Qingdao 266071, Peoples R China.
   [Duan, Delin] Qingdao Bright Moon Seaweed Grp Co Ltd, State Key Lab Bioact Seaweed Subst, Qingdao 266400, Peoples R China.
C3 Chinese Academy of Sciences; Institute of Oceanology, CAS; Laoshan
   Laboratory; Chinese Academy of Sciences; University of Chinese Academy
   of Sciences, CAS; Chinese Academy of Fishery Sciences; Yellow Sea
   Fisheries Research Institute, CAFS
RP Shao, ZR; Duan, DL (corresponding author), Chinese Acad Sci, Ctr Ocean Megasci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao 266071, Peoples R China.; Shao, ZR; Duan, DL (corresponding author), Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266237, Peoples R China.; Duan, DL (corresponding author), Qingdao Bright Moon Seaweed Grp Co Ltd, State Key Lab Bioact Seaweed Subst, Qingdao 266400, Peoples R China.
EM zrshao@qdio.ac.cn; dlduan@qdio.ac.cn
RI Duan, Delin/G-9002-2011; Lu, Chang/AAF-4827-2020
OI duan, delin/0000-0001-5356-5839
FU National Natural Science Foundation of China [41806175]; Marine Biology
   and Biotechnology Laboratory Youth Foundation [YQ2018NO06]; Shandong Key
   Research and Development Program [2018GHY115023]; Joint Research Project
   between China and Japan [2017YFE0130900]
FX This work was supported by the National Natural Science Foundation of
   China (no. 41806175), Marine Biology and Biotechnology Laboratory Youth
   Foundation (YQ2018NO06), Shandong Key Research and Development Program
   (2018GHY115023), and Joint Research Project between China and Japan (No.
   2017YFE0130900). These funders provided financial support for the
   purchase of instruments and reagents for research. Each of the funding
   bodies took part in the design of the study and collection, analysis,
   and interpretation of data, and the writing of the manuscript.
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NR 64
TC 13
Z9 13
U1 10
U2 47
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2229
J9 BMC PLANT BIOL
JI BMC Plant Biol.
PD JUN 11
PY 2020
VL 20
IS 1
AR 271
DI 10.1186/s12870-020-02422-3
PG 20
WC Plant Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences
GA MA9PA
UT WOS:000542241100002
PM 32527219
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU von Lukowicz, T
   Silacci, M
   Wyss, MT
   Trachsel, E
   Lohmann, C
   Buck, A
   Lüscher, TF
   Neri, D
   Matter, CM
AF von Lukowicz, Tobias
   Silacci, Michela
   Wyss, Matthias T.
   Trachsel, Eveline
   Lohmann, Christine
   Buck, Alfred
   Luescher, Thomas F.
   Neri, Dario
   Matter, Christian M.
TI Human antibody against C domain of tenascin-C visualizes murine
   atherosclerotic plaques ex vivo
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE atherosclerosis; autoradiography; molecular imaging; cardiology
   (basic/technical); correlative imaging
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ACUTE MYOCARDIAL-INFARCTION; PHAGE DISPLAY
   LIBRARY; ED-B DOMAIN; MONOCLONAL-ANTIBODIES; FIBRONECTIN; ANGIOGENESIS;
   EXPRESSION; AFFINITY; ISOFORM
AB Targeting proteins that are overexpressed in atherosclerotic plaques may open novel diagnostic applications. The C domain of tenascin-C is absent from normal adult tissues but can be inserted during tumor progression or tissue repair into the molecule by alternative splicing. We tested the ability of the human antibody G11, specific to this antigen, to reveal murine atherosclerotic plaques ex vivo. The antibody directed against the extra domain B of fibronectin (L19) was used as a reference. MethodsWe intravenously injected I-125-labeled G11 or L1 9 antibodies into apolipoprotein E-deficient (ApoE-/-) mice and harvested the aortae 4 or 24 h later. En face analyses of distal aortae and longitudinal sections of the aortic arch were performed to compare antibody uptake using autoradiography with plaque staining using oil red O. Plaque macrophages were detected by immunohistochemistry (anti-CD68 staining). Biodistribution of injected antibodies was investigated in aortae and blood at 4 and 24 h. Results: En face analyses revealed a significant correlation between radiolabeled G11 and fat-stained areas, increasing from 4 to 24 h, with a correlation coefficient of 0.92 (P < 0.0001) and an average signal-to-noise ratio of 104:1 at 24 h. Plaque imaging using L19 showed similar results (r = 0.86; P < 0.0001; signal-tonoise ratio, 72:1 at 24 h). Uptake of radiolabeled antibodies in histologic sections colocalized with fat staining and activated macrophages in aortic plaques. Biodistribution analyses confirmed specific accumulation in aortic plaques as well as rapid blood pool clearance of the antibodies 24 h after injection. Immunofluorescence analyses revealed increased expression of tenascin and fibronectin isoforms in macrophage-rich plaques. Conclusion: The antibody G11, specific to the C domain of tenascin-C, visualizes murine atherosclerotic plaques ex vivo. In conjunction with the increased expression of the C domain of tenascin-C in macrophage-rich plaques, the colocalization of G11 uptake with activated macrophages, and the favorable target-to-blood ratio at 24 h, this antibody may be useful for molecular imaging of advanced atherosclerotic plaques in the intact organism.
C1 Univ Zurich, Inst Physiol, CH-8057 Zurich, Switzerland.
   Zurich Univ Hosp, Cardiovasc Ctr, Zurich, Switzerland.
   Univ Zurich, Ctr Integrat Human Physiol, Zurich, Switzerland.
   Swiss Fed Inst Technol, Dept Chem & Appl Biosci, Zurich, Switzerland.
C3 University of Zurich; University of Zurich; University Zurich Hospital;
   University of Zurich; Zurich Center Integrative Human Physiology (ZIHP);
   Swiss Federal Institutes of Technology Domain; ETH Zurich
RP Matter, CM (corresponding author), Univ Zurich, Inst Physiol, Winterthurerstr 190, CH-8057 Zurich, Switzerland.
EM cmatter@physiol.unizh.ch
RI Müller, Christian/AAB-4783-2022; Wyss, Matthias/A-9659-2012; Neri,
   Dario/P-4368-2016
OI Neri, Dario/0000-0001-5234-7370
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NR 24
TC 32
Z9 34
U1 0
U2 5
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD APR
PY 2007
VL 48
IS 4
BP 582
EP 587
DI 10.2967/jnumed.106.036046
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 156KO
UT WOS:000245647000021
PM 17401095
OA Green Submitted, Bronze
DA 2025-04-10
ER

PT J
AU Jiang, SQ
   Ma, JH
   Wei, S
   Ren, PF
   Liu, JM
   Zhou, YY
   Liu, DQ
   Zhang, XH
AF Jiang, Siqi
   Ma, Jianhong
   Wei, Sheng
   Ren, Pengfei
   Liu, Jianmin
   Zhou, Yongying
   Liu, Daoquan
   Zhang, Xinhua
TI Identification of Hub Genes Associated with Progression and Prognosis of
   Bladder Cancer by Integrated Bioinformatics Analysis
SO ARCHIVOS ESPANOLES DE UROLOGIA
LA English
DT Article
DE bladder cancer; differential gene expression analysis; weighted gene
   co-expression network analysis; differential co-expression genes;
   biomarkers
ID LIGHT-CHAIN KINASE; ALTERNATIVE SPLICING EVENTS; MYOSIN HEAVY-CHAIN;
   ACTIN CYTOSKELETON; EXPRESSION; PROSTATE; COLON; METASTASIS; RECURRENCE;
   GUIDELINES
AB Background: Bladder cancer (BLCA) is an extremely common carcinoma of the urinary system that has a high incidence of relapse. Although intensive studies have investigated its pathology in the past decades, there are significant knowledge gaps regarding the characterization of the molecular processes underlying the progression of disease and consequently its prognosis. The purpose of current research was to identify significant genes that could serve as prognostic and progression biomarkers.Methods: Gene expression profiles were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Differential gene expression analysis (DGEA) and weighted gene co-expression network analysis (WGCNA) were conducted to recognize differential co-expression genes. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to explore gene function. Moreover, protein-protein inter-actions (PPI) network, overall survival (OS) and disease-free survival (DFS) were used to identify survival-related hub genes. Additionally, associations between these gene's expression and clinical parameters were determined. Finally, the Human Protein Atlas (HPA) database and qRT-PCR were used to validate gene's expression.Results: About 124 differential co-expression genes were identified. These genes were mainly enriched in muscle system process and muscle contraction (biological process, BP), contractile fiber, myofibril, sarcomere, focal adhesion and cell-substrate junc-tion (cellular component, CC) and actin binding (molecular function, MF) in GO enrichment analysis, while enriched in vascular smooth muscle contraction, focal adhesion, cardiac muscle contraction, hypertrophic cardiomyopathy, dilated cardiomyopathy and regulation of actin cytoskeleton in KEGG analysis. Furthermore, five survival-related hub genes (MYH11, ACTA2, CALD1, TPM1, MYLK) were identified via OS and DFS. In addition, these survival-related gene's expression was correlated with grade, stage and TNM stage. Finally, all survival-related hub genes were determined to be down-regulated in BLCA tissues by qRT-PCR and HPA databases.Conclusions: Our current study verified five new key genes in BLCA, which may participate in the prognosis and progression and serve as novel biomarkers of BLCA.
C1 [Jiang, Siqi] Jiujiang Univ, Sch Basic Med, Dept Clin Med, Jiujiang 332000, Jiangxi, Peoples R China.
   [Ma, Jianhong] Wuhan Univ, Zhongnan Hosp, Dept Gynecol & Obstet, Wuhan 430071, Hubei, Peoples R China.
   [Wei, Sheng] Tradit Chinese Med Hosp Xishui, Dept Urol, Huanggang 435500, Hubei, Peoples R China.
   [Ren, Pengfei; Liu, Jianmin; Zhou, Yongying; Liu, Daoquan; Zhang, Xinhua] Wuhan Univ, Zhongnan Hosp, Dept Urol, Wuhan 430071, Hubei, Peoples R China.
C3 Jiujiang University; Wuhan University; Wuhan University
RP Liu, DQ; Zhang, XH (corresponding author), Wuhan Univ, Zhongnan Hosp, Dept Urol, Wuhan 430071, Hubei, Peoples R China.
EM liudaoquan@whu.edu.cn; zhangxinhuad@163.com
RI ren, pengfei/JYP-6846-2024; jianmin, liu/KRQ-2607-2024; Jiang,
   Si-Qi/GSO-3136-2022
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NR 56
TC 3
Z9 3
U1 1
U2 11
PU INIESTARES, S.A.
PI MADRID
PA SAN GREGORIO, 8, 3 PTA. 4, MADRID, SPAIN
SN 0004-0614
EI 1576-8260
J9 ARCH ESP UROL
JI Arch. Esp. Urol.
PD NOV
PY 2022
VL 75
IS 9
BP 779
EP 790
DI 10.56434/j.arch.esp.urol.20227509.114
PG 12
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA 6X9RK
UT WOS:000896743500001
PM 36472061
DA 2025-04-10
ER

PT J
AU Goll, DE
   Thompson, VF
   Li, HQ
   Wei, W
   Cong, JY
AF Goll, DE
   Thompson, VF
   Li, HQ
   Wei, W
   Cong, JY
TI The calpain system
SO PHYSIOLOGICAL REVIEWS
LA English
DT Review
ID ACTIVATED NEUTRAL PROTEASE; CALCIUM-DEPENDENT PROTEASE; GIRDLE
   MUSCULAR-DYSTROPHY; MUSCLE-SPECIFIC CALPAIN; TRAUMATIC BRAIN-INJURY;
   CALMODULIN-LIKE DOMAIN; ACTIN-BINDING-PROTEIN; ELECTRON-MICROSCOPIC
   LOCALIZATION; CELL-PENETRATING INHIBITORS; SPECTRIN BREAKDOWN PRODUCTS
AB The calpain system originally comprised three molecules: two Ca2+-dependent proteases, mu-calpain and m-calpain, and a third polypeptide, calpastatin, whose only known function is to inhibit the two calpains. Both mu- and m-calpain are heterodimers containing an identical 28-kDa subunit and an 80-kDa subunit that shares 55-65% sequence homology between the two proteases. The crystallographic structure of m- calpain reveals six "domains" in the 80-kDa subunit: 1) a 19-amino acid NH2-terminal sequence; 2) and 3) two domains that constitute the active site, IIa and IIb; 4) domain III; 5) an 18-amino acid extended sequence linking domain III to domain IV; and 6) domain IV, which resembles the penta EF-hand family of polypeptides. The single calpastatin gene can produce eight or more calpastatin polypeptides ranging from 17 to 85 kDa by use of different promoters and alternative splicing events. The physiological significance of these different calpastatins is unclear, although all bind to three different places on the calpain molecule; binding to at least two of the sites is Ca2+ dependent. Since 1989, cDNA cloning has identified 12 additional mRNAs in mammals that encode polypeptides homologous to domains IIa and IIb of the 80-kDa subunit of mu- and m-calpain, and calpain-like mRNAs have been identified in other organisms. The molecules encoded by these mRNAs have not been isolated, so little is known about their properties. How calpain activity is regulated in cells is still unclear, but the calpains ostensibly participate in a variety of cellular processes including remodeling of cytoskeletal/membrane attachments, different signal transduction pathways, and apoptosis. Deregulated calpain activity following loss of Ca2+ homeostasis results in tissue damage in response to events such as myocardial infarcts, stroke, and brain trauma.
C1 Univ Arizona, Muscle Biol Grp, Tucson, AZ 85721 USA.
C3 University of Arizona
RP Univ Arizona, Muscle Biol Grp, Tucson, AZ 85721 USA.
EM darrel.goll@arizona.edu
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NR 504
TC 2321
Z9 2685
U1 7
U2 250
PU AMER PHYSIOLOGICAL SOC
PI Rockville
PA 6120 Executive Blvd, Suite 600, Rockville, MD, UNITED STATES
SN 0031-9333
EI 1522-1210
J9 PHYSIOL REV
JI Physiol. Rev.
PD JUL
PY 2003
VL 83
IS 3
BP 731
EP 801
DI 10.1152/physrev.00029.2002
PG 71
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 697KG
UT WOS:000183941300003
PM 12843408
DA 2025-04-10
ER

PT J
AU Deutsch, VR
   Pick, M
   Perry, C
   Grisaru, D
   Hemo, Y
   Golan-Hadari, D
   Grant, A
   Eldor, A
   Soreq, H
AF Deutsch, VR
   Pick, M
   Perry, C
   Grisaru, D
   Hemo, Y
   Golan-Hadari, D
   Grant, A
   Eldor, A
   Soreq, H
TI The stress-associated acetylcholinesterase variant AChE-R is expressed
   in human CD34<SUP>+</SUP> hematopoietic progenitors and its C-terminal
   peptide ARP promotes their proliferation
SO EXPERIMENTAL HEMATOLOGY
LA English
DT Article
ID GENE-EXPRESSION; BONE-MARROW; STEM-CELL; IN-VIVO; GLUCOCORTICOID
   RECEPTOR; SELF-RENEWAL; DIFFERENTIATION; BLOOD; SEQUENCE; GROWTH
AB Objective. Hematopoietic stress responses involve increases in leukocyte and platelet counts, implying the existence of stress responsive factors that modulate hematopoiesis. Acetylcholinesterase (AChE) is expressed in mammalian neurons and hematopoietic cells. In brain, it responds to stress by mRNA overexpression and alternative splicing, yielding the rare stress-associated "readthrough" AChE-R variant protein. This led us to explore the hematopoietic involvement of AChE-R and its cleavable C-terminal peptide ARP.
   Materials and Methods. AChE mRNA variants were labeled in CD34(+) hematopoietic progenitor cells by in situ hybridization. ARP expression was detected by multicolor flow cytometry. Bromo-deoxyuracil incorporation and viable cell counts served to evaluate the proliferative effects of ARP and suppressive effects of the AChE antisense oligonucleotide AS1 on CD34(+) cells.
   Results. The distal enhancer, proximal promoter, and first intron of the human AChE gene include consensus binding sites for hematopoietically active and stress-induced transcription factors. CD34(+) cells from human cord blood were found to express all three variant AChE mRNAs, having different intracellular distributions. ARP was found in 5 to 15% of adult peripheral blood, bone marrow, and fetal CD34(+) cells (both committed CD38(+) and uncommitted CD38(-)) and in acute myeloid leukemia blasts. Externally supplied ARP by itself facilitated the proliferation of CD34(+) cells in an antisense suppressible manner. When combined with early-acting cytokines, ARP enhanced survival and expansion of CD34(+) cells up to 28 days in culture.
   Conclusion. Our findings support ARP, the C-terminal peptide of AChE-R, as a new hematopoietic growth factor that may promote the myelopoietic expansion and thrombopoiesis characteristic of stress and may be used to enhance the efficiency of ex vivo expansion for bone marrow transplantation. (C) 2002 International Society for Experimental Hematology. Published by Elsevier Science Inc.
C1 Tel Aviv Univ, Sackler Fac Med, Tel Aviv Med Ctr, Dept Hematol, IL-69978 Tel Aviv, Israel.
   Tel Aviv Univ, Sackler Fac Med, Tel Aviv Med Ctr, Dept Obstet Gynecol, IL-69978 Tel Aviv, Israel.
   Tel Aviv Univ, Sackler Fac Med, Tel Aviv Med Ctr, Dept Orthoped, IL-69978 Tel Aviv, Israel.
   Hebrew Univ Jerusalem, Dept Biol Chem, Jerusalem, Israel.
C3 Tel Aviv University; Sackler Faculty of Medicine; Tel Aviv University;
   Sackler Faculty of Medicine; Tel Aviv University; Sackler Faculty of
   Medicine; Hebrew University of Jerusalem
RP Deutsch, VR (corresponding author), Tel Aviv Sourasky Med Ctr, Inst Hematol, 6 Weizman Str, IL-64239 Tel Aviv, Israel.
RI Soreq, Hermona/AFM-0869-2022
OI Soreq, Hermona/0000-0002-0955-526X
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NR 50
TC 60
Z9 64
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-472X
J9 EXP HEMATOL
JI Exp. Hematol.
PD OCT
PY 2002
VL 30
IS 10
BP 1153
EP 1161
AR PII S0301-472X(02)00900-1
DI 10.1016/S0301-472X(02)00900-1
PG 9
WC Hematology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Research & Experimental Medicine
GA 608YZ
UT WOS:000178877200008
PM 12384146
DA 2025-04-10
ER

PT J
AU Peters, DG
   Mitchell-Felton, H
   Kandarian, SC
AF Peters, DG
   Mitchell-Felton, H
   Kandarian, SC
TI Unloading induces transcriptional activation of the sarco(endo)plasmic
   reticulum Ca<SUP>2+</SUP>-ATPase 1 gene in muscle
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE reverse transcriptase-polymerase chain reaction; run-on assay
ID QUANTITATIVE RT-PCR; CALCIUM-PUMP GENE; SARCOPLASMIC-RETICULUM;
   SKELETAL-MUSCLE; THYROID-HORMONE; NEGATIVE REGULATOR; MOLECULAR-CLONING;
   CA-2+-ATPASE GENE; BINDING-SITE; CA-2+ ATPASE
AB Previous work showed that protein and mRNA levels of the "fast" isoform of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA1) are markedly increased in unloaded slow-twitch soleus muscles, suggesting pretranslational control of gene expression [L. M. Schulte, J. Navarro, and S. C. Kandarian. Am. J. Physiol. 264 (Cell Physiol. 33): C1308-C1315, 1993]. However, because of the difficulty of measuring transcription rates from whole muscle, transcriptional activation of the SERCA1 gene with unloading has not been confirmed. Because SERCA1 pre-mRNA levels can reflect transcriptional activity, in the present study SERCA1 introns were sequenced to allow intron-directed RT-PCR measurement of SERCA1 pre-mRNA. These data were then compared with changes in SERCA1 mRNA expression in control and unloaded soleus muscles. After 2, 4, and 10 days of unloading, SERCA1 pre-mRNA and mRNA transcript levels increased significantly by two-, three-, and sevenfold, respectively (P < 0.01). Parallel increases in SERCA1 pre-mRNA and mRNA suggest transcriptional activation of the endogenous SERCA1 gene by muscle unloading. SERCA2, the cardiac/slow-twitch skeletal muscle isoform, was not markedly increased by unloading, and RNase protection assays showed no change in alternative splicing of SERCA1 or SERCA2 primary transcripts. With use of in vivo plasmid injection, the activity of a reporter gene driven by 3.6 kb of the SERCA1 5'-flanking region increased fivefold in 7-day-unloaded soleus muscles. Comparison of the magnitude of transcriptional activation of endogenous and constructed SERCA1 genes by unloading confirms the fidelity of using intronic RT-PCR to examine muscle gene transcription rates and suggests that cis-acting elements sufficient for regulating unloading-induced transcriptional activation are contained in this promoter construct.
C1 Boston Univ, Dept Hlth Sci, Boston, MA 02215 USA.
C3 Boston University
RP Boston Univ, Dept Hlth Sci, 635 Commonwealth Ave,4th Fl, Boston, MA 02215 USA.
EM skandar@bu.edu
RI Peters, David/AAD-4629-2019
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NR 35
TC 31
Z9 34
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6143
EI 1522-1563
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD MAY
PY 1999
VL 276
IS 5
BP C1218
EP C1225
DI 10.1152/ajpcell.1999.276.5.C1218
PG 8
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA 195HR
UT WOS:000080245000026
DA 2025-04-10
ER

PT J
AU Sangiorgio, VFI
   Nam, A
   Chen, ZM
   Orazi, A
   Tam, W
AF Sangiorgio, Valentina Fabiola Ilenia
   Nam, Anna
   Chen, Zhengming
   Orazi, Attilio
   Tam, Wayne
TI GATA1 downregulation in prefibrotic and fibrotic stages of primary
   myelofibrosis and in the myelofibrotic progression of other
   myeloproliferative neoplasms
SO LEUKEMIA RESEARCH
LA English
DT Article
DE GATA1; BCR-ABL1 negative myeloproliferative neoplasms; Polycythemia
   vera; Essential thrombocythemia; Primary myelofibrosis; Pathogenesis;
   Fibrotic progression
AB GATA binding protein 1 (GATA1) is a transcription factor essential for effective erythropoiesis and mega-karyopoiesis. Two isoforms of GATA1 exist, derived from alternative splicing. "GATA1" is the full length and functionally active protein; "GATA1s" is the truncated isoform devoid of the activation domain, the function of which has not been fully elucidated.
   Reduced megakaryocytic expression of GATA1 has been linked to impaired hematopoiesis and bone marrow fibrosis in murine models and in vivo in patients affected by primary myelofibrosis (PMF). However, data is limited regarding GATA1 expression in other myeloproliferative neoplasms (MPN) such as pre-fibrotic PMF (prePMF), polycythemia vera (PV) and essential thrombocythemia (ET) and in their respective fibrotic progression.
   To assess whether an immunohistologic approach can be of help in separating different MPN, we have performed a comprehensive immunohistochemical evaluation of GATA1 expression in megakaryocytes within a cohort of BCR-ABL1 negative MPN. In order to highlight any potential differences between the two isoforms we tested two clones, one staining the sum of GATA1 and GATA1s ("clone 1"), the other staining GATA1 full length alone ("clone 2"). At the chronic phase, a significant reduction preferentially of GATA1 full length was seen in pre-fibrotic PMF, particularly compared to ET and PV; no significant differences were observed between PV and ET. The fibrotic progression of both PV and ET was associated with a significant reduction in GATA1, particularly affecting the GATA1 full length isoform. The fibrotic progression of pre-PMF to PMF was associated with a significant reduction of the overall GATA1 protein and a trend in reduction of GATA1s.
   Our findings support a role of GATA1 in the pathogenesis of BCR-ABL1 negative MPN, particularly in their fibrotic progression and suggest that the immunohistochemical evaluation of GATA1 may be of use in the differential diagnosis of these neoplasms.
C1 [Sangiorgio, Valentina Fabiola Ilenia] Royal London Hosp, Dept Cellular Pathol, London, England.
   [Sangiorgio, Valentina Fabiola Ilenia; Nam, Anna; Tam, Wayne] Weill Cornell Med, Dept Pathol & Lab Med, New York, NY USA.
   [Chen, Zhengming] Weill Cornell Med, Dept Populat Hlth Sci, New York, NY USA.
   [Orazi, Attilio] Texas Tech Univ, Paul L Foster Sch Med, Dept Pathol, Ctr Hlth Sci, El Paso, TX USA.
C3 Barts Health NHS Trust; Royal London Hospital; Cornell University; Weill
   Cornell Medicine; Cornell University; Weill Cornell Medicine; Texas Tech
   University System; Texas Tech University
RP Sangiorgio, VFI (corresponding author), Royal London Hosp, Dept Cellular Pathol, London, England.
EM valentina.sangiorgio@nhs.net; shn9035@med.cornell.edu;
   zhc2006@med.cornell.edu; attilio.orazi@ttuhsc.edu; wtam@med.cornell.edu
OI Chen, Zhengming/0000-0001-9437-6452
CR Barbui T, 2013, LEUKEMIA, V27, P1953, DOI 10.1038/leu.2013.74
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NR 18
TC 3
Z9 4
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
EI 1873-5835
J9 LEUKEMIA RES
JI Leuk. Res.
PD JAN
PY 2021
VL 100
AR 106495
DI 10.1016/j.leukres.2020.106495
PG 5
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA QH5WU
UT WOS:000618347200009
PM 33360878
DA 2025-04-10
ER

PT J
AU Williams, I
   Williams, C
   Siroky, B
   Bates, E
   Kovacs, G
   Peti-Peterdi, J
   Unlap, MT
   Bell, PD
AF Williams, I
   Williams, C
   Siroky, B
   Bates, E
   Kovacs, G
   Peti-Peterdi, J
   Unlap, MT
   Bell, PD
TI Regulation of mesangial cell Na<SUP>+</SUP>/Ca<SUP>2+</SUP> exchanger
   isoforms
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID CARDIAC NA+-CA2+ EXCHANGER; SODIUM-CALCIUM EXCHANGE; NA/CA EXCHANGER;
   CYTOSOLIC CA2+; RAT; EXPRESSION; CLONING; NCX1; TRANSPORT; PROTEIN
AB An isoform of the Na+/Ca2+ exchanger (SDNCX1.10) was cloned from mesangial cells of Sprague-Dawley rat. Regulation of this isoform was compared to two other clones that were derived from the Dahl/Rapp salt sensitive (SNCX) and salt resistant rat (RNCX). All isoforms differ at the alternative splice site and at amino acid 218 for SNCX. PKC activates RNCX but not SNCX while SDNCX1.10 was also activated by PKC. Regulation of exchanger activities by intracellular calcium ([Ca2+](i)), pH, and kinases was assessed using Na-dependent Ca-45(2+) uptake assays in OK-PTH cells expressing the vector, RNCX, SNCX, or SDNCX1.10. [Ca2+](i) was elevated from 50 to 125 nM (n = 4) with thapsigargin (40 nM) and reduced from 50 to 29 nM (n = 4) and 18 nM (n = 4) with 10 or 20 muM BAPTA, respectively. RNCX was active at all three [Ca2+](i) while SNCX and SDNCX1.10 were only active at lower [Ca2+](i). Varying extracellular pH (pH(e), without nigericin) or pH(e) and intracellular pH (pH(i), with 10 muM nigericin) from pH 7.4 to 6.2, 6.8, or 8.0 showed that SNCX activity was attenuated at both low and high pHs. SDNCX1.10 activity was attenuated only at pH 6.2 and 6.8 (with or without nigericin) while RNCX activity was attenuated at pH 6.2 (with or without nigericin) and pH 6.8 (with nigericin). Finally, only SDNCX1.10 activity was stimulated by 250 muM CPT-cAMP or 250 muM DB-cGMP treatment. Thus the differential regulation of [Ca2+](i) by these exchangers is dependent upon the pattern of cellular Na+/Ca2+ exchanger isoform expression. J. Cel L Physiol. 199: 181-193, 2004. (C) 2003 Wiley-Liss, Inc.
C1 Univ Alabama, Dept Physiol, Div Nephrol, Ctr Nephrol Res & Training, Birmingham, AL 35294 USA.
   Univ Alabama, Dept Med, Div Nephrol, Ctr Nephrol Res & Training, Birmingham, AL 35294 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham
RP Univ Alabama, UAB Stn, Sparks Ctr 865, Birmingham, AL 35294 USA.
EM pdbell@nrtc.dom.uab.edu
FU NHLBI NIH HHS [R01HL50163, 1K01HL67718-01] Funding Source: Medline
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NR 52
TC 2
Z9 3
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD MAY
PY 2004
VL 199
IS 2
BP 181
EP 193
DI 10.1002/jcp.10447
PG 13
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA 808OC
UT WOS:000220577400003
PM 15040000
DA 2025-04-10
ER

PT J
AU Lu, XH
   Timchenko, NA
   Timchenko, LT
AF Lu, XH
   Timchenko, NA
   Timchenko, LT
TI Cardiac elav-type RNA-binding protein (ETR-3) binds to RNA CUG
   repeats expanded in myotonic dystrophy
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID TRINUCLEOTIDE REPEAT; TRIPLET REPEAT; CTG REPEAT; REDUCES EXPRESSION;
   MESSENGER-RNA; SEX-LETHAL; GENE; EXPANSION; REGION; MICE
AB Myotonic dystrophy (DM) is a neuromuscular disorder associated with CTG triplet repeat expansion in the myotonin protein kinase gene (DMPK), We previously proposed a hypothesis suggesting that the expanded CUG repeats sequester specific RNA-binding proteins and that such a sequestration results in abnormal RNA processing of several RNAs containing CUG repeats in multiple tissues affected in patients with DM. One of the members of the CUG-binding proteins, CUG-BP, has been identified previously. Here we describe the second member of this family, elav-type ribonucleoprotein (ETR-3), which is highly expressed in heart and is able to interact with CUG repeats. Screening of a mouse liver cDNA library with a CUG-BP probe identified two mETR-3 cDNAs, Two additional cDNAs from mouse heart were amplified by RT-PCR, These cDNAs differ by several insertions/deletions and might be generated via alternative splicing. Mouse ETR-3 has a mel, wt of 50 kDa and displays a high level of homology to CUG-BP protein, The organization of the RNA-binding domains (RBDs) within the ETR-3 molecule is similar to one within CUG-BP, A study of mETR-3 RNA-binding activity showed that the mETR-3 binds to (CUG)(8) repeats. Sequence analysis of mETR-3 indicates the presence of several CUG repeats within the mETR-3 mRNA, Both CUG-BP and mETR-3 bind to mETR-3 mRNA via CUG repeats, suggesting the possible involvement of CUG-BP-like proteins in the regulation of mETR-3 processing. Analysis of the tissue distribution of ETR-3 showed that in human cells, ETR-3 mRNA is highly expressed in heart, but is undetectable in other tissues examined, Our results suggest the existence of a family of proteins that bind to CUG repeats and might be affected in DM by expansion of CUG repeats.
C1 Baylor Coll Med, Dept Med, Cardiol Sect, Houston, TX 77030 USA.
   Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA.
C3 Baylor College of Medicine; Baylor College of Medicine
RP Timchenko, LT (corresponding author), Baylor Coll Med, Dept Med, Cardiol Sect, 1 Baylor Plaza, Houston, TX 77030 USA.
FU NHLBI NIH HHS [HL54313-02] Funding Source: Medline; NIAMS NIH HHS
   [AR44387] Funding Source: Medline
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NR 35
TC 97
Z9 109
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD JAN
PY 1999
VL 8
IS 1
BP 53
EP 60
DI 10.1093/hmg/8.1.53
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 162ZF
UT WOS:000078377200006
PM 9887331
DA 2025-04-10
ER

PT J
AU Monsoro-Burq, AH
AF Monsoro-Burq, Anne H.
TI PAX transcription factors in neural crest development
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Pax1; Pax3; Pax7; Pax9; Splotch mutant; Waardenburg syndrome; Cardiac
   neural crest; Craniofacial skeleton; Melanocyte; Schwann cell; Sensory
   neuron
ID GENE REGULATORY NETWORK; PERSISTENT TRUNCUS ARTERIOSUS; POSTERIOR
   NONAXIAL MESODERM; SPLOTCH MUTANT MOUSE; WAARDENBURG-SYNDROME; PLATE
   BORDER; PAIRED-BOX; CELL DIFFERENTIATION; POINT MUTATION; NERVOUS-SYSTEM
AB The nine vertebrate PAX transcription factors (PAX1-PAX9) play essential roles during early development and organogenesis. Pax genes were identified in vertebrates using their homology with the Drosophila melanogaster paired gene DNA-binding domain. PAX1-9 functions are largely conserved throughout vertebrate evolution, in particular during central nervous system and neural crest development. The neural crest is a vertebrate invention, which gives rise to numerous derivatives during organogenesis, including neurons and glia of the peripheral nervous system, craniofacial skeleton and mesenchyme, the heart outflow tract, endocrine and pigment cells. Human and mouse spontaneous mutations as well as experimental analyses have evidenced the critical and diverse functions of PAX factors during neural crest development. Recent studies have highlighted the role of PAX3 and PAX7 in neural crest induction. Additionally, several PAX proteins - PAX1, 3, 7, 9 - regulate cell proliferation, migration and determination in multiple neural crest-derived lineages, such as cardiac, sensory, and enteric neural crest, pigment cells, glia, craniofacial skeleton and teeth, or in organs developing in close relationship with the neural crest such as the thymus and parathyroids. The diverse PAX molecular functions during neural crest formation rely on fine-tuned modulations of their transcriptional transactivation properties. These modulations are generated by multiple means, such as different roles for the various isoforms (formed by alternative splicing), or posttranslational modifications which alter protein-DNA binding, or carefully orchestrated protein-protein interactions with various co-factors which control PAX proteins activity. Understanding these regulations is the key to decipher the versatile roles of PAX transcription factors in neural crest development, differentiation and disease. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Monsoro-Burq, Anne H.] Univ Paris Saday, Univ Paris 11, Ctr Univ, F-91405 Orsay, France.
   [Monsoro-Burq, Anne H.] Inst Curie, Div Res, Ctr Univ, F-91405 Orsay, France.
   [Monsoro-Burq, Anne H.] Univ Paris Saday, UMR 3347, CNRS, U1021,Inserm,Ctr Univ, F-91405 Orsay, France.
C3 Universite Paris Saclay; UNICANCER; Universite PSL; Institut Curie;
   Universite Paris Saclay; Universite Paris Saclay; Centre National de la
   Recherche Scientifique (CNRS); CNRS - National Institute for Biology
   (INSB); Universite PSL; UNICANCER; Institut Curie; Institut National de
   la Sante et de la Recherche Medicale (Inserm)
RP Monsoro-Burq, AH (corresponding author), Inst Curie, Div Res, Ctr Univ, Batiment 110, F-91405 Orsay, France.
EM anne-helene.monsoro-burq@curie.fr
RI Monsoro-Burq, Anne/F-7075-2013
OI Monsoro-Burq, Anne H./0000-0003-2427-982X
FU Fondation pour la Recherche Medicale (FRM) [DEQ20150331733]; Agence
   Nationale pour la Recherche (ANR); Association pour la Recherche contre
   le Cancer (ARC) [PJA20131200185]
FX I am grateful to C. Borday, A. Figueiredo, and P. Pla for their comments
   on the manuscript. Research in the Monsoro-Burq team is supported by
   grants from Fondation pour la Recherche Medicale (FRM, DEQ20150331733),
   Agence Nationale pour la Recherche (ANR, Programmes blancs 2011 et
   2015), and Association pour la Recherche contre le Cancer (ARC,
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NR 119
TC 78
Z9 97
U1 0
U2 48
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD AUG
PY 2015
VL 44
BP 87
EP 96
DI 10.1016/j.semcdb.2015.09.015
PG 10
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA CW7NT
UT WOS:000365186700012
PM 26410165
DA 2025-04-10
ER

PT J
AU Polampalli, S
   Choughule, A
   Negi, N
   Shinde, S
   Baisane, C
   Amre, P
   Subramanian, PG
   Gujral, S
   Prabhash, K
   Parikh, P
AF Polampalli, S.
   Choughule, A.
   Negi, N.
   Shinde, S.
   Baisane, C.
   Amre, P.
   Subramanian, P. G.
   Gujral, S.
   Prabhash, K.
   Parikh, P.
TI Analysis and comparison of clinicohematological parameters and molecular
   and cytogenetic response of two Bcr/Abl fusion transcripts
SO GENETICS AND MOLECULAR RESEARCH
LA English
DT Article
DE Bcr/Abl fusion transcripts; b3a2; b2a2; Thrombocytosis; Molecular
   response
ID CHRONIC MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; HYBRID
   MESSENGER-RNA; EARLY CHRONIC PHASE; PHILADELPHIA-CHROMOSOME; BCR GENE;
   ESSENTIAL THROMBOCYTHEMIA; BREAKPOINT LOCATION; PLATELET COUNTS;
   TYROSINE KINASE
AB Different forms of p210 are produced by alternative splicing, namely b2a2 and b3a2. There have been many contrasting data establishing a relationship between the two Bcr/Abl transcripts and platelet counts and also response to treatment. However, the data published to date have been on a small group of patients. The aim of the present study was to determine whether there was any difference between clinical and hematological parameters at diagnosis between the two Bcr/Abl fusion transcripts in our population, and whether the two transcripts responded differently or similarly to imatinib treatment. RT-PCR was performed in 202 cases for detection of Bcr/Abl transcripts in newly diagnosed chronic myelogenous leukemia cases in one year. The two transcripts were compared and correlated with clinical, hematological and FISH data and with response to treatment. A total of 138 cases were of b3a2 and 64 were of b2a2 transcript. There was no correlation between the hematological parameters and the type of transcript. There was a significant association of blast crisis with b2a2, especially with myeloid blast crisis. When compared to FISH results, 10% of b3a2 were found to have a significant association with 5' Abl deletion as compared to 3% of b2a2. On analyzing the therapeutic response, we did not find any difference between the two transcripts. In conclusion, our findings confirm that the b3a2 type transcript is not significantly associated with thrombocytosis, that the short transcript, b2a2, occurs with acute phase, i.e., blast crisis, and that there is no difference in treatment response between the two transcripts. However, further studies are required to understand the molecular pathways involved in the Bcr/Abl mechanism.
C1 [Polampalli, S.; Choughule, A.; Negi, N.; Shinde, S.; Subramanian, P. G.; Gujral, S.] Tata Mem Hosp, Dept Med Oncol, Mol Biol Lab, Mumbai 400012, Maharashtra, India.
   [Baisane, C.; Amre, P.] Tata Mem Hosp, Dept Hematopathol, Mol Biol Lab, Mumbai 400012, Maharashtra, India.
   [Prabhash, K.; Parikh, P.] Tata Mem Hosp, Canc Cytogenet Lab, Mumbai 400012, Maharashtra, India.
C3 Tata Memorial Centre (TMC); Tata Memorial Hospital; Tata Memorial Centre
   (TMC); Tata Memorial Hospital; Tata Memorial Centre (TMC); Tata Memorial
   Hospital
RP Polampalli, S (corresponding author), Tata Mem Hosp, Dept Med Oncol, Mol Biol Lab, Mumbai 400012, Maharashtra, India.
EM drsunitap@yahoo.co.in
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NR 34
TC 34
Z9 38
U1 0
U2 0
PU FUNPEC-EDITORA
PI RIBEIRAO PRETO
PA RUA FLORIANO PEIXOTO 2444, ALTO DA BOA VISTA, RIBEIRAO PRETO, SP 00000,
   BRAZIL
SN 1676-5680
J9 GENET MOL RES
JI Genet. Mol. Res.
PY 2008
VL 7
IS 4
BP 1138
EP 1149
DI 10.4238/vol7-4gmr485
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 362WF
UT WOS:000260227200016
PM 19048492
OA Bronze
DA 2025-04-10
ER

PT J
AU Sugiyama, N
   Andersson, S
   Lathe, R
   Fan, X
   Alonso-Magdalena, P
   Schwend, T
   Nalvarte, I
   Warner, M
   Gustafsson, JÅ
AF Sugiyama, N.
   Andersson, S.
   Lathe, R.
   Fan, X.
   Alonso-Magdalena, P.
   Schwend, T.
   Nalvarte, I.
   Warner, M.
   Gustafsson, J- A.
TI Spatiotemporal dynamics of the expression of estrogen receptors in the
   postnatal mouse brain
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE 3 beta Adiol; central nervous system; cytochrome P-450 enzyme system;
   estrogen receptor-beta; neuronal development; puberty
ID CENTRAL-NERVOUS-SYSTEM; IMMATURE FEMALE RATS; KNOCKOUT MICE; ER-BETA;
   SEXUAL-DIFFERENTIATION; PERIPHERAL-BLOOD; CORTICAL-NEURONS; SPLICE
   VARIANT; ALPHA; IDENTIFICATION
AB This study reports on the spatiotemporal dynamics of the expression of estrogen receptors (ERs) in the mouse central nervous system (CNS) during the early postnatal and the peripubertal period. At postnatal day 7 (P7), neurons with strong nuclear immunostaining for both ER alpha and ER beta 1 were widely distributed throughout the brain. Sucrose density gradient sedimentation followed by western blotting supported the histochemical evidence for high levels of both ERs at P7. Over the following 2 days, there was a rapid downregulation of ERs. At P9, ER alpha expression was visible only in the hypothalamic area. Decline in ER beta 1 expression was slower than that of ER alpha, and ER alpha-negative, ER beta 1-positive cells were observed in the dentate gyrus and walls of third ventricle. Between P14 and P35, ERs were undetectable except for the hypothalamic area. As before P7, the ovary does not produce estrogen but does produce 5 alpha-androstane-3 beta, 17 beta-diol (3 beta Adiol), an estrogenic metabolite of dihydrotestosterone, we examined the effects of high levels of 3 beta Adiol in the postnatal period. We used CYP7B1 knockout mice which cannot hydroxylate and inactivate 3 beta Adiol. The brains of these mice are abnormally large with reduced apoptosis. In the early postnatal period, there was 1-week delay in the timing of the reduction in ER expression in the brain. These data reveal that the time when ERs might be activated in the brain is limited to the first 8 postnatal days. In addition, the importance of aromatase has to be reconsidered as the alternative estrogen, 3 beta Adiol, is important in neuronal function in the postnatal brain.
C1 [Sugiyama, N.; Andersson, S.; Fan, X.; Alonso-Magdalena, P.; Schwend, T.; Nalvarte, I.; Warner, M.; Gustafsson, J- A.] Karolinska Inst, Dept Biosci & Nutr, Novum, SE-14186 Stockholm, Sweden.
   [Lathe, R.] Pieta Res, Edinburgh, Midlothian, Scotland.
C3 Karolinska Institutet
RP Gustafsson, JÅ (corresponding author), Karolinska Inst, Dept Biosci & Nutr, Novum, SE-14186 Stockholm, Sweden.
EM jan-ake.gustafsson@ki.se
RI Nalvarte, Ivan/V-3849-2019; Alonso-Magdalena, Paloma/AAH-2076-2021;
   Sugiyama, Nobuhiro/C-6388-2008
OI Lathe, Richard/0000-0001-9698-9834; Nalvarte, Ivan/0000-0001-6828-2583;
   warner, margaret/0000-0002-7946-2675; ALONSO MAGDALENA,
   PALOMA/0000-0003-1065-5388
FU Shinshu University School of Medicine; Mochida Memorial Foundation for
   Medical and Pharmaceutical Research; Swedish Cancer Fund; EU Integrated
   Project CRESCENDO; KaroBio AB
FX The excellent technical participation of Christina Thulin-Andersson and
   Makbule Sagici is gratefully acknowledged. This study was supported by
   Study Abroad Support from Shinshu University School of Medicine, Study
   Abroad Support from Mochida Memorial Foundation for Medical and
   Pharmaceutical Research, the Swedish Cancer Fund, the EU Integrated
   Project CRESCENDO, and KaroBio AB.
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NR 54
TC 39
Z9 39
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD FEB
PY 2009
VL 14
IS 2
BP 223
EP 232
DI 10.1038/mp.2008.118
PG 10
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 395VD
UT WOS:000262550700011
PM 18982005
DA 2025-04-10
ER

PT J
AU Lee, EHY
   Hsieh, YP
   Yang, CL
   Tsai, KJ
   Liu, CH
AF Lee, EHY
   Hsieh, YP
   Yang, CL
   Tsai, KJ
   Liu, CH
TI Induction of integrin-associated protein (IAP) mRNA expression during
   memory consolidation in rat hippocampus
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE alternative splicing forms; hippocampus; inhibitory avoidance learning;
   integrin-associated protein; reverse transcription-polymerase chain
   reaction
ID LONG-TERM POTENTIATION; OVARIAN TUMOR-MARKER; EXTRACELLULAR-MATRIX;
   SIGNAL-TRANSDUCTION; CELLS; THROMBOSPONDIN; RECEPTOR; IDENTIFICATION;
   GLYCOPROTEIN; ADHESION
AB We have previously demonstrated that hippocampal integrin-associated protein (IAP) gene expression is associated with memory formation in a one-way inhibitory avoidance learning in rats. In the present study, we further investigated the role and mechanism of IAP involved in memory consolidation in rats. Because of the minute amount of IAP present in the brain, we have adopted the quantitative reverse transcription-polymerase chain reaction (RT-PCR) method. Our results revealed that hippocampal IAP mRNA expression is approximately fourfold higher in rats showing good memory retention (GM, retention score of 600 s) at 3 h, but not at other time points, after training when compared with the poor memory rats (retention score < 80 s). On the other hand, integrin alpha v mRNA level was markedly increased (similar to twofold), while integrin beta 3 mRNA level was decreased (similar to 50%) at 1 h post-training. Further, separate sets of RT-PCR analysis revealed that IAP5 and IAP6 mRNA expressions, but not that of IAP7, were markedly increased in GM rats 3 h post-training. Moreover, regional distribution studies revealed that different isoforms of the IAP gene are similarly distributed in different brain areas, while IAP7 has been the predominant form present in astrocyte cells. These results together suggest that IAP mRNA expression is indeed induced upon training, rather than that the GM rats have constitutively higher levels of IAP. The unparallel change of IAP and integrin mRNA expressions as far as time-course is concerned suggests that they are possibly involved in different forms and stages of memory processing. Further, IAP5 and IAP6 are more closely associated with memory consolidation, while IAP7 may constitute the major isotype for signal transduction in astrocyte cells.
C1 Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
   Natl Def Med Ctr, Grad Inst Life Sci, Taipei, Taiwan.
C3 Academia Sinica - Taiwan; National Defense Medical Center
RP Lee, EHY (corresponding author), Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
RI Lee, Eminy/S-7014-2018; Tsai, Kuen-Jer/B-9393-2009
OI Ma, Yun Li/0000-0002-6321-8889; Lee, Eminy/0000-0001-6342-0940; Tsai,
   Kuen-Jer/0000-0002-2170-9735
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NR 35
TC 21
Z9 26
U1 0
U2 1
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD MAR
PY 2000
VL 12
IS 3
BP 1105
EP 1112
DI 10.1046/j.1460-9568.2000.00985.x
PG 8
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 300NH
UT WOS:000086258700035
PM 10762341
DA 2025-04-10
ER

PT J
AU Aleem, AA
   Elsaid, MF
   Chalhoub, N
   Chakroun, A
   Mohamed, KAS
   AlShami, R
   Kuzu, O
   Mohamed, RB
   Ibrahim, K
   AlMudheki, N
   Osman, O
   Ross, ME
   ELalamy, O
AF Aleem, Alice Abdel
   Elsaid, Mahmoud F.
   Chalhoub, Nader
   Chakroun, Almahdi
   Mohamed, Khalid A. S.
   AlShami, Rana
   Kuzu, Omer
   Mohamed, Reem B.
   Ibrahim, Khalid
   AlMudheki, Noora
   Osman, Omar
   Ross, M. Elizabeth
   ELalamy, Osama
TI Clinical and genomic characteristics of LAMA2 related congenital
   muscular dystrophy in a patients' cohort from Qatar. A population
   specific founder variant
SO NEUROMUSCULAR DISORDERS
LA English
DT Article
DE LAMA2-RD; MDC1A; Merosin deficiency congenital muscular dystrophy;
   Osteopenia in MDC1A; LAMA2 Founder mutation in Qatar; Genomic modifiers
ID CORTICAL DYSPLASIA; MEROSIN; PHENOTYPE; EPILEPSY; GENOTYPE/PHENOTYPE;
   CLASSIFICATION; PREVALENCE; MANAGEMENT; MUTATION
AB Congenital LAMA2 related muscular dystrophy (LAMA2-RD), the most commonly recognized type of congenital muscular dystrophies, has been described in patients' cohorts from Europe and the UK but not from Middle-Eastern. This study aimed to reveal the prevalence, clinical and genomic characteristics of congenital LAMA2-RD in a patient's cohort of 17 families (21 patients) from the Gulf and Middle East. Affected subjects exhibited the classic phenotype of generalized hypotonia, developmental delay, and progressive muscular weakness. Despite the homogeneous background of most of our patients, clinical variability was evident; however, none of our patients was able to achieve independent ambulation. The associated features of nephrocalcinosis, infantile-onset osteopenia, and cardiac arrest were first described in this study. LAMA2 mutations constituted 48% of the genetic causes underlying congenital muscular dystrophies (CMDs) in our patients. We estimated a point prevalence of 0.8 in 100.000 for LAMA2-RD in Qatar, relatively higher compared to that described in Europe's studies. The founder mutation and high rate of consanguinity are potential contributors. This study identified five LAMA2 truncating variants, two novel and three recurrent, of which the c.6488delA-frameshift that was found in 12 unrelated Qatari families, highlighting a founder mutation in Qatari patients. The two novel variants involved an acceptor splice site and N-terminus deletion that removes the LAMA2 promoter, exon1, and part of intron1. The "residual" expression of LAMA2 transcript and protein associated with this large N-terminus deletion suggested an alternative promoter that, while seems to be activated, acts less efficiently. (C) 2020 Elsevier B.V. All rights reserved.
C1 [Aleem, Alice Abdel] Weill Cornell Med Qatar, Dept Neurol, PO 24144, Doha, Qatar.
   [Aleem, Alice Abdel; Chalhoub, Nader; Chakroun, Almahdi; Kuzu, Omer; Ross, M. Elizabeth] Weill Cornell Med, Dept Ctr Neurogenet, Brain & Mind Res Inst, New York, NY USA.
   [Elsaid, Mahmoud F.; Mohamed, Khalid A. S.; AlShami, Rana; Ibrahim, Khalid] Hamad Med Corp, Dept Neuropediat, Doha, Qatar.
   [Elsaid, Mahmoud F.; Mohamed, Khalid A. S.; AlShami, Rana; Mohamed, Reem B.; Ibrahim, Khalid] Sidra Med, Doha, Qatar.
   [Mohamed, Reem B.] Hamad Med Corp, Dept Pediat, Doha, Qatar.
   [AlMudheki, Noora] Hamad Med Corp, Dept Physiotherapy, Doha, Qatar.
   [Osman, Omar] Hamad Med Corp, Dept Radiol, Doha, Qatar.
   [ELalamy, Osama] Hamad Med Corp, Dept Adult Neurol, Doha, Qatar.
C3 Qatar Foundation (QF); Weill Cornell Medical College Qatar; Cornell
   University; Weill Cornell Medicine; Hamad Medical Corporation; Sidra
   Medical & Research Center; Hamad Medical Corporation; Hamad Medical
   Corporation; Hamad Medical Corporation; Hamad Medical Corporation
RP Aleem, AA (corresponding author), Weill Cornell Med Qatar, Qatar Fdn, Dept Neurol, PO 24144, Doha, Qatar.
EM aka2005@qatar-med.cornell.edu
RI osman, Omar/KFA-6361-2024; Aleem, Alice/AAY-2598-2020; CHAKROUN,
   Almahdi/V-1009-2018
OI CHAKROUN, Almahdi/0000-0003-1124-7765; Abdel Aleem,
   Alice/0000-0001-5137-3382
FU PPM1 grant from the Qatar National Research Fund, a member of Qatar
   Foundation [PPM1-1206-150013]
FX We thank patients and families for their participation in the study.
   This publication was made possible by PPM1 grant [PPM1-1206-150013, AAA
   principal investigator] from the Qatar National Research Fund, a member
   of Qatar Foundation. The findings achieved herein are solely the
   responsibility of the author[s]
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NR 39
TC 17
Z9 17
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD JUN
PY 2020
VL 30
IS 6
BP 457
EP 471
DI 10.1016/j.nmd.2020.03.009
PG 15
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA LZ3RU
UT WOS:000541146600003
PM 32444167
DA 2025-04-10
ER

PT J
AU Golembiewska, E
   Stepniewska, J
   Kabat-Koperska, J
   Kedzierska, K
   Domanski, M
   Ciechanowski, K
AF Golembiewska, Edyta
   Stepniewska, Joanna
   Kabat-Koperska, Joanna
   Kedzierska, Karolina
   Domanski, Maciej
   Ciechanowski, Kazimierz
TI The Role of Klotho Protein in Chronic Kidney Disease: Studies in Animals
   and Humans
SO CURRENT PROTEIN & PEPTIDE SCIENCE
LA English
DT Review
DE Cardiovascular disease; chronic kidney disease; dialysis; FGF-23; Klotho
   protein; kidney transplantation
ID GROWTH-FACTOR 23; PERITONEAL-DIALYSIS PATIENTS; SOLUBLE KLOTHO;
   TRANSPLANT RECIPIENTS; PARATHYROID KLOTHO; PHOSPHATE; CHANNEL;
   CALCIFICATION; METABOLISM; EXPRESSION
AB The identification of Klotho gene was a major discovery as the gene encodes a protein regulating multiple functions. A defect in Klotho gene expression in mice results in a phenotype of premature aging including shortened life span, growth retardation, hypogonadism, skin and muscle atrophies, vascular calcification, cognition impairment, motor neuron degeneration and others. This phenotype is associated with phosphate balance disorders and underlines the major function of Klotho in mineral metabolism. As another 2 related paralogs were discovered (beta-Klotho, which is involved in bile acid and energy metabolism, and gamma-Klotho, with a yet to be defined function), this led to the revised naming of Klotho as alpha-Klotho. Two forms of alpha-Klotho protein have been reported: a membrane-bound and a soluble one. Membrane Klotho forms a complex with fibroblast growth factor (FGF) receptors and functions as an obligate co-receptor for the FGF-23 phosphatonin in distal tubules. The soluble form of Klotho seems to function as a humoral factor and regulates glycoproteins on the cell surface including ion channels and growth factors. There is data suggesting that soluble Klotho exerts phosphaturic effects independently of FGF-23. Circulating soluble Klotho is produced either by proteolytic cleavage of the extracellular domain of the transmembrane form by two membrane-anchored proteases (ADAM10 and ADAM17) or by alternative mRNA splicing. In animal models Klotho has been shown to exert pleiotropic actions, including cytoprotection, anti-oxidation, anti-apoptosis, protection of vasculature, promotion of angiogenesis and vascularization, inhibition of fibrogenesis and preservation of stem cells. The exact diagnostic and therapeutic role of Klotho in humans is not fully known yet. The article presents the role of Klotho in physiology and different stages of chronic kidney disease (CKD).
C1 [Golembiewska, Edyta; Stepniewska, Joanna; Kabat-Koperska, Joanna; Kedzierska, Karolina; Domanski, Maciej; Ciechanowski, Kazimierz] Pomeranian Med Univ, Dept Nephrol Transplantol & Internal Med, Powstancow Wielkopolskich 72, PL-70111 Szczecin, Poland.
C3 Pomeranian Medical University
RP Golembiewska, E (corresponding author), Pomeranian Med Univ, Dept Nephrol Transplantol & Internal Med, Powstancow Wielkopolskich 72, PL-70111 Szczecin, Poland.
EM irys@pum.edu.pl
RI Ciechanowski, Kazimierz/A-5675-2016; Golembiewska, Edyta/AAX-3165-2021;
   Golembiewska, Edyta/B-2957-2016
OI Golembiewska, Edyta/0000-0001-6461-1570; Ciechanowski,
   Kazimierz/0000-0003-2758-8871
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NR 43
TC 17
Z9 20
U1 1
U2 14
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-2037
EI 1875-5550
J9 CURR PROTEIN PEPT SC
JI Curr. Protein Pept. Sci.
PY 2016
VL 17
IS 8
BP 821
EP 826
DI 10.2174/1389203717666160526123646
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA ED1AS
UT WOS:000388576500010
PM 27226196
DA 2025-04-10
ER

PT J
AU Nicod, N
   Parker, RS
   Giordano, E
   Maestro, V
   Davalos, A
   Visioli, F
AF Nicod, Nathalie
   Parker, Robert S.
   Giordano, Elena
   Maestro, Virginia
   Davalos, Alberto
   Visioli, Francesco
TI Isomer-specific effects of conjugated linoleic acid on HDL functionality
   associated with reverse cholesterol transport
SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY
LA English
DT Article
DE HDL functionality; Conjugated linoleic acid; SR-BI; Atherosclerosis;
   Intestine
ID FATTY-ACIDS; CACO-2 CELLS; LIPID-METABOLISM; GENE-EXPRESSION; KNOCKOUT
   MICE; ATHEROSCLEROSIS; LIPOPROTEIN; EFFLUX; LDL; ABCA1
AB High-density lipoproteins (HDLs) are atheroprotective because of their role in reverse cholesterol transport. The intestine is involved in this process because it synthesizes HDL, removes cholesterol from plasma and excretes it into the lumen. We investigated the role of selected dietary fatty acids on intestinal cholesterol uptake and HDL functionality. Caco-2 monolayers grown on Transwells were supplemented with either palmitic, palmitoleic, oleic, linoleic, docosahexaenoic, eicosapentaenoic, arachidonic or conjugated linoleic acids (CLAs): c9,t11-CLA; t9,t11-CLA; c10,t12-CLA. Cells synthesized HDL in the basolateral compartment for 24 h in the absence or presence of an antibody to SR-BI (aSR-BI), which inhibits its interaction with HDL Free cholesterol (FC) accumulated to a greater extent in the presence than in the absence of aSR-BI, indicating net uptake of FC by SR-BI. Uptake's efficiency was significantly decreased when cells were treated with c9,t11-CLA relative to the other fatty acids. These differences were associated with lower HDL functionality, since neither SR-BI protein expression nor expression and alternative splicing of other genes involved lipid metabolism were affected. Only INSIG2 expression was decreased, with no increase of its target genes. Increasing pre-beta-HDL synthesis, by inducing ABCA1 and adding APOA1, resulted in reduced uptake of FC by SR-BI after c9, t11-CLA treatment, indicating reduced functionality of pre-beta-HDL Conversely, treatment with c9,t11-CLA resulted in a greater uptake of FC and esterified cholesterol from mature HDL Therefore, Caco-2 monolayers administered c9,t11-CLA produced a nonfunctional pre-beta-HDL but took up cholesterol more efficiently via SR-BI from mature HDL. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Nicod, Nathalie; Giordano, Elena; Maestro, Virginia; Davalos, Alberto; Visioli, Francesco] CSIC, CEI UAM, Madrid Inst Adv Studies IMDEA Food, Lab Funct Foods, Madrid, Spain.
   [Parker, Robert S.] Cornell Univ, Div Nutr Sci, Ithaca, NY USA.
C3 IMDEA Food Institute; Consejo Superior de Investigaciones Cientificas
   (CSIC); Cornell University
RP Visioli, F (corresponding author), IMDEA Food, Ctra Cantoblanco 8, Madrid 28049, Spain.
EM francesco.visioli@imdea.org
RI Davalos, Alberto/AAA-9949-2021; Visioli, Francesco/J-9356-2013
OI Davalos, Alberto/0000-0001-5709-6443; Visioli,
   Francesco/0000-0002-1756-1723
FU Programa de actividades en tecnologias ALIBIRD-CM de la Comunidad de
   Madrid [S2013/ABU-2728]
FX BMS212122 was a kind gift from Bristol Myers Squibb. Belen Garcia
   provided skillful technical assistance. FEDER Funds. Programa de
   actividades en tecnologias ALIBIRD-CM S2013/ABU-2728 de la Comunidad de
   Madrid.
CR [Anonymous], COCHRANE DB SYST REV
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NR 41
TC 8
Z9 10
U1 1
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0955-2863
EI 1873-4847
J9 J NUTR BIOCHEM
JI J. Nutr. Biochem.
PD FEB
PY 2015
VL 26
IS 2
BP 165
EP 172
DI 10.1016/j.jnutbio.2014.10.002
PG 8
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA CB4DL
UT WOS:000349578300008
PM 25468613
DA 2025-04-10
ER

PT J
AU Horton, JD
   Shimomura, I
   Ikemoto, S
   Bashmakov, Y
   Hammer, RE
AF Horton, JD
   Shimomura, I
   Ikemoto, S
   Bashmakov, Y
   Hammer, RE
TI Overexpression of sterol regulatory element-binding protein-1a in mouse
   adipose tissue produces adipocyte hypertrophy, increased fatty acid
   secretion, and fatty liver
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LEUCINE ZIPPER PROTEIN; COENZYME-A SYNTHETASE; ACYL-COA SYNTHETASE;
   TRANSGENIC MICE; DIABETES-MELLITUS; GENE-EXPRESSION; TRANSCRIPTION
   FACTOR; INSULIN-RESISTANCE; NUCLEAR SREBP-1C; CULTURED-CELLS
AB Sterol regulatory element-binding proteins (SREBPs) are a family of membrane-bound transcription factors that regulate cholesterol and fatty acid homeostasis. In mammals, three SREBP isoforms designated SREBP-1a, SREBP-1c, and SREBP-2 have been identified. SREBP-1a and SREBP-1c are derived from the same gene by virtue of alternatively spliced first exons. SREBP-1a has a longer transcriptional activation domain and is a more potent transcriptional activator than SREBP-1c in cultured cells and liver. Here, we describe the physiologic consequences of overexpressing the nuclear form of SREBP-1a (nSREBP-1a) in adipocytes of mice using the adipocyte-specific aP2 promoter (aP2-nSREBP-1a). The transgenic aP2-nSREBP-1a mice developed markedly enlarged white and brown adipocytes that were fully differentiated. Adipocytes isolated from aP2-nSREBP-1a mice had significantly increased rates of fatty acid synthesis and enhanced fatty acid secretion. The increased production and release of fatty acids from adipocytes led, in turn, to a fatty liver. Overexpression of the alternative SREBP-1 isoform, nSREBP-1c, in adipose tissue inhibits adipocyte differentiation; as a result, the transgenic nSREBP-1c mice develop a syndrome resembling human lipodystrophy, which includes a loss of peripheral white adipose tissue, diabetes, and fatty livers (Shimomura, I., Hammer, R. E., Richardson, J. A., Ikemoto, S., Bashmakov, Y., Goldstein, J. L., and Brown, M. S. ( 1998) Genes Dev. 12, 3182-3194). In striking contrast, nSREBP-1a overexpression in fat resulted in the hypertrophy of fully differentiated adipocytes, no diabetes, and mild hepatic steatosis. These results suggest that nSREBP-1a and nSREBP-1c have distinct roles in adipocyte fat metabolism in vivo.
C1 Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75390 USA.
   Univ Texas, SW Med Ctr, Dept Mol Genet, Dallas, TX 75390 USA.
   Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA.
   Univ Texas, SW Med Ctr, Howard Hughes Med Inst, Dallas, TX 75390 USA.
C3 University of Texas System; University of Texas Southwestern Medical
   Center Dallas; University of Texas Dallas; University of Texas System;
   University of Texas Southwestern Medical Center Dallas; University of
   Texas Dallas; University of Texas System; University of Texas
   Southwestern Medical Center Dallas; University of Texas Dallas;
   University of Texas System; University of Texas Southwestern Medical
   Center Dallas; Howard Hughes Medical Institute; University of Texas
   Dallas
RP Univ Texas, SW Med Ctr, Dept Biochem, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM Robert.hammer@utsouthwestern.edu
OI Hammer, Robert E./0000-0001-5487-7551; Ikemoto,
   Shinji/0000-0002-2291-2735
FU NHLBI NIH HHS [HL-20948] Funding Source: Medline
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NR 35
TC 172
Z9 200
U1 1
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI ROCKVILLE
PA 11200 ROCKVILLE PIKE, SUITE 302, ROCKVILLE, MD, UNITED STATES
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 19
PY 2003
VL 278
IS 38
BP 36652
EP 36660
DI 10.1074/jbc.M306540200
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 721LR
UT WOS:000185318300096
PM 12855691
OA hybrid
DA 2025-04-10
ER

PT J
AU Fiermonte, G
   Dolce, V
   Palmieri, F
AF Fiermonte, G
   Dolce, V
   Palmieri, F
TI Expression in Escherichia coli, functional characterization, and
   tissue distribution of isoforms A and B of the phosphate carrier from
   bovine mitochondria
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BEEF-HEART MITOCHONDRIA; RAT-LIVER MITOCHONDRIA; TRANSPORT PROTEIN;
   N-ETHYLMALEIMIDE; SACCHAROMYCES-CEREVISIAE; OXOGLUTARATE CARRIER; GENES;
   YEAST; CARDIOLIPIN; SUBUNIT
AB The two isoforms of the mammalian mitochondrial phosphate carrier (PiC), A and B, differing in the sequence near the N terminus, arise from alternative splicing of a primary transcript of the Pic gene (Dolce, V., Iacobazzi, V., Palmieri, F., and Walker, J. E. (1994) J. Biol. Chem. 269, 10451-10460). To date, the PiC isoforms A and B have not been studied at the protein level. To explore the tissue-distribution and the potential functional differences between the two isoforms, polyclonal site-directed antibodies specific for PiC-A and PiC-B were raised, and the two bovine isoforms were obtained by expression in Escherichia coli and reconstituted into phospholipid vesicles. Western blot analysis demonstrated that isoform A is present in high amounts in heart, skeletal muscle, and diaphragm mitochondria, whereas isoform B is present in the mitochondria of all tissues examined. Heart and liver bovine mitochondria contained 69 and 0 pmol of PiC-A/mg of protein, and 10 and 8 pmol of PiC-B/mg of protein, respectively. In the reconstituted system the pure recombinant isoforms A and B both catalyzed the two known modes of transport (P-i/P-i antiport and P-i/H+ symport) and exhibited similar properties of substrate specificity and inhibitor sensitivity. However, they strongly differed in their kinetic parameters. The transport affinities of isoform B for phosphate and arsenate were found to be 3-fold lower than those of isoform A Furthermore, the maximum transport rate of isoform B is about 3-fold higher than that of isoform A. These results support the hypothesis that the sequence divergence between PiC-A and PiC-B may have functional significance in determining the affinity and the translocation rate of the substrate through the PiC molecule.
C1 Univ Bari, Dept Pharmaco Biol, Biochem & Mol Biol Lab, I-70125 Bari, Italy.
C3 Universita degli Studi di Bari Aldo Moro
RP Univ Bari, Dept Pharmaco Biol, Biochem & Mol Biol Lab, Via E Orabona 4, I-70125 Bari, Italy.
EM fpalm@farmbiol.uniba.it
RI Dolce, Vincenza/HLX-3233-2023; Fiermonte, Giuseppe/D-3680-2018
OI Fiermonte, Giuseppe/0000-0002-6764-9395; Dolce,
   Vincenza/0000-0003-2966-4866
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NR 54
TC 123
Z9 128
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD AUG 28
PY 1998
VL 273
IS 35
BP 22782
EP 22787
DI 10.1074/jbc.273.35.22782
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 114NY
UT WOS:000075616600087
PM 9712911
OA hybrid
DA 2025-04-10
ER

PT J
AU Lee, CS
   Han, H
   Kim, BS
   Lee, SM
   Hwang, JS
   Kang, SW
   Lee, BH
   Kim, HR
AF Lee, CS
   Han, H
   Kim, BS
   Lee, SM
   Hwang, JS
   Kang, SW
   Lee, BH
   Kim, HR
TI Wax moth, Galleria mellonella, high density lipophorin receptor::
   alternative splicing, tissue-specific expression, and developmental
   regulation
SO INSECT BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Article
DE Galleria mellonella; Lepidoptera; lipophorin receptor; VLDL receptor;
   O-linked sugar domain; 20-hydroxyecdysone
ID LIPOPROTEIN RECEPTOR; INSECT LIPOPROTEIN; GENE-EXPRESSION;
   SALIVARY-GLANDS; CELLS EXPRESS; BINDING; DROSOPHILA; LARVAL; ECDYSONE;
   ENDOCYTOSIS
AB A lipophorin (Lp) receptor cDNA from the fat body of Galleria mellonella (Lepidoptera) was cloned and sequenced. This is the first result in this order, Lepidoptera. It showed the pattern of the VLDL receptor belonging to the LDL receptor family. Sequence homology with other Lp receptors in insects, Locusta migratoria and Aedes aegypti, was 70 and 61%, respectively and each domain was highly conserved. Polyclonal anti-Lp receptor antibody prepared against expressed Lp receptor fragment between ligand binding domain and EGF-precursor homology domain (R305rD549 of amino acid residues) specifically detected the Lp receptor. Through immuno-blotting, the Lp receptor of larval fat body has an approximate molecular mass of about 97 and 110 kDa under non-reducing and reducing conditions, respectively. This result was in agreement with that of the ligand-blotting. The variant Lp receptors were expressed in the fat body of G. mellonella; one is an Lp receptor which lacks 84 bp of O-linked sugar domain and the other is a full length form of the Lp receptor. Both forms were detected by the polyclonal anti-Lp receptor antibody. The Lp receptor from the fat body of G. mellonella was differently expressed depending on the tissue and the developmental stage with specific abundance in prepupal stage. A steroid hormone, 20-hydroxyecdysone (20-HE) plays a crucial role in insect development. With regards to this conception, day 1-2 last instar larvae were treated with 20-HE and drastic induction of the Lp receptor was observed 48 It after treatment. It was also observed that cholesterol caused an induction of the Lp receptor. (C) 2003 Elsevier Ltd. All rights reserved.
C1 Korea Univ, Sch Life Sci & Biotechnol, Lab Anim Macromol Physiol & Biochem, Seoul 136701, South Korea.
   Natl Inst Agr Sci & Technol, Dept Sericulture & Entomol, Suwon 441701, South Korea.
   SUNY Buffalo, Sch Med, Dept Physiol & Biophys, Buffalo, NY 14215 USA.
   Miryang Natl Univ, Dept Sericulturre & Entomol, Miryang 627130, South Korea.
C3 Korea University; State University of New York (SUNY) System; University
   at Buffalo, SUNY; Pusan National University
RP Korea Univ, Sch Life Sci & Biotechnol, Lab Anim Macromol Physiol & Biochem, Seoul 136701, South Korea.
EM kimhr@mail.korea.ac.kr
RI ; Han, Jikhyon/L-7891-2014
OI Lee, Chang Seok/0000-0002-7513-7621; Han, Jikhyon/0000-0002-7767-3305
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NR 35
TC 35
Z9 40
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0965-1748
EI 1879-0240
J9 INSECT BIOCHEM MOLEC
JI Insect Biochem. Mol. Biol.
PD AUG
PY 2003
VL 33
IS 8
BP 761
EP 771
DI 10.1016/S0965-1748(03)00066-3
PG 11
WC Biochemistry & Molecular Biology; Entomology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Entomology
GA 706LR
UT WOS:000184455600002
PM 12878223
DA 2025-04-10
ER

PT J
AU Desind, SZ
   Bell, SK
   Davidson, ZM
   Lutz, CS
AF Desind, Samuel Z.
   Bell, Samira K.
   Davidson, Zachary M.
   Lutz, Carol S.
TI Long noncoding RNAs and their complex role in shaping and regulating
   arachidonic acid metabolism: Learning to love the (not-really) junk
SO WILEY INTERDISCIPLINARY REVIEWS-RNA
LA English
DT Review
DE arachidonic acid; COX-2; inflammatory signaling; long noncoding RNA;
   miRNA
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; NF-KAPPA-B; MESSENGER-RNA;
   PROSTAGLANDIN SYNTHASE; COX-2 EXPRESSION; GASTROINTESTINAL TOXICITY;
   HEPATOCELLULAR-CARCINOMA; PROMOTES PROLIFERATION; UP-REGULATION; CANCER
AB Long noncoding RNAs (lncRNAs) have emerged as critical regulators in numerous biological processes. The arachidonic acid (AA) metabolic pathway is a fundamental biochemical pathway responsible for the enzymatic conversion of AA, a 20-carbon omega-six polyunsaturated fatty acid, into a variety of potent lipid signaling molecules known as eicosanoids. Eicosanoids are produced through the cyclooxygenase and lipoxygenase arms of the AA pathway and have diverse biological roles in both healthy and disease states, including cancer and inflammatory diseases. Cyclooxygenase 2 (COX-2), the inducible, rate-limiting enzyme of the cyclooxygenase arm, produces two main forms of eicosanoids: prostaglandins and thromboxanes. AA metabolized through the lipoxygenase arm by the action of 5-lipoxygenase (ALOX5) produces eicosanoids known as leukotrienes. COX-2 and ALOX5 gene expression are regulated through many different lncRNAs and microRNA (miRNA)-mediated mechanisms. As previously reviewed, noncoding RNAs affect transcription, splicing, alternative polyadenylation, messenger RNA stability, translation, and miRNA regulation of COX-2 and ALOX5 (Lutz and Cornett, 2013, Wiley Interdisciplinary Reviews. RNA, 4(5), 593-605). This current review discusses the intricate roles of lncRNAs, including MALAT1, NEAT1, HOTAIR, PACER, and others, in modulating the AA pathway. In this review update, we will delve into advancements in our understanding of AA gene expression regulation. We will explore the mechanisms of lncRNAs and their associated miRNAs and proteins known to regulate key components of the AA signaling pathway. We will also discuss the therapeutic potential of targeting lncRNA-mediated regulation, with a focus on modulating COX-2 and ALOX5 activity and downstream eicosanoid production for applications in inflammatory and oncological conditions. This article is categorized under: Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs RNA in Disease and Development > RNA in Disease
C1 [Desind, Samuel Z.; Bell, Samira K.; Davidson, Zachary M.; Lutz, Carol S.] Univ Med & Dent New Jersey, Dept Microbiol Biochem & Mol Genet, Rutgers Biomed & Hlth Sci, Newark, NJ 07103 USA.
   [Desind, Samuel Z.; Bell, Samira K.; Davidson, Zachary M.; Lutz, Carol S.] Rutgers Sch Grad Studies, Newark, NJ USA.
   [Lutz, Carol S.] Rutgers Biomed & Hlth Sci New Jersey Med Sch, Dept Microbiol, Biochem & Mol Genet, Newark, NJ 07103 USA.
   [Lutz, Carol S.] Rutgers Sch Grad Studies, Newark, NJ 07103 USA.
C3 Rutgers University System; Rutgers University New Brunswick; Rutgers
   University Biomedical & Health Sciences; Rutgers University System;
   Rutgers University New Brunswick; Rutgers University Biomedical & Health
   Sciences
RP Lutz, CS (corresponding author), Rutgers Biomed & Hlth Sci New Jersey Med Sch, Dept Microbiol, Biochem & Mol Genet, Newark, NJ 07103 USA.; Lutz, CS (corresponding author), Rutgers Sch Grad Studies, Newark, NJ 07103 USA.
EM lutzcs@njms.rutgers.edu
OI Desind, Samuel/0000-0001-9900-4973; Lutz, Carol/0000-0002-7283-072X;
   Bell, Samira/0009-0003-8548-7646
FU New Jersey Commission on Cancer Research, Predoctoral fellowship to
   S.Z.D.; NJCCR predoctoral fellowship; NJHF; Cheers
FX This work was supported by an NJCCR predoctoral fellowship to SZD and an
   NJHF grant to CSL. Cheers to all.
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NR 131
TC 0
Z9 0
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-7004
EI 1757-7012
J9 WIRES RNA
JI Wiley Interdiscip. Rev.-RNA
PD JAN
PY 2024
VL 15
IS 1
DI 10.1002/wrna.1828
EA NOV 2023
PG 21
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA NV8K1
UT WOS:001108547200001
PM 37994271
OA hybrid
DA 2025-04-10
ER

PT J
AU Denz, CR
   Zhang, C
   Jia, PP
   Du, JF
   Huang, XP
   Dube, S
   Thomas, A
   Poiesz, BJ
   Dube, DK
AF Denz, Christopher R.
   Zhang, Chi
   Jia, Pingping
   Du, Jianfeng
   Huang, Xupei
   Dube, Syamalima
   Thomas, Anish
   Poiesz, Bernard J.
   Dube, Dipak K.
TI Absence of Mutation at the 5′-Upstream Promoter Region of the TPM4 Gene
   From Cardiac Mutant Axolotl (Ambystoma mexicanum)
SO CARDIOVASCULAR TOXICOLOGY
LA English
DT Article
DE Tropomyosin; Promoter; Ambystoma mexicanum; Myofibrillogenesis
ID SERUM RESPONSE FACTOR; ALPHA-TROPOMYOSIN GENE; TISSUE-SPECIFIC
   TRANSCRIPTION; LIGHT CHAIN-2 PROMOTER; ACTIN GENE; SKELETAL-MUSCLE;
   XENOPUS EMBRYOS; EXPRESSION; ISOFORMS; SMOOTH
AB Tropomyosins are a family of actin-binding proteins that show cell-specific diversity by a combination of multiple genes and alternative RNA splicing. Of the 4 different tropomyosin genes, TPM4 plays a pivotal role in myofibrillogenesis as well as cardiac contractility in amphibians. In this study, we amplified and sequenced the upstream regulatory region of the TPM4 gene from both normal and mutant axolotl hearts. To identify the cis-elements that are essential for the expression of the TPM4, we created various deletion mutants of the TPM4 promoter DNA, inserted the deleted segments into PGL3 vector, and performed promoter-reporter assay using luciferase as the reporter gene. Comparison of sequences of the promoter region of the TPM4 gene from normal and mutant axolotl revealed no mutations in the promoter sequence of the mutant TPM4 gene. CArG box elements that are generally involved in controlling the expression of several other muscle-specific gene promoters were not found in the upstream regulatory region of the TPM4 gene. In deletion experiments, loss of activity of the reporter gene was noted upon deletion which was then restored upon further deletion suggesting the presence of both positive and negative cis-elements in the upstream regulatory region of the TPM4 gene. We believe that this is the first axolotl promoter that has ever been cloned and studied with clear evidence that it functions in mammalian cell lines. Although striated muscle-specific cis-acting elements are absent from the promoter region of TPM4 gene, our results suggest the presence of positive and negative cis-elements in the promoter region, which in conjunction with positive and negative trans-elements may be involved in regulating the expression of TPM4 gene in a tissue-specific manner.
C1 [Denz, Christopher R.; Dube, Syamalima; Thomas, Anish; Poiesz, Bernard J.; Dube, Dipak K.] SUNY Upstate Med Univ, Dept Med, Syracuse, NY 13210 USA.
   [Zhang, Chi; Jia, Pingping; Du, Jianfeng; Huang, Xupei] Florida Atlantic Univ, Dept Biomed Sci, Boca Raton, FL 33431 USA.
C3 State University of New York (SUNY) System; State University of New York
   (SUNY) Upstate Medical Center; State University System of Florida;
   Florida Atlantic University
RP Dube, DK (corresponding author), SUNY Upstate Med Univ, Dept Med, 750 E Adams St, Syracuse, NY 13210 USA.
EM dubed@upstate.edu
RI Huang, xp/JRX-2837-2023; Du, Jian/IXD-1367-2023
OI Thomas, Anish/0000-0003-3293-3115
FU American Heart Association (NY Affiliate) [951038T]; Department of
   Medicine; NIH [S6- GM073621]; AHA Great Southeast Affiliate
   [09GRNT2400138]; American Heart Association (AHA) [09GRNT2400138]
   Funding Source: American Heart Association (AHA)
FX The work was supported by grants from American Heart Association (NY
   Affiliate # 951038T) and from the Department of Medicine to DKD and NIH
   S6- GM073621 and AHA Great Southeast Affiliate (09GRNT2400138) to XH.
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NR 37
TC 10
Z9 10
U1 0
U2 3
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1530-7905
J9 CARDIOVASC TOXICOL
JI Cardiovasc. Toxicol.
PD SEP
PY 2011
VL 11
IS 3
BP 235
EP 243
DI 10.1007/s12012-011-9117-z
PG 9
WC Cardiac & Cardiovascular Systems; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Toxicology
GA 798UC
UT WOS:000293236700005
PM 21626230
DA 2025-04-10
ER

PT J
AU Zhang, XJ
   Li, GY
   Jiang, HY
   Li, LM
   Ma, JG
   Li, HM
   Chen, JP
AF Zhang, Xiujuan
   Li, Guanyu
   Jiang, Haiying
   Li, Linmiao
   Ma, Jinge
   Li, Huiming
   Chen, Jinping
TI Full-length transcriptome analysis of Litopenaeus vannamei
   reveals transcript variants involved in the innate immune system
SO FISH & SHELLFISH IMMUNOLOGY
LA English
DT Article
DE The Pacific white shrimp; Litopenaeus vannamei; Isoform sequencing;
   Immune molecules
ID PACIFIC WHITE SHRIMP; L-TYPE LECTIN; GENE; HEPATOPANCREAS; EXPRESSION;
   IDENTIFICATION; ANTIBACTERIAL; CONSTRUCTION; COMBINATION; DISCOVERY
AB To better understand the immune system of shrimp, this study combined PacBio isoform sequencing (Iso-Seq) and Illumina paired-end short reads sequencing methods to discover full-length immune-related molecules of the Pacific white shrimp, Litopenaeus vannamei. A total of 72,648 nonredundant full-length transcripts (unigenes) were generated with an average length of 2545 bp from five main tissues, including the hepatopancreas, cardiac stomach, heart, muscle, and pyloric stomach. These unigenes exhibited a high annotation rate (62,164, 85.57%) when compared against NR, NT, Swiss-Prot, Pfam, GO, KEGG and COG databases. A total of 7544 putative long noncoding RNAs (lncRNAs) were detected and 1164 nonredundant full-length transcripts (449 UniTransModels) participated in the alternative splicing (AS) events. Importantly, a total of 5279 nonredundant full-length unigenes were successfully identified, which were involved in the innate immune system, including 9 immunerelated processes, 19 immune-related pathways and 10 other immune-related systems. We also found wide transcript variants, which increased the number and function complexity of immune molecules; for example, toll-like receptors (TLRs) and interferon regulatory factors (IRFs). The 480 differentially expressed genes (DEGs) were significantly higher or tissue-specific expression patterns in the hepatopancreas compared with that in other four tested tissues (FDR < 0.05). Furthermore, the expression levels of six selected immune-related DEGs and putative IRFs were validated using real-time PCR technology, substantiating the reliability of the PacBio Iso-seq results. In conclusion, our results provide new genetic resources of long-read full-length transcripts data and information for identifying immune-related genes, which are an invaluable transcriptomic resource as genomic reference, especially for further exploration of the innate immune and defense mechanisms of shrimp.
C1 [Zhang, Xiujuan; Li, Guanyu; Jiang, Haiying; Li, Linmiao; Ma, Jinge; Li, Huiming; Chen, Jinping] Guangdong Inst Appl Biol Resources, Guangdong Publ Lab Wild Anim Conservat & Utilizat, Guangdong Key Lab Anim Conservat & Resource Utili, Guangzhou 510260, Guangdong, Peoples R China.
C3 Guangdong Academy of Sciences; Institute of Zoology, Guangdong Academy
   of Sciences
RP Chen, JP (corresponding author), Guangdong Inst Appl Biol Resources, Guangdong Publ Lab Wild Anim Conservat & Utilizat, Guangdong Key Lab Anim Conservat & Resource Utili, Guangzhou 510260, Guangdong, Peoples R China.
EM Chenjp@giabr.gd.cn
OI Chen, Jinping/0000-0002-0808-6617
FU Funds of Technology Transfer from Guangdong Academy of Sciences and
   Zhongshan [2016G1FC0008]; Guangzhou Science Technology and Innovation
   Commission [201804020080]; National Natural Science Fund of China
   [31802279]; GDAS Special Project of Science and Technology Development
   [2017GDASCX-0107, 2018GDASCX-0107]; Planning funds of Scientific and
   Technological of Guangdong Province [2016B070701016]
FX This work was supported by the Funds of Technology Transfer from
   Guangdong Academy of Sciences and Zhongshan [2016G1FC0008], the
   Guangzhou Science Technology and Innovation Commission [201804020080],
   the National Natural Science Fund of China [31802279], the GDAS Special
   Project of Science and Technology Development [2017GDASCX-0107 and
   2018GDASCX-0107], and the Planning funds of Scientific and Technological
   of Guangdong Province [2016B070701016].
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NR 55
TC 47
Z9 51
U1 5
U2 53
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1050-4648
EI 1095-9947
J9 FISH SHELLFISH IMMUN
JI Fish Shellfish Immunol.
PD APR
PY 2019
VL 87
BP 346
EP 359
DI 10.1016/j.fsi.2019.01.023
PG 14
WC Fisheries; Immunology; Marine & Freshwater Biology; Veterinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Fisheries; Immunology; Marine & Freshwater Biology; Veterinary Sciences
GA HS7ZA
UT WOS:000464086600038
PM 30677515
DA 2025-04-10
ER

PT J
AU Sánchez-Lanzas, R
   Alvarez-Castelao, B
   Bermejo, T
   Ayuso, T
   Tuñón, T
   Castaño, JG
AF Sanchez-Lanzas, Raul
   Alvarez-Castelao, Beatriz
   Bermejo, Teresa
   Ayuso, Teresa
   Tunon, Teresa
   Castano, Jose G.
TI Protein degradation in a LAMP-2-deficient B-lymphoblastoid cell line
   from a patient with Danon disease
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Article
DE Danon disease; LAMP-2; Autophagy; Ubiquitin proteasome;
   Chaperone-mediated autophagy; Alpha-synuclein; IkappaB; Rcan1;
   glyceraldehyde-3-phosphate dehydrogenase
ID CHAPERONE-MEDIATED AUTOPHAGY; CLASS-II PRESENTATION; ALPHA-SYNUCLEIN;
   LYSOSOMAL PROTEOLYSIS; SELECTIVE PATHWAY; STORAGE DISEASE; LAMP-2;
   PROTEASOME; MECHANISM; COMPLEX
AB Danon disease, a condition characterized by cardiomyopathy, myopathy, and intellectual disability, is caused by mutations in the LAMP-2 gene. Lamp-2A protein, generated by alternative splicing from the Lamp-2 pre-mRNA, is reported to be the lysosomal membrane receptor essential for the chaperone-mediated autophagic pathway (CMA) aimed to selective protein targeting and translocation into the lysosomal lumen for degradation. To study the relevance of Lamp-2 in protein degradation, a lymphoblastoid cell line was obtained by EBV transformation of B-cells from a Danon patient. The derived cell line showed no significant expression of Lamp-2 protein. The steady-state mRNA and protein levels of alpha-synuclein, IKB alpha, Rcan1, and glyceraldehyde-3-phosphate dehydrogenase, four proteins reported to be selective substrates of the CMA pathway, were similar in control and Lamp-2-deficient cells. Inhibition of protein synthesis showed that the half-life of alpha-synuclein, IKB alpha, and Rcan1 was similar in control and Lamp-2-deficient cells, and its degradation prevented by proteasome inhibitors. Both in control and Lamp-2-deficient cells, induction of CMA and macroautophagy by serum and aminoacid star-vation of cells for 8 h produced a similar decrease in IKB alpha and Rcan1 protein levels and was prevented by the addition of lysosome and autophagy inhibitors. In conclusion, the results presented here showed that Lamp-2 deficiency in human lymphoblastoid cells did not modify the steady-state levels or the degradation of several protein substrates reported as selective substrates of the CMA pathway. (C) 2016 Elsevier B.V. All rights reserved.
C1 [Sanchez-Lanzas, Raul; Alvarez-Castelao, Beatriz; Bermejo, Teresa; Castano, Jose G.] UAM CSIC, Inst Invest Biomed Alberto Sols, Dept Bioquim, Madrid 28029, Spain.
   [Sanchez-Lanzas, Raul; Alvarez-Castelao, Beatriz; Bermejo, Teresa; Castano, Jose G.] UAM, Ctr Invest Biomed Red Enfermedades Neurodegenrat, Fac Med, Madrid 28029, Spain.
   [Ayuso, Teresa] Complejo Hosp Navarra, Dept Neurol, Pamplona 31008, Spain.
   [Tunon, Teresa] Complejo Hosp Navarra, Anat Patol, Pamplona 31008, Spain.
   [Tunon, Teresa] Inst Invest Biomed Navarra IdisNa, Biobanco Tejidos Neurol, Ctr Invest Biomed, Pamplona 31008, Spain.
   [Alvarez-Castelao, Beatriz] Max Planck Inst Brain Res, Synapt Plast, D-60438 Frankfurt, Germany.
C3 Consejo Superior de Investigaciones Cientificas (CSIC); CSIC - Instituto
   de Investigaciones Biomedicas Alberto Sols (IIBM); CIBERNED; Autonomous
   University of Madrid; Servicio Navarro de Salud - Osasunbidea; Servicio
   Navarro de Salud - Osasunbidea; Max Planck Society
RP Castaño, JG (corresponding author), Univ Autonoma Madrid, Fac Med, CSIC, Dept Bioquim, E-28029 Madrid, Spain.; Castaño, JG (corresponding author), Univ Autonoma Madrid, Fac Med, CSIC, Inst Invest Biomed Alberto Sols, E-28029 Madrid, Spain.
EM joseg.castano@uam.es
RI Tuñón, María/L-2456-2017; alvarez-castelao, beatriz/W-1707-2018
OI Sanchez, Raul/0000-0002-6179-6546
FU MINECO [SAF-2012-3455]; Comunidad de Madrid [P2010_BMD2331]; CIBERNED
FX This work was supported by grants from MINECO SAF-2012-3455, Comunidad
   de Madrid P2010_BMD2331, and CIBERNED to JGC.
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NR 38
TC 2
Z9 2
U1 2
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0925-4439
EI 0006-3002
J9 BBA-MOL BASIS DIS
JI Biochim. Biophys. Acta-Mol. Basis Dis.
PD AUG
PY 2016
VL 1862
IS 8
BP 1423
EP 1432
DI 10.1016/j.bbadis.2016.04.014
PG 10
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA DO5LA
UT WOS:000377823400006
PM 27130438
OA Bronze
DA 2025-04-10
ER

PT J
AU Cummings, BB
   Karczewski, KJ
   Kosmicki, JA
   Seaby, EG
   Watts, NA
   Singer-Berk, M
   Mudge, JM
   Karjalainen, J
   Satterstrom, FK
   O'Donnell-Luria, AH
   Poterba, T
   Seed, C
   Solomonson, M
   Alfoldi, J
   Daly, MJ
   MacArthur, DG
AF Cummings, Beryl B.
   Karczewski, Konrad J.
   Kosmicki, Jack A.
   Seaby, Eleanor G.
   Watts, Nicholas A.
   Singer-Berk, Moriel
   Mudge, Jonathan M.
   Karjalainen, Juha
   Satterstrom, F. Kyle
   O'Donnell-Luria, Anne H.
   Poterba, Timothy
   Seed, Cotton
   Solomonson, Matthew
   Alfoldi, Jessica
   Daly, Mark J.
   MacArthur, Daniel G.
CA Genome Aggregation Database Prod T
   Genome Aggregation Database Consor
TI Transcript expression-aware annotation improves rare variant
   interpretation
SO NATURE
LA English
DT Article
ID GENES; ARRHYTHMIA; MUTATIONS
AB The acceleration of DNA sequencing in samples from patients and population studies has resulted in extensive catalogues of human genetic variation, but the interpretation of rare genetic variants remains problematic. A notable example of this challenge is the existence of disruptive variants in dosage-sensitive disease genes, even in apparently healthy individuals. Here, by manual curation of putative loss-of-function (pLoF) variants in haploinsufficient disease genes in the Genome Aggregation Database (gnomAD)(1), we show that one explanation for this paradox involves alternative splicing of mRNA, which allows exons of a gene to be expressed at varying levels across different cell types. Currently, no existing annotation tool systematically incorporates information about exon expression into the interpretation of variants. We develop a transcript-level annotation metric known as the 'proportion expressed across transcripts', which quantifies isoform expression for variants. We calculate this metric using 11,706 tissue samples from the Genotype Tissue Expression (GTEx) project(2) and show that it can differentiate between weakly and highly evolutionarily conserved exons, a proxy for functional importance. We demonstrate that expression-based annotation selectively filters 22.8% of falsely annotated pLoF variants found in haploinsufficient disease genes in gnomAD, while removing less than 4% of high-confidence pathogenic variants in the same genes. Finally, we apply our expression filter to the analysis of de novo variants in patients with autism spectrum disorder and intellectual disability or developmental disorders to show that pLoF variants in weakly expressed regions have similar effect sizes to those of synonymous variants, whereas pLoF variants in highly expressed exons are most strongly enriched among cases. Our annotation is fast, flexible and generalizable, making it possible for any variant file to be annotated with any isoform expression dataset, and will be valuable for the genetic diagnosis of rare diseases, the analysis of rare variant burden in complex disorders, and the curation and prioritization of variants in recall-by-genotype studies.
C1 [Cummings, Beryl B.; Karczewski, Konrad J.; Kosmicki, Jack A.; Seaby, Eleanor G.; Watts, Nicholas A.; Singer-Berk, Moriel; Karjalainen, Juha; Satterstrom, F. Kyle; O'Donnell-Luria, Anne H.; Poterba, Timothy; Solomonson, Matthew; Alfoldi, Jessica; Daly, Mark J.; MacArthur, Daniel G.] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA 02142 USA.
   [Cummings, Beryl B.; Karczewski, Konrad J.; Kosmicki, Jack A.; Seaby, Eleanor G.; Watts, Nicholas A.; Karjalainen, Juha; Satterstrom, F. Kyle; Poterba, Timothy; Seed, Cotton; Solomonson, Matthew; Alfoldi, Jessica; Daly, Mark J.; MacArthur, Daniel G.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
   [Cummings, Beryl B.] Harvard Med Sch, Program Biol & Biomed Sci, Boston, MA 02115 USA.
   [Kosmicki, Jack A.] Harvard Med Sch, Program Bioinformat & Integrat Genom, Boston, MA 02115 USA.
   [Seaby, Eleanor G.] Univ Hosp Southampton, Genom Informat Grp, Southampton, Hants, England.
   [Mudge, Jonathan M.] European Bioinformat Inst, European Mol Biol Lab, Wellcome Genome Campus, Cambridge, England.
   [Karjalainen, Juha; Satterstrom, F. Kyle; Poterba, Timothy; Seed, Cotton] Broad Inst MIT & Harvard, Stanley Ctr Psychiat Res, Cambridge, MA 02142 USA.
   [O'Donnell-Luria, Anne H.] Boston Childrens Hosp, Div Genet & Genom, Boston, MA USA.
   [O'Donnell-Luria, Anne H.] Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA.
   [MacArthur, Daniel G.] Garvan Inst Med Res, Ctr Populat Genom, Syndney, Australia.
   [MacArthur, Daniel G.] UNSW Sydney, Sydney, NSW, Australia.
   [MacArthur, Daniel G.] Murdoch Childrens Res Inst, Ctr Populat Genom, Melbourne, Vic, Australia.
C3 Harvard University; Massachusetts Institute of Technology (MIT); Broad
   Institute; Harvard University; Harvard University Medical Affiliates;
   Massachusetts General Hospital; Harvard University; Harvard Medical
   School; Harvard University; Harvard Medical School; European Molecular
   Biology Laboratory (EMBL); European Bioinformatics Institute; Harvard
   University; Massachusetts Institute of Technology (MIT); Broad
   Institute; Harvard University; Harvard University Medical Affiliates;
   Boston Children's Hospital; Harvard University; Harvard Medical School;
   University of New South Wales Sydney; Murdoch Children's Research
   Institute
RP MacArthur, DG (corresponding author), Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA 02142 USA.; MacArthur, DG (corresponding author), Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.; MacArthur, DG (corresponding author), Garvan Inst Med Res, Ctr Populat Genom, Syndney, Australia.; MacArthur, DG (corresponding author), UNSW Sydney, Sydney, NSW, Australia.; MacArthur, DG (corresponding author), Murdoch Childrens Res Inst, Ctr Populat Genom, Melbourne, Vic, Australia.
EM d.macarthur@garvan.org.au
RI MacArthur, Daniel/E-3275-2010; Seaby, Eleanor/AAM-7744-2020; Daly,
   Mark/B-2453-2017; Glaser, Benjamin/F-8411-2017; Erdmann,
   Jeanette/P-7513-2014; Ma, Ronald/C-2788-2009; Bown, Matthew/P-1957-2016;
   Benjamin, Emelia/E-7103-2011; sokol, harry/E-2290-2019; Loos,
   Ruth/Q-2862-2016; Rioux, John D./A-9599-2015
OI Lehtimaki, Terho/0000-0002-2555-4427; Tai, E Shyong/0000-0003-2929-8966;
   Ware, James/0000-0002-6110-5880; Cibulskis,
   Kristian/0000-0003-1343-1582; Glaser, Benjamin/0000-0003-4711-5000;
   Erdmann, Jeanette/0000-0002-4486-6231; Beaugerie,
   Laurent/0000-0002-5012-4146; O'Donnell-Luria, Anne/0000-0001-6418-9592;
   ELOSUA, ROBERTO/0000-0001-8235-0095; Armean, Irina/0000-0002-1043-4756;
   Ma, Ronald/0000-0002-1227-803X; Seaby, Eleanor/0000-0002-6814-8648;
   Bown, Matthew/0000-0002-6180-3611; Tuomi,
   Tiinamaija/0000-0002-8306-6202; Farkkila, Martti/0000-0002-0250-8559;
   Benjamin, Emelia/0000-0003-4076-2336; McGovern,
   Dermot/0000-0001-5621-759X; Mudge, Jonathan/0000-0003-4789-7495;
   Melander, Olle/0000-0002-2581-484X; sokol, harry/0000-0002-2914-1822;
   Gauthier, Laura/0009-0003-6679-9433; Loos, Ruth/0000-0002-8532-5087;
   Kaprio, Jaakko/0000-0002-3716-2455; Rioux, John D./0000-0001-7560-8326;
   Palotie, Aarno/0000-0002-2527-5874; Satterstrom,
   Frederick/0000-0001-6187-7680; solinas, emilia/0000-0003-3532-1317;
   Solomonson, Matthew/0000-0002-5344-9026; MacArthur,
   Daniel/0000-0002-5771-2290
FU NIDDK [U54 DK105566]; NIGMS [F32 GM115208, R01 GM104371]; Broad
   Institute; NICHD [K12 HD052896]; National Human Genome Research
   Institute of the National Institutes of Health [U41HG007234]; MRC
   [MR/R006237/1, MC_UP_1102/20] Funding Source: UKRI
FX We thank all of the research participants for contributing their data.
   This work was supported by NIDDK U54 DK105566, NIGMS R01 GM104371, and
   the Broad Institute. KJK was supported by NIGMS F32 GM115208. A.O.L was
   supported by NICHD K12 HD052896. The GENCODE project is supported by the
   National Human Genome Research Institute of the National Institutes of
   Health under Award Number U41HG007234. The results published here are in
   part based on data: (1) generated by The Cancer Genome Atlas (TCGA)
   managed by the NCI and NHGRI (accession: phs000178.v10.p8); information
   about TCGA can be found at http://cancergenome.nih.gov; (2) generated by
   the Genotype-Tissue Expression Project (GTEx) managed by the NIH Common
   Fund and NHGRI (accession: phs000424.v7.p2); (3) generated by the Exome
   Sequencing Project, managed by NHLBI; and (4) generated by the
   Alzheimer's Disease Sequencing Project (ADSP), managed by the NIA and
   NHGRI (accession: phs000572. v7.p4). We thank E. Pierce-Hoffman for
   previous analysis and thoughts on characterizing loss-of-function
   variants in haploinsufficient genes. We thank the iPSYCH/SSI/Broad
   Institute psychiatric genetics study for the use of exome count data. We
   have complied with all relevant ethical regulations. This study was
   overseen by the Broad Institute's Office of Research Subject Protection
   and the Partners Human Research Committee, and was given a determination
   of Not Human Subjects Research. Informed consent was obtained from all
   participants. The content is solely the responsibility of the authors
   and does not necessarily represent the official views of the National
   Institutes of Health.
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NR 51
TC 115
Z9 128
U1 0
U2 21
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD MAY 28
PY 2020
VL 581
IS 7809
BP 452
EP +
DI 10.1038/s41586-020-2329-2
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA NX9ZL
UT WOS:000576060200005
PM 32461655
OA hybrid, Green Published, Green Submitted
DA 2025-04-10
ER

PT J
AU Brini, M
   Carafoli, E
AF Brini, Marisa
   Carafoli, Ernesto
TI Calcium Pumps in Health and Disease
SO PHYSIOLOGICAL REVIEWS
LA English
DT Review
ID PLASMA-MEMBRANE CA2+; HAILEY-HAILEY-DISEASE; SECRETORY PATHWAY
   CA2+/MN2+-ATPASE; TWITCH SKELETAL-MUSCLE; NITRIC-OXIDE SYNTHASE; CARDIAC
   SARCOPLASMIC-RETICULUM; P-TYPE ATPASE; NMR SOLUTION STRUCTURE;
   SQUAMOUS-CELL TUMORS; INTRACELLULAR CA2+
AB Brini M, Carafoli E. Calcium Pumps in Health and Disease. Physiol Rev 89: 1341-1378, 2009; doi:10.1152/physrev.00032.2008.-Ca2+-ATPases (pumps) are key actors in the regulation of Ca2+ in eukaryotic cells and are thus essential to the correct functioning of the cell machinery. They have high affinity for Ca2+ and can efficiently regulate it down to very low concentration levels. Two of the pumps have been known for decades (the SERCA and PMCA pumps); one (the SPCA pump) has only become known recently. Each pump is the product of a multigene family, the number of isoforms being further increased by alternative splicing of the primary transcripts. The three pumps share the basic features of the catalytic mechanism but differ in a number of properties related to tissue distribution, regulation, and role in the cellular homeostasis of Ca2+. The molecular understanding of the function of the pumps has received great impetus from the solution of the three-dimensional structure of one of them, the SERCA pump. These spectacular advances in the structure and molecular mechanism of the pumps have been accompanied by the emergence and rapid expansion of the topic of pump malfunction, which has paralleled the rapid expansion of knowledge in the topic of Ca2+-signaling dysfunction. Most of the pump defects described so far are genetic: when they are very severe, they produce gross and global disturbances of Ca2+ homeostasis that are incompatible with cell life. However, pump defects may also be of a type that produce subtler, often tissue-specific disturbances that affect individual components of the Ca2+-controlling and/or processing machinery. They do not bring cells to immediate death but seriously compromise their normal functioning.
C1 [Carafoli, Ernesto] Univ Padua, Dept Biochem, I-35131 Padua, Italy.
   Univ Padua, Dept Expt Vet Sci, I-35131 Padua, Italy.
   Venetian Inst Mol Med, Padua, Italy.
C3 University of Padua; University of Padua; Veneto Institute Molecular
   Medicine
RP Carafoli, E (corresponding author), Univ Padua, Dept Biochem, Viale G Colombo 3, I-35131 Padua, Italy.
EM ernesto.carafoli@unipd.it
RI Brini, Marisa/JCE-4293-2023; Carafoli, Ernesto/K-5192-2016
OI Carafoli, Ernesto/0000-0002-7826-0094; Brini, Marisa/0000-0001-5141-0243
FU Italian Ministry of University and Research [FIRB2001]; Telethon
   Foundation [GGP04169]; FP6 program of the European Union
   [LSH-2003-2.1.3-3]; Human Frontier Science Program Organization; Italian
   National Research Council
FX The original work by the authors has been supported over the years by
   grants from the Italian Ministry of University and Research (FIRB2001 to
   E. Carafoli; PRIN 2003 and 2005 to M. Brini), the Telethon Foundation
   (Project GGP04169 to M. Brini), the FP6 program of the European Union
   (FP6 Network of Excellence NeuroNe, LSH-2003-2.1.3-3 and Integrated
   Project Eurohear to E. Carafoli), the Human Frontier Science Program
   Organization (to E. Carafoli), and the Italian National Research Council
   (to M. Brini).
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NR 332
TC 481
Z9 548
U1 2
U2 69
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0031-9333
EI 1522-1210
J9 PHYSIOL REV
JI Physiol. Rev.
PD OCT
PY 2009
VL 89
IS 4
BP 1341
EP 1378
DI 10.1152/physrev.00032.2008
PG 38
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 500LX
UT WOS:000270304700007
PM 19789383
DA 2025-04-10
ER

PT J
AU Facchin, F
   Canaider, S
   Vitale, L
   Frabetti, F
   Griffoni, C
   Lenzi, L
   Casadei, R
   Strippoli, P
AF Facchin, Federica
   Canaider, Silvia
   Vitale, Lorenza
   Frabetti, Flavia
   Griffoni, Cristiana
   Lenzi, Luca
   Casadei, Raffaella
   Strippoli, Pierluigi
TI Identification and analysis of human RCAN3 (DSCR1L2) mRNA
   and protein isoforms
SO GENE
LA English
DT Article
DE alternative splicing; GST fusion protein assay; yeast cotransformation;
   quantitative relative RT-PCR; TNNI3
ID DEPENDENT TRANSCRIPTIONAL PATHWAY; SYNDROME CRITICAL REGION;
   DOWN-SYNDROME; TROPONIN-I; GENE FAMILY; CALCINEURIN; EXPRESSION;
   SKELETAL; GENOME; INHIBITOR
AB Human RCAN3 (Regulator of calcineurin 3; previously known as DSCR1L2, Down syndrome critical region gene 1-like 2) is a five-exon gene mapped on chromosome I and belongs to the human RCAN gene family which also includes RCAN1 and RCAN2. The novel denomination RCAN for genes and proteins, instead of DSCR1L (Down syndrome critical region gene I-like) has recently been widely discussed. The aim of the present work was to perform a multiple approach analysis of five RCAN3 mRNA and encoded protein isoforms, two of which have been identified for the first time in this research. The two new RCAN3 mRNA isoforms, RCAN3-2,4,5, which lacks exon 3, and RCAN3-2,3,5, which lacks exon 4, were identified during RCAN3 RT-PCR (reverse transcription-polymerase chain reaction) cloning, the product of which unexpectedly revealed the presence of five isoforms as opposed to the three previously known. In order to analyze the expression pattern of the five RCAN3 mRNA isoforms in seven different human tissues, a quantitative relative RT-PCR was performed: interestingly, all isoforms are present in all tissues investigated, with a statistically significant constant prevalence of RCAN3 isoform (the most complete, "reference" isoform). The RCAN3 locus expression level was comparable in all seven tissues analyzed, considering all isoforms, which indicates a ubiquitous expression of this human RCAN family member. To date two possible interactors have been described for this protein: human cardiac troponin 1 (TNNI3) and calcineurin. Here we report the interaction between the new RCAN3 variants and TNNI3, demonstrated by both yeast cotransformation and by the GST (glutathione-sepharose transferase) fusion protein assay, as was to be expected from the presence of exon 2 whose product has been seen to be sufficient for binding to TNNI3. (c) 2007 Elsevier B.V. All rights reserved.
C1 [Facchin, Federica; Canaider, Silvia; Vitale, Lorenza; Frabetti, Flavia; Lenzi, Luca; Casadei, Raffaella; Strippoli, Pierluigi] Univ Bologna, Dept Histol Embryol & Appl Biol, I-40126 Bologna, Italy.
   [Griffoni, Cristiana] Univ Bologna, Dept Expt Biol, I-40126 Bologna, Italy.
C3 University of Bologna; University of Bologna
RP Strippoli, P (corresponding author), Univ Bologna, Dept Histol Embryol & Appl Biol, Via Belmeloro 8, I-40126 Bologna, Italy.
EM pierluigi.strippoli@unibo.it
RI Griffoni, Cristiana/D-3031-2019; Casadei, Raffaella/K-1730-2015
OI Griffoni, Cristiana/0000-0001-8344-7534; STRIPPOLI,
   PIERLUIGI/0000-0001-8769-8832
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NR 37
TC 13
Z9 16
U1 0
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-1119
EI 1879-0038
J9 GENE
JI Gene
PD JAN 15
PY 2008
VL 407
IS 1-2
BP 159
EP 168
DI 10.1016/j.gene.2007.10.006
PG 10
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 259CW
UT WOS:000252917700016
PM 18022329
DA 2025-04-10
ER

PT J
AU Park, S
   DiMaio, TA
   Scheef, EA
   Sorenson, CM
   Sheibani, N
AF Park, SunYoung
   DiMaio, Terri A.
   Scheef, Elizabeth A.
   Sorenson, Christine M.
   Sheibani, Nader
TI PECAM-1 regulates proangiogenic properties of endothelial cells through
   modulation of cell-cell and cell-matrix interactions
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE angiogenesis; retinal endothelial cells; CD31; osteopontin;
   thrombospondins; tenascin-C; adherens junctions; endothelial nitric
   oxide synthase
ID NITRIC-OXIDE SYNTHASE; ADHESION MOLECULE-1 PECAM-1; EXPRESSION PATTERN;
   VE-CADHERIN; PECAM-1-DEFICIENT MICE; VASCULAR-PERMEABILITY; RETINAL
   VASCULATURE; HEMATOPOIETIC-CELLS; SHEAR-STRESS; ANGIOGENESIS
AB Park SY, DiMaio TA, Scheef EA, Sorenson CM, Sheibani N. PECAM-1 regulates proangiogenic properties of endothelial cells through modulation of cell-cell and cell-matrix interactions. Am J Physiol Cell Physiol 299: C1468-C1484, 2010. First published September 1, 2010; doi:10.1152/ajpcell.00246.2010.-Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is a member of the immunoglobulin superfamily of cell adhesion molecules with important roles in angiogenesis and inflammation. However, the molecular and cellular mechanisms, and the role that specific PECAM-1 isoforms play in these processes, remain elusive. We recently showed attenuation of retinal vascular development and neovascularization in PECAM-1-deficient (PECAM-1-/-) mice. To gain further insight into the role of PECAM-1 in these processes, we isolated primary retinal endothelial cells (EC) from wild-type (PECAM-1+/+) and PECAM-1-/- mice. Lack of PECAM-1 had a significant impact on endothelial cell-cell and cell-matrix interactions, resulting in attenuation of cell migration and capillary morphogenesis. Mechanistically these changes were associated with a significant decrease in expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability in PECAM-1-/- retinal EC. PECAM-1-/- retinal EC also exhibited a lower rate of apoptosis under basal and challenged conditions, consistent with their increased growth rate. Furthermore, reexpression of PECAM-1 was sufficient to restore migration and capillary morphogenesis of null cells in an isoform-specific manner. Thus PECAM-1 expression modulates proangiogenic properties of EC, and these activities are significantly influenced by alternative splicing of its cytoplasmic domain.
C1 [Park, SunYoung; DiMaio, Terri A.; Scheef, Elizabeth A.; Sheibani, Nader] Univ Wisconsin, Dept Ophthalmol & Visual Sci, Sch Med & Publ Hlth, Madison, WI 53792 USA.
   [Sorenson, Christine M.] Univ Wisconsin, Dept Pediat, Sch Med & Publ Hlth, Madison, WI 53792 USA.
   [Sheibani, Nader] Univ Wisconsin, Dept Pharmacol, Sch Med & Publ Hlth, Madison, WI 53792 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison
RP Sheibani, N (corresponding author), Univ Wisconsin, Dept Ophthalmol & Visual Sci, Sch Med & Publ Hlth, 600 Highland Ave,K6-485 CSC, Madison, WI 53792 USA.
EM nsheibanikar@wisc.edu
RI Sheibani, Nader/AAG-2379-2020
FU National Institutes of Health (NIH) [EY-16995, EY-18179]; University of
   Wisconsin Paul P. Carbone Cancer Center [P30-CA-014520]; Research to
   Prevent Blindness [P30-EY-16665]; American Diabetes Association
   [1-10-BS-160]; Retina Research Foundation; American Heart Association
   [0950057G]
FX This work was supported by National Institutes of Health (NIH) Grants
   EY-16995 and EY-18179 (Sheibani), P30-CA-014520 University of Wisconsin
   Paul P. Carbone Cancer Center support grant, and P30-EY-16665 and an
   unrestricted departmental award from Research to Prevent Blindness. N.
   Sheibani is a recipient of a Research Award from the American Diabetes
   Association (1-10-BS-160) and the Retina Research Foundation. C. M.
   Sorenson is a recipient of an American Heart Association research award
   (0950057G).
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NR 56
TC 70
Z9 89
U1 0
U2 10
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6143
EI 1522-1563
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD DEC
PY 2010
VL 299
IS 6
BP C1468
EP C1484
DI 10.1152/ajpcell.00246.2010
PG 17
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA 688BC
UT WOS:000284822100029
PM 20810911
OA Green Published
DA 2025-04-10
ER

PT J
AU Liu, L
   Markus, I
   Vandenberg, RJ
   Neilan, BA
   Murray, M
   Burcher, E
AF Liu, L
   Markus, I
   Vandenberg, RJ
   Neilan, BA
   Murray, M
   Burcher, E
TI Molecular identification and characterization of three isoforms of
   tachykinin NK1-like receptors in the cane toad Bufo
   marinus
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
   PHYSIOLOGY
LA English
DT Article
DE bufokinin; tachykinin receptors; sequencing and cloning; Xenopus oocyte
   expression; amphibian
ID SUBSTANCE-P RECEPTOR; HUMAN NEUROKININ-1 RECEPTOR; PROTEIN-COUPLED
   RECEPTOR; FUNCTIONAL EXPRESSION; HUMAN BRAIN; BINDING; PEPTIDE;
   LOCALIZATION; GENE; ORGANIZATION
AB The tachykinin peptide bufokinin, isolated from the cane toad intestine, is important in intestinal and cardiovascular regulation in the toad. In this study, three tachykinin NK1-like receptor isoforms, bNK(1)-A, bNK(1)-B, and bNK(1)-C, encoding proteins of 309, 390, and 371 amino acids, respectively, were cloned from the toad brain and intestine. These isoforms differ only at the intracellular COOH terminus. The bNK(1)-A and bNK(1)-B isoforms are similar to the truncated and full-length forms of the mammalian NK1 receptor, whereas bNK(1)-C is unique and does not correspond to any previously described receptor. RT-PCR studies demonstrated that three isoform transcripts are widely distributed in the toad with high expression in gut, spinal cord, brain, lung, and skeletal muscle. When expressed in COS-7 cells, bufokinin showed similar high affinity (IC50 0.6 - 0.8 nM) in competing for I-125-labeled Bolton-Hunter bufokinin binding at all receptors, but the binding affinities of substance P (SP) and neurokinin A (NKA) were very different at each isoform. When expressed in Xenopus oocytes, the truncated isoform, bNK(1)-A, was inactive, whereas bNK(1)-B and bNK(1)-C produced changes in chloride current when stimulated by tachykinins ( minimum concentrations: bufokinin, 0.1 nM; SP, 1 nM; and NKA, 10 nM). A marked desensitization of the response was seen to subsequent applications of tachykinins, as experienced by the mammalian NK1 receptor. In summary, our study describing three isoforms of NK1-like receptor from the toad suggests that the alternative splicing of NK1 receptor is a physiologically conserved mechanism and raises a fundamental question as to the physiological role of each isoform.
C1 Univ New S Wales, Sch Med Sci, Sydney, NSW 2052, Australia.
   Univ New S Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW 2052, Australia.
   Univ Sydney, Dept Pharmacol, Sydney, NSW 2006, Australia.
C3 University of New South Wales Sydney; University of New South Wales
   Sydney; University of Sydney
RP Univ New S Wales, Sch Med Sci, Sydney, NSW 2052, Australia.
EM lu.liu@unsw.edu.au
RI Neilan, Brett/AGW-6984-2022; lu, liu/AAJ-1122-2020; Vandenberg,
   Robert/E-6018-2016; Neilan, Brett/I-5767-2012
OI Liu, Lu/0000-0001-8338-1168; Vandenberg, Robert/0000-0003-1523-4814;
   Neilan, Brett/0000-0001-6113-772X
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NR 39
TC 11
Z9 13
U1 0
U2 3
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6119
EI 1522-1490
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD SEP
PY 2004
VL 287
IS 3
BP R575
EP R585
DI 10.1152/ajpregu.00051.2004
PG 11
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 845NI
UT WOS:000223251200013
PM 15155274
DA 2025-04-10
ER

PT J
AU Eckhardt, ERM
   Cai, L
   Sun, B
   Webb, NR
   van der Westhuyzen, DR
AF Eckhardt, ERM
   Cai, L
   Sun, B
   Webb, NR
   van der Westhuyzen, DR
TI High density lipoprotein uptake by scavenger receptor SR-BII
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID B TYPE-I; MICROVILLAR CHANNEL FORMATION; CHOLESTERYL ESTER UPTAKE;
   SELECTIVE LIPID UPTAKE; HDL PARTICLE UPTAKE; APOPROTEIN-A-I;
   CELL-SURFACE; APOLIPOPROTEIN-E; ADRENAL-CELLS; METABOLISM
AB Scavenger receptor class B, type I (SR-BI) mediates selective uptake of high density lipoprotein (HDL) lipids. It is unclear whether this process occurs at the cell membrane or via endocytosis. Our group previously identified an alternative mRNA splicing variant of SR-BI, named SR-BII, with an entirely different, yet highly conserved cytoplasmic C terminus. In this study we aimed to compare HDL uptake by both isoforms. Whereas SR-BI was mainly (similar to70%) localized on the surface of transfected Chinese hamster ovary cells, as determined by biotinylation, HDL binding at 4 degreesC, and studies of enhanced green fluorescent protein-tagged SR-BI/II fusion proteins, the majority of SR-BII ( similar to 80-90%) was expressed intracellularly. The cellular distribution of SR-BI was not affected by deletion of the C terminus, which suggests that the distinct C terminus of SR-BII is responsible for its intracellular expression. Pulse-chase experiments showed that SR-BII rapidly internalized HDL protein, whereas in the case of SR-BI most HDL protein remained surface bound. Like its ligand, SR-BII was more rapidly endocytosed compared with SR-BI. Despite more rapid HDL uptake by SR-BII than SR-BI, selective cholesteryl ether uptake was significantly lower. Relative to their levels of expression at the cell surface, however, both isoforms mediated selective uptake with similar efficiency. HDL protein that was internalized by SR-BII largely co-localized with transferrin in the endosomal recycling compartment. Within the endosomal recycling compartment of SR-BII cells, there was extensive co-localization of internalized HDL lipid and protein. These results do not support a model that selective lipid uptake by SR-BI requires receptor/ligand recycling within the cell. We conclude that SR-BII may influence cellular cholesterol trafficking and homeostasis in a manner that is distinct from SR-BI.
C1 Univ Kentucky, Med Ctr, Dept Internal Med, MN 520, Lexington, KY 40536 USA.
   Dept Vet Affairs Med Ctr, Lexington, KY 40536 USA.
C3 University of Kentucky; US Department of Veterans Affairs; Veterans
   Health Administration (VHA); Lexington VA Medical Center
RP Univ Kentucky, Med Ctr, Dept Internal Med, MN 520, 800 Rose St, Lexington, KY 40536 USA.
EM dvwest1@uky.edu
RI Sun, Bing/D-3758-2009; Webb, Nancy/AAL-7030-2021
OI Cai, Lei/0000-0001-8535-530X; Eckhardt, Erik/0000-0002-3015-5180
FU NHLBI NIH HHS [HL63763] Funding Source: Medline
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NR 44
TC 87
Z9 100
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI ROCKVILLE
PA 11200 ROCKVILLE PIKE, SUITE 302, ROCKVILLE, MD, UNITED STATES
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 2
PY 2004
VL 279
IS 14
BP 14372
EP 14381
DI 10.1074/jbc.M313793200
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 807CB
UT WOS:000220478500133
PM 14726519
DA 2025-04-10
ER

PT J
AU Briggs, MM
   Schachat, F
AF Briggs, MM
   Schachat, F
TI Early specialization of the superfast myosin in extraocular and
   laryngeal muscles
SO JOURNAL OF EXPERIMENTAL BIOLOGY
LA English
DT Article
DE extraocular; laryngeal; muscle; 5 ' untranslated region; exon; myosin
   heavy chain
ID HEAVY-CHAIN GENE; B/EPSILON-CRYSTALLIN GENE; JAW-CLOSING MUSCLES;
   AMINO-ACID-SEQUENCE; TROPONIN-T; XENOPUS-LAEVIS; MESSENGER-RNA; THIN
   FILAMENT; EXPRESSION; RAT
AB Extraocular muscle (EOM) exhibits high-velocity, low-tension contractions compared with other vertebrate striated muscles, These distinctive properties have been associated with a novel myosin heavy chain (My HC) isoform, MyHC-EO. An atypical MyHC, MyHC IIL, has also been identified in laryngeal muscles that have similarly fast contractile properties. It co-migrates with MyHC-EO on high-resolution SDS gels, but appeared to be encoded by a different mRNA, We combined CNBr peptide maps and full-length cDNA sequences to show that rabbit muscle EO and IIL MyHCs are identical, Analysis of the 5' untranslated region (5'UTR) of the mRNAs identified three variants that result from a combination of alternative splicing and multiple transcription initiation sites. This complex pattern of 5'UTRs has not been reported previously for MyHC genes. We identified the human homologue of the MyHC-EO gene in GenBank, and analyzed the 5' upstream region, which revealed a paucity of muscle-specific transcription factor binding sites compared with the other MyHC genes. These features are likely to be critical to the unique regulation and tissue-specific expression of the MyHC-EO/IIL gene.
   Phylogenetic analysis indicates that MyHC-EO/IIL diverged from an ancestral MyHC gene to generate the first specialized fast myosin, The catalytic S1 head domain is more closely related to the fast MyHCs, while the rod is more closely related to the slow/cardiac MyHCs. The exon boundaries of the MyHC-EO are identical to those of the embryonic MyTHC gene and virtually identical to those of the alpha and beta cardiac genes. This implies that most of the current exon boundaries were present in the ancestral gene, predating the duplications that generated the family of skeletal and cardiac myosin genes.
C1 Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA.
C3 Duke University
RP Duke Univ, Med Ctr, Dept Cell Biol, Box 3011, Durham, NC 27710 USA.
EM m.briggs@cellbio.duke.edu
FU NEI NIH HHS [EY11377] Funding Source: Medline
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NR 66
TC 43
Z9 45
U1 0
U2 7
PU COMPANY BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING, STATION RD, HISTON, CAMBRIDGE CB24 9LF, ENGLAND
SN 0022-0949
EI 1477-9145
J9 J EXP BIOL
JI J. Exp. Biol.
PD AUG
PY 2000
VL 203
IS 16
BP 2485
EP 2494
PG 10
WC Biology; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Zoology
GA 356YW
UT WOS:000089472600011
PM 10903163
DA 2025-04-10
ER

PT J
AU Hsu, SY
   Mukda, S
   Leu, S
AF Hsu, Shu-Yuan
   Mukda, Sujira
   Leu, Steve
TI Expression and Distribution Pattern of Pnn in Ischemic Cerebral Cortex
   and Cultured Neural Cells Exposed to Oxygen-Glucose Deprivation
SO BRAIN SCIENCES
LA English
DT Article
DE Pnn; Pinin; oxygen-glucose deprivation and reoxygenation; ischemic
   stroke
ID PININ; COMPLEX; CANCER; STROKE; ASAP
AB Pinin (Pnn), a multifunctional protein, participates in embryonic development as well as in cellular apoptosis, proliferation, and migration through regulating mRNA alternative splicing and gene transcription. Previous studies have shown that Pnn plays important roles in neural system development and the expression level of Pnn in astrocytes is altered by ischemic stress and associated with cellular apoptosis. In the present study, we further utilized primary cultured rat neurons and astrocytes with oxygen-glucose deprivation (OGD) and a mouse model with middle cerebral artery occlusion (MCAO)-induced ischemic stroke to examine the effect of ischemic stress on Pnn expression and distribution in different types of neural cells. Under normoxia, Pnn is mainly localized in the nuclear speckle of primary cultured neurons. The expression level of Pnn was increased after the OGD treatment and then decreased in the reoxygenation period. Moreover, the cytoplasmic expression of Pnn was observed in neurons with OGD and reoxygenation (OGD/R). Unlike that in neurons, the Pnn expression in astrocytes was decreased after OGD treatment and then gradually increased during the reoxygenation period. Of interest, the nuclear-cytoplasmic translocation of Pnn was not observed in astrocytes with OGD/R. In the MCAO mouse model, the neuronal expression of Pnn in the peri-ischemic region was reduced by three days post induction of ischemic stroke. However, the Pnn expression in astrocytes was not altered. Moreover, the nuclear speckle distribution of Pnn in neurons was also diminished following ischemic stroke. In conclusion, the Pnn expression and distribution after OGD and during reoxygenation showed distinct manners in neurons and astrocytes, implying that Pnn may play different roles in different types of neural cells in the stress response to ischemic injury.
C1 [Hsu, Shu-Yuan] Chang Gung Univ, Grad Inst Biomed Sci, Coll Med, Dept Anat, Taoyuan 33302, Taiwan.
   [Hsu, Shu-Yuan; Leu, Steve] Kaohsiung Chang Gung Mem Hosp, Inst Translat Res Biomed, Kaohsiung 83301, Taiwan.
   [Mukda, Sujira] Mahidol Univ, Inst Mol Biosci, Res Ctr Neurosci, Salaya 73170, Nakhon Pathom, Thailand.
   [Leu, Steve] Kaohsiung Med Univ, Coll Life Sci, Dept Biotechnol, Kaohsiung 807808, Taiwan.
C3 Chang Gung University; Chang Gung Memorial Hospital; Mahidol University;
   Kaohsiung Medical University
RP Leu, S (corresponding author), Kaohsiung Chang Gung Mem Hosp, Inst Translat Res Biomed, Kaohsiung 83301, Taiwan.; Leu, S (corresponding author), Kaohsiung Med Univ, Coll Life Sci, Dept Biotechnol, Kaohsiung 807808, Taiwan.
EM hsusy@mail.cgu.edu.tw; sujira.muk@mahidol.edu; leu@mail.cgu.edu.tw
RI Leu, Steve/D-6807-2011
OI Leu, Steve/0000-0002-1738-1028
FU International Brain Research Organization (IBRO) 2016 Research
   Fellowship
FX We thank Chang Gung Memorial Foundation Kaohsiung Chang Gung Memorial
   Hospital Tissue Bank Core Lab and Biobank (CLRPG810032) for excellent
   technical support. S.M. was supported by an International Brain Research
   Organization (IBRO) 2016 Research Fellowship during her tenure as a
   Visiting Faculty at the Institute for Translational Research in
   Biomedicine, Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
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NR 28
TC 4
Z9 4
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3425
J9 BRAIN SCI
JI Brain Sci.
PD OCT
PY 2020
VL 10
IS 10
AR 708
DI 10.3390/brainsci10100708
PG 10
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA OJ6TT
UT WOS:000584091800001
PM 33027948
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU McClarrinon, M
   Gilkey, L
   Watral, V
   Fox, B
   Bullock, C
   Fradkin, L
   Liggitt, D
   Roche, L
   Bussey, LB
   Fox, E
   Gorman, C
AF McClarrinon, M
   Gilkey, L
   Watral, V
   Fox, B
   Bullock, C
   Fradkin, L
   Liggitt, D
   Roche, L
   Bussey, LB
   Fox, E
   Gorman, C
TI In vivo studies of gene expression via transient transgenesis
   using lipid-DNA delivery
SO DNA AND CELL BIOLOGY
LA English
DT Article
ID PRE-MESSENGER-RNA; HUMAN CYTOMEGALO-VIRUS; IMMEDIATE EARLY GENE;
   EPSTEIN-BARR-VIRUS; MAMMALIAN-CELLS; IN-VIVO; FUNCTIONAL GENOMICS;
   SPLICE-SITE; BETA-GALACTOSIDASE; LIPOSOME COMPLEXES
AB As the sequencing of the human genome proceeds, the need for a new screen for in vivo function is becoming apparent. Many investigators are turning to various transgenic models as a means of studying function. However, these approaches are very time consuming, with a transgene-expressing mouse model often taking months to establish. We have developed an efficient system for delivering genes in vivo, which allows the gene product to be studied as early as 24 h after introduction into the mouse model. The delivery system employs a novel cationic lipid, 1-[2-(9-(Z) -octadecenoyloxy)ethyl]-2-(8-(Z)-heptadecenyl)-3-(hydroxyethyl)imidazolinium chloride (DOTIM), and a neutral lipid, cholesterol, complexed with an expression vector containing the reporter gene chloramphenicol acetyl transferase (CAT), After a single intravenous injection of these complexes, several tissues were seen to express the transgene, High, persistent expression in the vascular endothelial cells in the mouse lung was obtained. Delivery of DNA in vivo has been evaluated by quantitative polymerase chain reaction and protein expression by CAT activity assays, In vivo studies showed reproducible expression in more than 500 mice injected via the tail vein. An early peak of expression was followed by lower, but sustained, expression for > 50 days. Transgene expression of CAT could also be identified by immunohistochemistry staining in mouse lung and appeared to be located within the capillaries. The pattern of in vivo expression could be modulated and targeted to specific organs by altering the lipid-DNA formulation. New expression vectors with altered introns and polyadenylation sites further improved expression. The expression reported here may be sufficient in magnitude, duration, and flexibility to be an attractive alternative, in some cases, to establishing transgenic animals by stable gene transfer.
C1 Valentis Inc, Burlingame, CA 94010 USA.
   Oregon State Univ, DiaXot, Corvallis, OR 97331 USA.
   Univ Washington, Dept Comparat Anat, Seattle, WA 98195 USA.
C3 Oregon State University; University of Washington; University of
   Washington Seattle
RP Valentis Inc, 863A Mitten Rd, Burlingame, CA 94010 USA.
EM dliggitt@valentis.com
RI Torres-de la Roche, Luz Angela/L-4281-2013
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NR 54
TC 9
Z9 9
U1 0
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5498
EI 1557-7430
J9 DNA CELL BIOL
JI DNA Cell Biol.
PD JUL
PY 1999
VL 18
IS 7
BP 533
EP 547
DI 10.1089/104454999315088
PG 15
WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
GA 220UY
UT WOS:000081686900002
PM 10433552
DA 2025-04-10
ER

PT J
AU Lee, JD
   Hsiao, KM
   Chang, PJ
   Chen, CC
   Kuo, YW
   Huang, YC
   Hsu, HL
   Lin, YH
   Wu, CY
   Huang, YC
   Lee, M
   Hsu, CY
   Pan, YT
   Kuo, CY
   Lin, CH
AF Lee, Jiann-Der
   Hsiao, Kuang-Ming
   Chang, Pey-Jium
   Chen, Chih-Cheng
   Kuo, Ya-Wen
   Huang, Yen-Chu
   Hsu, Huan-Lin
   Lin, Ya-Hui
   Wu, Chih-Ying
   Huang, Ying-Chih
   Lee, Meng
   Hsu, Chia-Yu
   Pan, Yi-Ting
   Kuo, Chih-Yu
   Lin, Chun-Hsien
TI A common polymorphism decreases LRP1 mRNA stability and is
   associated with increased plasma factor VIII levels
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Article
DE Low density lipoprotein receptor-related; protein 1; Codon optimality;
   Genetic polymorphism; Factor VIII; Messenger RNA stability
ID RECEPTOR-RELATED PROTEIN; VON-WILLEBRAND-FACTOR; SMOOTH-MUSCLE CELLS;
   GENE-EXPRESSION; LDLR LOCUS; DISEASE; RISK; INHIBITION; SCAVENGER;
   FAMILY
AB The low -density lipoprotein receptor-related protein 1 (LRP1) gene is associated with increased levels of plasma factor VIII (FVIII). We aimed to explore eight functional genetic LRP1 variants for their potential roles in regulating FVIII levels and acute ischemic stroke (AIS). This genetic association study enrolled 192 patients with AIS and 134 controls. There were no significant differences in the genetic frequency of the eight functional single-nucleotide polymorphisms (SNPs) between the control and AIS groups. However, while analyzing the association between the eight SNPs and plasma FVIII levels, subjects with T/T genotype of rs1800137 (vs. CC + CT) were found to be associated with higher FVIII levels (23.5 IU/dL; 95% confidence interval, 7.4-39.5 IU/dL; P = 0.0044) after adjusting for age, gender, estimated glomerular filtration rate, 0 blood type, inflammatory state, and body mass index.
   An analysis of the mRNA stability and abundance was designed and performed using minigene system transfected into HepG2 cells to assess the possible differences in mRNA stabilities between rs1800137 CC (rs1800137C) and TT (rs1800137T) genotypes. Site-directed mutagenesis revealed that rs1800137T accounts for the observed decrease in mRNA stability. The SNP rs1800137, located in exon 8, has been identified as an exonsplicing enhancer in silico. However, alternative splicing of LRP1 without inclusion of exon 8 was not identified. In transfected HepG2 cells, cycloheximide slowed down the degradation of the rs1800137T-containing minigene. These results demonstrate that synonymous SNP rs1800137 can lead to increased plasma FVIII levels due to decreased mRNA stability via translation-dependent mRNA degradation associated with codon optimality.
C1 [Lee, Jiann-Der; Huang, Yen-Chu; Hsu, Huan-Lin; Lin, Ya-Hui; Wu, Chih-Ying; Huang, Ying-Chih; Lee, Meng; Hsu, Chia-Yu; Pan, Yi-Ting; Kuo, Chih-Yu; Lin, Chun-Hsien] Chang Gung Mem Hosp Chiayi, Dept Neurol, 6 W Sec,Jiapu Rd, Puzi 613, Chiayi, Taiwan.
   [Lee, Jiann-Der; Huang, Yen-Chu; Lee, Meng] Chang Gung Univ, Coll Med, Sch Tradit Chinese Med, Taoyuan, Taiwan.
   [Hsiao, Kuang-Ming] Natl Chung Cheng Univ, Dept Life Sci, Chiayi, Taiwan.
   [Chang, Pey-Jium] Chang Gung Univ, Grad Inst Clin Med Sci, Coll Med, Taoyuan, Taiwan.
   [Chen, Chih-Cheng] Chang Gung Univ, Coll Med, Chang Gung Mem Hosp Chiayi, Div Hematol & Oncol,Dept Med, Taoyuan, Taiwan.
   [Kuo, Ya-Wen] Chung Hwa Univ Med Technol, Dept Nursing, Coll Med & Life Sci, Tainan, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; National Chung
   Cheng University; Chang Gung University; Chang Gung University; Chang
   Gung Memorial Hospital; Chung Hua University
RP Lee, JD (corresponding author), Chang Gung Mem Hosp Chiayi, Dept Neurol, 6 W Sec,Jiapu Rd, Puzi 613, Chiayi, Taiwan.
EM jdlee540908@gmail.com
RI Huang, Yenchu/AAO-1140-2020; Hsu, Chia-Yu/ABB-5867-2021; Chen,
   Chien-Hung/AFU-7949-2022
OI Chang, Pey-Jium/0000-0002-6492-0346; Lee, Meng/0000-0002-7491-0571;
   Huang, Yenchu/0000-0001-7885-6376; Chen, Chih-Cheng/0000-0002-6794-7229;
   Lee, Jiann-Der/0000-0001-6310-0488
FU Chang Gung Medicine Research Project [CMRPG6E0321, 6C0363]
FX This work was supported by grants from the Chang Gung Medicine Research
   Project (CMRPG6E0321, 6C0363).
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NR 50
TC 6
Z9 6
U1 0
U2 4
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0925-4439
EI 1879-260X
J9 BBA-MOL BASIS DIS
JI Biochim. Biophys. Acta-Mol. Basis Dis.
PD JUN
PY 2017
VL 1863
IS 6
BP 1690
EP 1698
DI 10.1016/j.bbadis.2017.04.015
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA EZ4TE
UT WOS:000404704600050
PM 28431990
OA Bronze
DA 2025-04-10
ER

PT J
AU Wilson, PM
   LaBonte, MJ
   Lenz, HJ
AF Wilson, Peter M.
   LaBonte, Melissa J.
   Lenz, Heinz-Josef
TI Assessing the in vivo efficacy of biologic antiangiogenic therapies
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE Ziv-aflibercept (VEGF Trap); Bevacizumab; Angiogenesis;
   Antiangiogenesis; Biomarkers; Review; Vascular endothelial growth factor
   (VEGF)
ID ENDOTHELIAL GROWTH-FACTOR; METASTATIC COLORECTAL-CANCER; B VEGF-B;
   TUMOR-GROWTH; PATHOLOGICAL ANGIOGENESIS; SPLICE ISOFORMS; BEVACIZUMAB;
   BIOMARKERS; SURVIVAL; CELLS
AB To review key clinical issues underlying the assessment of in vivo efficacy when using antiangiogenic therapies for cancer treatment.
   Literature relevant to use of antiangiogenic therapies in cancer was reviewed, with particular emphasis on the assessment of in vivo efficacy of these agents, as well as additional angiogenic factors that could play a role in escape from angiogenesis inhibition.
   In order to grow and metastasize, tumors need to continually acquire new blood supplies; therefore, therapeutic inhibition of angiogenesis has become a component of anticancer treatment for many tumor types. Bevacizumab, a humanized monoclonal antibody directed at vascular endothelial growth factor A (VEGF-A), has shown activity in combination with chemotherapy in metastatic colorectal cancer. Nevertheless, the use of antiangiogenic therapies remains suboptimal; specifically, optimal dose, duration of therapy, and combination of agents remain unknown. Also, at present, it is not possible to determine which patients are most likely to respond to a given form of antiangiogenic therapy. There has been increased recognition of alternative pathways possibly associated with disease progression in patients undergoing antiangiogenic therapy targeted at VEGF-A. Multiligand-targeted antiangiogenic therapies, such as ziv-aflibercept (formerly known as aflibercept, VEGF Trap), are currently undergoing clinical evaluation. Ziv-aflibercept forms monomeric complexes with VEGF-A, VEGF-B, and PlGF, which have a long half-life, allowing optimization of ziv-aflibercept doses and angiogenic blockage.
   Although antiangiogenic therapies have increased treatment options for cancer patients, their use is limited by a lack of established and standardized methodology to evaluate their efficacy in vivo. Circulating endothelial cells, hypertension, and several molecular and imaging-based markers have potential for use as biomarkers in these patients and may better define appropriate patient populations.
C1 [Wilson, Peter M.; Lenz, Heinz-Josef] Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
   [LaBonte, Melissa J.] Azusa Pacific Univ, Sch Liberal Arts & Sci, Dept Biol & Chem, Azusa, CA USA.
C3 University of Southern California; Azusa Pacific University
RP Wilson, PM (corresponding author), Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, 1441 Eastlake Ave,RM5322, Los Angeles, CA 90033 USA.
EM pmwilson@usc.edu
OI LaBonte, Melissa/0000-0002-0354-413X
FU sanofi-aventis U.S. LLC; Regeneron Pharmaceuticals, Inc.
FX Medical editorial writing assistance was provided by Samantha Taylor,
   PhD, Phase Five Communications Inc. and funded by sanofi-aventis U.S.
   LLC and Regeneron Pharmaceuticals, Inc. The authors retained full
   editorial control over the content of the manuscript and received no
   compensation from any party for their work. Dr. Lenz has served as a
   consultant to Genentech and received clinical trial support from
   sanofi-aventis and Genentech.
CR Adams B, 2011, SANOFI AVENTIS LUNG
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NR 56
TC 18
Z9 19
U1 0
U2 20
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JAN
PY 2013
VL 71
IS 1
BP 1
EP 12
DI 10.1007/s00280-012-1978-8
PG 12
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 063MW
UT WOS:000313004900001
PM 23053262
DA 2025-04-10
ER

PT J
AU Kondo, S
   Scheef, EA
   Sheibani, N
   Sorenson, CM
AF Kondo, Shuji
   Scheef, Elizabeth A.
   Sheibani, Nader
   Sorenson, Christine M.
TI PECAM-1 isoform-specific regulation of kidney endothelial cell migration
   and capillary morphogenesis
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE CD31; alternative splicing; angiogenesis; integrins; extracellular
   matrix
ID ADHESION MOLECULE-1 PECAM-1; INTEGRIN-MEDIATED ADHESION; EXPRESSION
   PATTERN; RETINAL VASCULATURE; HEMATOPOIETIC-CELLS; CYTOPLASMIC DOMAIN;
   PLATELET; ANGIOGENESIS; THROMBOSPONDIN-1; ACTIVATION
AB Platelet endothelial cell adhesion molecule-1 (PECAM-1) has been implicated in angiogenesis through its involvement in endothelial cell-cell and cell-matrix interactions and signal transduction. Recent studies indicate that the cytoplasmic domain of PECAM-1 plays an important role in its cell adhesive and signaling properties. However, the role PECAM-1 isoforms play during angiogenic events such as cell adhesion and migration requires further delineation. To gain insight into the role PECAM-1 plays during vascular development and angiogenesis, we examined the expression pattern of PECAM-1 isoforms during kidney vascularization. We show that multiple isoforms of PECAM-1 are expressed during renal vascular development with different frequencies. The PECAM-1 that lacks exons 14 and 15 (Delta 14&15) was the predominant isoform detected in the renal vasculature. To further study PECAM-1 isoform-specific functions we isolated kidney endothelial cells (EC) from wild-type and PECAM-1-deficient (PECAM-1-/-) mice with B4-lectin-coated magnetic beads. PECAM-1-/- kidney EC showed reduced migration, inability to undergo capillary morphogenesis in Matrigel, dense peripheral focal adhesions, and peripheral cortical actin distribution compared with wild-type cells. PECAM-1-/- kidney EC secreted increased amounts of fibronectin and decreased amounts of tenascin-C and thrombospondin-1. Reexpression of Delta 14&15, but not full-length, PECAM-1 in PECAM-1-/- kidney EC restored cell migration and capillary morphogenesis defects. Thus PECAM-1 may regulate the adhesive and migratory properties of kidney EC in an isoform-specific fashion through modulation of integrin activity and extracellular matrix protein expression. Our results indicate that regulated expression of specific PECAM-1 isoforms may enable EC to accommodate the different stages of angiogenesis.
C1 Univ Wisconsin, Sch Med & Publ Hlth, Dept Pediat, Madison, WI 53792 USA.
   Univ Wisconsin, Sch Med & Publ Hlth, Dept Ophthalmol & Visual Sci, Madison, WI 53792 USA.
   Univ Wisconsin, Sch Med & Publ Hlth, Dept Pharmacol, Madison, WI 53792 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison
RP Sorenson, CM (corresponding author), Univ Wisconsin, Sch Med & Publ Hlth, Dept Pediat, 600 Highland Ave,H4-444 CSC, Madison, WI 53792 USA.
EM cmsorenson@wisc.edu
RI Sheibani, Nader/AAG-2379-2020
FU NEI NIH HHS [P30 EY016665] Funding Source: Medline; NIDDK NIH HHS
   [DK-67120] Funding Source: Medline
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NR 51
TC 47
Z9 55
U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6143
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD JUN
PY 2007
VL 292
IS 6
BP C2070
EP C2083
DI 10.1152/ajpcell.00489.2006
PG 14
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA 188RI
UT WOS:000247936600008
PM 17563397
DA 2025-04-10
ER

PT J
AU Niino, YS
   Kawashima, I
   Iguchi, Y
   Kanda, H
   Ogura, K
   Mita-Yoshida, K
   Ono, T
   Yamazaki, M
   Sakimura, K
   Yogosawa, S
   Yoshida, K
   Shioda, S
   Gotoh, T
AF Niino, Yuko S.
   Kawashima, Ikuo
   Iguchi, Yoshinobu
   Kanda, Hiroaki
   Ogura, Kiyoshi
   Mita-Yoshida, Kaoru
   Ono, Tomio
   Yamazaki, Maya
   Sakimura, Kenji
   Yogosawa, Satomi
   Yoshida, Kiyotsugu
   Shioda, Seiji
   Gotoh, Takaya
TI PKCδ deficiency inhibits fetal development and is associated with heart
   elastic fiber hyperplasia and lung inflammation in adult PKCδ knockout
   mice
SO PLOS ONE
LA English
DT Article
ID PROTEIN-KINASE-C; PROTEOLYTIC ACTIVATION; RETINOIC ACID; APOPTOSIS;
   ISOFORM; CELLS; IDENTIFICATION; SUPPRESSION; MECHANISMS; SURVIVAL
AB Protein kinase C-delta (PKC delta) has a caspase-3 recognition sequence in its structure, suggesting its involvement in apoptosis. In addition, PKC delta was recently reported to function as an anti-cancer factor. The generation of a PKC delta knockout mouse model indicated that PKC delta plays a role in B cell homeostasis. However, the Pkcrd gene, which is regulated through complex transcription, produces multiple proteins via alternative splicing. Since gene mutations can result in the loss of function of molecular species required for each tissue, in the present study, conditional PKC delta knockout mice lacking PKC delta I, II, IV, V, VI, and VII were generated to enable tissue-specific deletion of PKC delta using a suitable Cre mouse. We generated PKC delta-null mice that lacked whole-body expression of PKC delta. PKC delta+/- parental mice gave birth to only 3.4% PKC delta-/- offsprings that deviated significantly from the expected Mendelian ratio (chi 2(2) = 101.7, P < 0.001). Examination of mice on embryonic day 11.5 (E11.5) showed the proportion of PKC delta-/- mice implanted in the uterus in accordance with Mendelian rules; however, approximately 70% of the fetuses did not survive at E11.5. PKC delta-/- mice that survived until adulthood showed enlarged spleens, with some having cardiac and pulmonary abnormalities. Our findings suggest that the lack of PKC delta may have harmful effects on fetal development, and heart and lung functions after birth. Furthermore, our study provides a reference for future studies on PKC delta deficient mice that would elucidate the effects of the multiple protein variants in mice and decipher the roles of PKC delta in various diseases.
C1 [Niino, Yuko S.; Shioda, Seiji] Showa Univ Med, Dept Anat, Shinagawa Ku, Tokyo, Japan.
   [Kawashima, Ikuo; Ogura, Kiyoshi] Tokyo Metropolitan Inst Med Sci, Lab Biomembrane, Setagaya Ku, Tokyo, Japan.
   [Iguchi, Yoshinobu] Tokyo Metropolitan Inst Med Sci, Technol Res Div, Setagaya Ku, Tokyo, Japan.
   [Kanda, Hiroaki] Saitama Canc Ctr, Dept Pathol, Saitama, Saitama, Japan.
   [Mita-Yoshida, Kaoru; Ono, Tomio] Tokyo Metropolitan Inst Med Sci, Lab Transgen Technol, Setagaya Ku, Tokyo, Japan.
   [Yamazaki, Maya; Sakimura, Kenji] Niigata Univ, Brain Res Inst, Dept Cellular Neurobiol, Niigata, Japan.
   [Yogosawa, Satomi; Yoshida, Kiyotsugu] Jikei Univ, Sch Med, Dept Biochem, Minato Ku, Tokyo, Japan.
   [Niino, Yuko S.; Gotoh, Takaya] Daito Bunka Univ, Dept Hlth Sci, Fac Sports & Hlth Sci, Higashimatsuyama, Saitama, Japan.
   [Yamazaki, Maya] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
   [Sakimura, Kenji] Niigata Univ, Brain Res Inst, Dept Anim Model Dev, Niigata, Japan.
   [Shioda, Seiji] Shonan Univ Med Sci, Dept Clin Pharm, Totsuka Ku, Yokohama, Kanagawa, Japan.
C3 Tokyo Metropolitan Institute of Medical Science; Tokyo Metropolitan
   Institute of Medical Science; Tokyo Metropolitan Institute of Medical
   Science; Niigata University; Jikei University; University of California
   System; University of California San Francisco; Niigata University
RP Gotoh, T (corresponding author), Daito Bunka Univ, Dept Hlth Sci, Fac Sports & Hlth Sci, Higashimatsuyama, Saitama, Japan.
EM gotoh_tky@ic.daito.ac.jp
RI Yoshida, Kiyotsugu/A-1646-2014
FU JSPS KAKENHI [JP 16H06276, 21590204, 15K10689]; Grants-in-Aid for
   Scientific Research [21590204, 15K10689] Funding Source: KAKEN
FX This work was supported by the JSPS KAKENHI Grant-in-Aid for Scientific
   Research (C) grant numbers 21590204:YSN and 15K10689: YSN, and JSPS
   KAKENHI Grant Number JP 16H06276 (AdAMS):HK. The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript. We thank the Media Technology Laboratory
   of Tokyo Metropolitan Institute of Medical Science for photographs and
   figures of mice and their tissues. We would like to thank Dr. T.
   Nakamachi and Dr. J. Watanabe for their cooperation in producing and
   maintaining PKC delta KO mice.
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NR 51
TC 5
Z9 5
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PY 2021
VL 16
IS 7
AR e0253912
DI 10.1371/journal.pone.0253912
PG 18
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA TC7AG
UT WOS:000668791400093
PM 34197550
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Wang, DR
   Zhang, H
   Li, M
   Frid, MG
   Flockton, AR
   McKeon, BA
   Yeager, ME
   Fini, MA
   Morrell, NW
   Pullamsetti, SS
   Velegala, S
   Seeger, W
   McKinsey, TA
   Sucharov, CC
   Stenmark, KR
AF Wang, Daren
   Zhang, Hui
   Li, Min
   Frid, Maria G.
   Flockton, Amanda R.
   McKeon, B. Alexandre
   Yeager, Michael E.
   Fini, Mehdi A.
   Morrell, Nicholas W.
   Pullamsetti, Soni S.
   Velegala, Sivareddy
   Seeger, Werner
   McKinsey, Timothy A.
   Sucharov, Carmen C.
   Stenmark, Kurt R.
TI MicroRNA-124 Controls the Proliferative, Migratory, and Inflammatory
   Phenotype of Pulmonary Vascular Fibroblasts
SO CIRCULATION RESEARCH
LA English
DT Article
DE anoxia; hypertension; pulmonary; migration; neoplasms; proliferation
ID TRACT-BINDING-PROTEIN; HISTONE DEACETYLASES; CHRONIC HYPOXIA;
   CELL-PROLIFERATION; DOWN-REGULATION; KEY REGULATOR; MESSENGER-RNA;
   PROMOTES; CANCER; GROWTH
AB Rationale: Pulmonary hypertensive remodeling is characterized by excessive proliferation, migration, and proinflammatory activation of adventitial fibroblasts. In culture, fibroblasts maintain a similar activated phenotype. The mechanisms responsible for generation/maintenance of this phenotype remain unknown.
   Objective: We hypothesized that aberrant expression of microRNA-124 (miR-124) regulates this activated fibroblast phenotype and sought to determine the signaling pathways through which miR-124 exerts effects.
   Methods and Results: We detected significant decreases in miR-124 expression in fibroblasts isolated from calves and humans with severe pulmonary hypertension. Overexpression of miR-124 by mimic transfection significantly attenuated proliferation, migration, and monocyte chemotactic protein-1 expression of hypertensive fibroblasts, whereas anti-miR-124 treatment of control fibroblasts resulted in their increased proliferation, migration, and monocyte chemotactic protein-1 expression. Furthermore, the alternative splicing factor, polypyrimidine tract-binding protein 1, was shown to be a direct target of miR-124 and to be upregulated both in vivo and in vitro in bovine and human pulmonary hypertensive fibroblasts. The effects of miR-124 on fibroblast proliferation were mediated via direct binding to the 3 untranslated region of polypyrimidine tract-binding protein 1 and subsequent regulation of Notch1/phosphatase and tensin homolog/FOXO3/p21Cip1 and p27Kip1 signaling. We showed that miR-124 directly regulates monocyte chemotactic protein-1 expression in pulmonary hypertension/idiopathic pulmonary arterial hypertension fibroblasts. Furthermore, we demonstrated that miR-124 expression is suppressed by histone deacetylases and that treatment of hypertensive fibroblasts with histone deacetylase inhibitors increased miR-124 expression and decreased proliferation and monocyte chemotactic protein-1 production.
   Conclusions: Stable decreases in miR-124 expression contribute to an epigenetically reprogrammed, highly proliferative, migratory, and inflammatory phenotype of hypertensive pulmonary adventitial fibroblasts. Thus, therapies directed at restoring miR-124 function, including histone deacetylase inhibitors, should be investigated.
C1 [Wang, Daren; Zhang, Hui; Li, Min; Frid, Maria G.; Flockton, Amanda R.; McKeon, B. Alexandre; Yeager, Michael E.; Fini, Mehdi A.] Univ Colorado, Dept Pediat, Aurora, CO 80045 USA.
   [McKinsey, Timothy A.; Sucharov, Carmen C.] Univ Colorado, Dept Med, Aurora, CO 80045 USA.
   [Stenmark, Kurt R.] Univ Colorado, Dept Med & Pediat, Aurora, CO 80045 USA.
   [Morrell, Nicholas W.] Univ Colorado, Dept Med, Aurora, CO 80045 USA.
   [Pullamsetti, Soni S.; Velegala, Sivareddy; Seeger, Werner] Univ Colorado, Dept Lung Dev & Remodeling, Aurora, CO 80045 USA.
   [Zhang, Hui] Univ Colorado, Dept Med, Aurora, CO 80045 USA.
   [Morrell, Nicholas W.] Univ Cambridge, Cambridge, England.
   [Morrell, Nicholas W.] Addenbrookes Hosp, Cambridge, England.
   [Morrell, Nicholas W.] Papworth Hosp, Cambridge CB3 8RE, England.
   Max Planck Inst Heart & Lung Res, Bad Nauheim, Germany.
   [Pullamsetti, Soni S.; Velegala, Sivareddy; Seeger, Werner] Univ Giessen, Bad Nauheim, Germany.
   [Pullamsetti, Soni S.; Velegala, Sivareddy; Seeger, Werner] Marburg Lung Ctr, Bad Nauheim, Germany.
   [Zhang, Hui] China Med Univ, Shengjing Hosp, Shenyang, Peoples R China.
C3 University of Colorado System; University of Colorado Anschutz Medical
   Campus; University of Colorado System; University of Colorado Anschutz
   Medical Campus; University of Colorado System; University of Colorado
   Anschutz Medical Campus; University of Colorado System; University of
   Colorado Anschutz Medical Campus; University of Colorado System;
   University of Colorado Anschutz Medical Campus; University of Colorado
   System; University of Colorado Anschutz Medical Campus; University of
   Cambridge; University of Cambridge; Cambridge University Hospitals NHS
   Foundation Trust; Addenbrooke's Hospital; Papworth Hospital; Max Planck
   Society; Justus Liebig University Giessen; China Medical University
RP Stenmark, KR (corresponding author), Univ Colorado, 12700 E 19th Ave,Room 6124, Aurora, CO 80045 USA.
EM Kurt.Stenmark@ucdenver.edu
RI stenmark, kurt/AFI-6776-2022
OI Seeger, Werner/0000-0003-1946-0894; Morrell,
   Nicholas/0000-0001-5700-9792; Pullamsetti, Soni
   Savai/0000-0003-0440-8831
FU National Institutes of Health Axis grant [1R01 HL114887-01, 5P01
   HL014985-39, 2 T32 HL07171-36]
FX This work was supported, in part, by National Institutes of Health Axis
   grant 1R01 HL114887-01, Program Project grant 5P01 HL014985-39, and
   Training grant 2 T32 HL07171-36.
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NR 80
TC 167
Z9 184
U1 0
U2 29
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0009-7330
EI 1524-4571
J9 CIRC RES
JI Circ.Res.
PD JAN 3
PY 2014
VL 114
IS 1
BP 67
EP 78
DI 10.1161/CIRCRESAHA.114.301633
PG 12
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
   Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Hematology
GA AG7GQ
UT WOS:000335586700013
PM 24122720
OA Green Accepted, Bronze
DA 2025-04-10
ER

PT J
AU Nuutinen, T
   Suuronen, T
   Kauppinen, A
   Salminen, A
AF Nuutinen, Tapio
   Suuronen, Tiina
   Kauppinen, Anu
   Salminen, Antero
TI Clusterin: A forgotten player in Alzheimer's disease
SO BRAIN RESEARCH REVIEWS
LA English
DT Review
DE Alzheimer; ApoJ; Clusterin; Complement; Dementia; Inflammation; Cerebral
   amyloid angiopathy
ID APOLIPOPROTEIN-J CLUSTERIN; BLOOD-BRAIN-BARRIER; CEREBRAL AMYLOID
   ANGIOPATHY; EXTRACELLULAR CHAPERONE CLUSTERIN; HEAT-SHOCK PROTEINS;
   SMOOTH-MUSCLE-CELLS; HISTONE DEACETYLASE INHIBITORS;
   HIGH-DENSITY-LIPOPROTEIN; CENTRAL-NERVOUS-SYSTEM; GROWTH-FACTOR-BETA
AB Clusterin, also known as apolipoprotein J, is a versatile chaperone molecule which contains several amphipathic and coiled-coil alpha-helices, typical characteristics of small heat shock proteins. in addition, clusterin has three large intrinsic disordered regions, so-called molten globule domains, which can stabilize stressed protein structures. Twenty years ago, it was demonstrated that the expression of clusterin was clearly increased in Alzheimer's disease (AD). Later it was observed that clusterin can bind amyloid-beta peptides and prevent their fibrillization. Clusterin is also involved in the clearance of amyloid-beta peptides and fibrils by binding to megalin receptors and enhancing their endocytosis within glial cells. Clusterin is a complement inhibitor and can suppress complement activation observed in AD. Clusterin is also present in lipoprotein particles and regulates cholesterol and lipid metabolism of brain which is disturbed in AD. Clusterin is a stress-induced chaperone which is normally secreted but in conditions of cellular stress, it can be transported to cytoplasm where it can bind to Bax protein and inhibit neuronal apoptosis. Clusterin can also bind to Smad2/3 proteins and potentiate the neuroprotective TGF beta signaling. An alternative splicing can produce a variant isoform of clusterin which can be translocated to nuclei where it induces apoptosis. The role of nuclear clusterin in AD needs to be elucidated. We will review here the extensive literature linking clusterin to AD and examine the recent progress in clusterin research with the respect to AD pathology. Though clusterin can be viewed as a multipotent guardian of brain, it is unable to prevent the progressive neuropathology in chronic AD. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Nuutinen, Tapio; Suuronen, Tiina; Kauppinen, Anu; Salminen, Antero] Univ Kuopio, Dept Neurosci & Neurol, FIN-70211 Kuopio, Finland.
   [Salminen, Antero] Kuopio Univ Hosp, Dept Neurol, FIN-70211 Kuopio, Finland.
C3 University of Eastern Finland; Kuopio University Hospital
RP Salminen, A (corresponding author), Univ Kuopio, Dept Neurosci & Neurol, POB 1627, FIN-70211 Kuopio, Finland.
EM antero.salminen@uku.fi
FU Academy of Finland; Finnish Eye Foundation; University of Kuopio,
   Finland
FX This study was financially supported by grants from the Academy of
   Finland, The Finnish Eye Foundation and the University of Kuopio,
   Finland. The authors thank Dr. Ewen MacDonald for checking the language
   of the manuscript.
CR [Anonymous], BJR S, DOI DOI 10.1259/BJR/18105113]
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PY 2009
VL 61
IS 2
BP 89
EP 104
DI 10.1016/j.brainresrev.2009.05.007
PG 16
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 511MI
UT WOS:000271169000005
PM 19651157
DA 2025-04-10
ER

PT J
AU Ziche, M
   Maglione, D
   Ribatti, D
   Morbidelli, L
   Lago, CT
   Battisti, M
   Paoletti, I
   Barra, A
   Tucci, M
   Parise, G
   Vincenti, V
   Granger, HJ
   Viglietto, G
   Persico, MG
AF Ziche, M
   Maglione, D
   Ribatti, D
   Morbidelli, L
   Lago, CT
   Battisti, M
   Paoletti, I
   Barra, A
   Tucci, M
   Parise, G
   Vincenti, V
   Granger, HJ
   Viglietto, G
   Persico, MG
TI Placenta growth factor-1 is chemotactic, mitogenic, and angiogenic
SO LABORATORY INVESTIGATION
LA English
DT Article
ID VASCULAR-PERMEABILITY FACTOR; ENDOTHELIAL-CELL MITOGEN; TYROSINE KINASE;
   CHORIOALLANTOIC MEMBRANE; MESSENGER-RNAS; CHICK-EMBRYO; FACTOR PIGF;
   IN-VITRO; RECEPTOR; HEPARIN
AB The placental-derived growth factor (PIGF) is a dimeric glycoprotein showing a high degree of sequence similarity to the vascular endothelial growth factor. Alternative splicing of the PIGF primary transcript gives rise to two forms, named PIGF-1 and PIGF-2, which differ only in the insertion of a highly basic 21-amino acid stretch at the carboxyl end. The presence of the PIGF mRNA in thyroid, placenta, lung, and goiter has indicated the tissues where this factor functions. However, the role of PIGF in vascular development has not yet been clearly established. In the present study, we described the purification of PIGF-1 from overexpressing eukaryotic cells and then measured the angiogenic activity of the purified PIGF-1 in vivo in the rabbit cornea and the chick chorioallantoic membrane assays. In both in vivo assays, PIGF-1 induced a strong neovascularization process that was blocked by affinity-purified anti-PIGF-1 antibody. In the avascular cornea, PIGF-1 induced angiogenesis in a dose-dependent manner and seemed to be at least as effective (if not more effective) than vascular endothelial growth factor and basic fibroblast growth factor under the same conditions and at the same concentration. PIGF-1 was shown to induce cell growth and migration of endothelial cells from bovine coronary postcapillary venules and from human umbilical veins. In these two in vitro assays, PIGF-1 seemed to have a comparable effect to that of vascular endothelial growth factor and basic fibroblast growth factor on the cultured microvascular endothelium leg, capillary venule endothelial cells). In summary, this is the first study to demonstrate that PIGF-1 can induce angiogenesis in vivo and stimulate the migration and proliferation of endothelial cells in vitro.
C1 CNR,INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY.
   UNIV FLORENCE,DEPT PHARMACOL,FLORENCE,ITALY.
   GEYMONAT SPA,ANAGNI,ITALY.
   UNIV BARI,INST HUMAN ANAT HISTOL & GEN EMBRYOL,BARI,ITALY.
   FDN G PASCALE,IST NAZL TUMORI NAPOLI,NAPLES,ITALY.
   TEXAS A&M UNIV,HLTH SCI CTR,MICROCIRCULAT RES INST,COLLEGE STN,TX.
   TEXAS A&M UNIV,HLTH SCI CTR,DEPT MED PHYSIOL,COLLEGE STN,TX.
C3 Consiglio Nazionale delle Ricerche (CNR); Istituto di Genetica e
   Biofisica "Adriano Buzzati-Traverso" (IGB-CNR); University of Florence;
   Universita degli Studi di Bari Aldo Moro; IRCCS Fondazione Pascale;
   Texas A&M University System; Texas A&M University College Station; Texas
   A&M Health Science Center; Texas A&M University System; Texas A&M
   University College Station; Texas A&M Health Science Center
RI Morbidelli, Lucia/AAC-7858-2020; Viglietto, Giuseppe/AAC-2852-2019
FU NHLBI NIH HHS [HL-21498] Funding Source: Medline
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NR 44
TC 235
Z9 274
U1 0
U2 8
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD APR
PY 1997
VL 76
IS 4
BP 517
EP 531
PG 15
WC Medicine, Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pathology
GA WU670
UT WOS:A1997WU67000008
PM 9111514
DA 2025-04-10
ER

PT J
AU Turner, AJ
   Murphy, LJ
AF Turner, AJ
   Murphy, LJ
TI Molecular pharmacology of endothelin converting enzymes
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Review
DE endothelin; endothelin converting enzyme; metallopeptidase;
   endopeptidase-24.11; phosphoramidon; thiorphan; endothelium
ID NEUTRAL ENDOPEPTIDASE 24.11; KIDNEY MICROVILLAR MEMBRANE; PORCINE BIG
   ENDOTHELIN-1; LEUKEMIA ANTIGEN CALLA; RAT LUNG; CATHEPSIN-D;
   METALLOPROTEINASE INHIBITOR; SYNAPTIC-MEMBRANES; RENAL DIPEPTIDASE;
   TRANSITION-STATE
AB A critical processing step in endothelin biosynthesis is the conversion of the intermediate ''big endothelin'' to its biologically active product catalysed by endothelin converting enzyme (ECE). In this commentary we discuss critically the cellular location, structure, and activity of the isoforms of ECE. The current evidence supporting a metallopeptidase ECE as the physiological regulator of endothelin production is described. Its sensitivity to inhibition by the fungal metabolite phosphoramidon and subsequent cloning of the enzyme indicate it to be a type II integral membrane protein homologous with neutral endopeptidase-24.11 (E-24.11), the major neuropeptide-degrading ectoenzyme in brain and other tissues. Unlike E-24.11, however, ECE exists as a disulphide-linked dimer of subunit M(r), 120-130 kDa and is not inhibited by other E-24.11 inhibitors such as thiorphan. Alternative splicing produces two forms of ECE with distinct N-terminal tails. These isoforms of ECE-1 show similar specificity converting big endothelin-l (ET-1) to ET-1 but big ET-2 and big ET-3 are converted much less efficiently. This suggests that additional forms of ECE remain to be isolated. Immunocytochemical studies indicate a predominant cell surface location for ECE-1, like E-24.11. This is consistent with the conversion of exogenous big ET-1 when administered in vivo and the inhibition of this event by phosphoramidon. However, mature ET-1 can be detected in intracellular vesicles in endothelial cells, suggesting that some processing occurs in the constitutive secretory pathway. This may be mediated by ECE-2, a recently cloned member of the E-24.11/ECE family which has an acidic pH optimum. Selective inhibitors of ECE may have therapeutic applications in cardiovascular and renal medicine.
RP Turner, AJ (corresponding author), UNIV LEEDS,DEPT BIOCHEM & MOLEC BIOL,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND.
FU Wellcome Trust Funding Source: Medline
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NR 127
TC 218
Z9 236
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0006-2952
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD JAN 26
PY 1996
VL 51
IS 2
BP 91
EP 102
DI 10.1016/0006-2952(95)02036-5
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TL773
UT WOS:A1996TL77300001
PM 8615890
DA 2025-04-10
ER

PT J
AU Llamusi, B
   Bargiela, A
   Fernandez-Costa, JM
   Garcia-Lopez, A
   Klima, R
   Feiguin, F
   Artero, R
AF Llamusi, Beatriz
   Bargiela, Ariadna
   Fernandez-Costa, Juan M.
   Garcia-Lopez, Amparo
   Klima, Raffaella
   Feiguin, Fabian
   Artero, Ruben
TI Muscleblind, BSF and TBPH are mislocalized in the muscle sarcomere of a
   Drosophila myotonic dystrophy model
SO DISEASE MODELS & MECHANISMS
LA English
DT Article
ID FRONTOTEMPORAL LOBAR DEGENERATION; EXPANDED CUG REPEAT; DILATED
   CARDIOMYOPATHY; TDP-43 PROTEINOPATHY; SPATIAL-PATTERNS; STRESS GRANULES;
   GENE-EXPRESSION; RNA TOXICITY; IN-VIVO; Z-DISC
AB Myotonic dystrophy type 1 (DM1) is a genetic disease caused by the pathological expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene. In the DMPK transcripts, the CUG expansions sequester RNA-binding proteins into nuclear foci, including transcription factors and alternative splicing regulators such as MBNL1. MBNL1 sequestration has been associated with key features of DM1. However, the basis behind a number of molecular and histological alterations in DM1 remain unclear. To help identify new pathogenic components of the disease, we carried out a genetic screen using a Drosophila model of DM1 that expresses 480 interrupted CTG repeats, i(CTG)480, and a collection of 1215 transgenic RNA interference (RNAi) fly lines. Of the 34 modifiers identified, two RNA-binding proteins, TBPH (homolog of human TAR DNA-binding protein 43 or TDP-43) and BSF (Bicoid stability factor; homolog of human LRPPRC), were of particular interest. These factors modified i(CTG) 480 phenotypes in the fly eye and wing, and TBPH silencing also suppressed CTG-induced defects in the flight muscles. In Drosophila flight muscle, TBPH, BSF and the fly ortholog of MBNL1, Muscleblind (Mbl), were detected in sarcomeric bands. Expression of i(CTG) 480 resulted in changes in the sarcomeric patterns of these proteins, which could be restored by coexpression with human MBNL1. Epistasis studies showed that Mbl silencing was sufficient to induce a subcellular redistribution of TBPH and BSF proteins in the muscle, which mimicked the effect of i(CTG) 480 expression. These results provide the first description of TBPH and BSF as targets of Mbl-mediated CTG toxicity, and they suggest an important role of these proteins in DM1 muscle pathology.
C1 [Llamusi, Beatriz; Bargiela, Ariadna; Fernandez-Costa, Juan M.; Garcia-Lopez, Amparo; Artero, Ruben] Univ Valencia, Dept Genet, Translat Genom Grp, Valencia 46100, Spain.
   [Klima, Raffaella; Feiguin, Fabian] ICGEB, I-34149 Trieste, Italy.
C3 University of Valencia; International Center for Genetic Engineering &
   Biotechnology (ICGEB)
RP Artero, R (corresponding author), Univ Valencia, Dept Genet, Translat Genom Grp, Doctor Moliner 50, Valencia 46100, Spain.
EM ruben.artero@uv.es
RI Bargiela, Ariadna/ABF-9125-2020; Fernandez-Costa, Juan/Q-1670-2015;
   Feiguin, Fabian/ABC-2514-2020; Artero, Ruben/K-6815-2014; llamusi,
   Beatriz/M-4449-2015
OI Fernandez-Costa, Juan M./0000-0002-1854-6082; Artero,
   Ruben/0000-0003-1596-047X; Bargiela, Ariadna/0000-0003-4336-2522;
   llamusi, Beatriz/0000-0002-2694-1293
FU Genoma Espana Foundation, Generalitat Valenciana [Prometeo/2010/081];
   Ministerio de Ciencia e Innovacion [BFU2009-10940]; Generalitat
   Valenciana [Prometeo/2010/081]; Fundacion Ramon Areces and Caja Navarra;
   Ministerio de Educacion y Ciencia
FX This work was supported by research grants from Genoma Espana
   Foundation, Generalitat Valenciana (Prometeo/2010/081) and Ministerio de
   Ciencia e Innovacion (BFU2009-10940) to R.A.A.B. was supported by
   Generalitat Valenciana (Prometeo/2010/081). J.M.F.C. was supported by a
   predoctoral fellowship from Generalitat Valenciana and grants from
   Fundacion Ramon Areces and Caja Navarra. A.G.L. was supported by a FPU
   fellowship from Ministerio de Educacion y Ciencia.
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NR 64
TC 37
Z9 42
U1 0
U2 10
PU COMPANY BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING, STATION RD, HISTON, CAMBRIDGE CB24 9LF, ENGLAND
SN 1754-8403
EI 1754-8411
J9 DIS MODEL MECH
JI Dis. Model. Mech.
PD JAN
PY 2013
VL 6
IS 1
BP 184
EP 196
DI 10.1242/dmm.009563
PG 13
WC Cell Biology; Medicine, Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine; Pathology
GA 088VQ
UT WOS:000314865700019
PM 23118342
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Harris, PC
   Rossetti, S
AF Harris, PC
   Rossetti, S
TI Molecular genetics of autosomal recessive polycystic kidney disease
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Review
DE autosomal recessive polycystic kidney disease; ARPKD; congenital hepatic
   fibrosis; Caroli's disease; PKHDI; fibrocystin; mutation analysis;
   genotype/phenotype correlations; cilia; DHPLC
ID CONGENITAL HEPATIC-FIBROSIS; RIGHT AXIS DETERMINATION; PKHD1 CANDIDATE
   GENE; CLINICAL-EXPERIENCE; PRENATAL-DIAGNOSIS; PRIMARY CILIUM; PHYSICAL
   MAP; PROTEIN; ARPKD; MUTATIONS
AB Autosomal recessive polycystic kidney disease (ARPKD) is a severe form of inherited childhood nephropathy (similar to1:20,000 live births) characterized by fusiform dilatation of collecting ducts and congenital hepatic fibrosis. Up to 30% die as neonates due to respiratory insufficiency and the majority of surviving infants develop hypertension. Progression to end stage renal disease occurs in 20-45% of cases within 15 years but a proportion maintain renal function into adulthood where complications of liver disease predominate. The ARPKD disease gene, PKHD1, has recently been identified through analysis of an orthologous animal model, the PCK rat. PKHD1 is a large gene (similar to470 kb) with 67 exons from which multiple transcripts may be generated by alternative splicing. It is highly expressed in kidney, with lower levels in liver and pancreas. The ARPKD protein, fibrocystin (4074 aa and 447 kDa), is predicted to be an integral membrane, receptor-like protein containing multiple copies of an Ig-like domain (TIG). Fibrocystin is localized to the branching ureteric bud, collecting and biliary ducts, consistent with the disease phenotype, and often absent from ARPKD tissue. In common with other PKD-related proteins, fibrocystin is localized to the primary cilia of renal epithelial cells, reinforcing the link between ciliary dysfunction and cyst development. Screens of PKHD1 have revealed H 9 different mutations of various types spread throughout the gene. Several ancestral changes have been described, some localized to specific geographic populations. The majority of patients are compound heterozygotes and preliminary genotype/phenotype studies associate two truncating mutations with severe disease. The complexities of PKHD1, marked allelic heterogeneity and high level of missense changes complicate gene-based diagnostics. (C) 2003 Elsevier Inc. All rights reserved.
C1 Mayo Clin, Coll Med, Div Nephrol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Mayo Clin, Coll Med, Div Nephrol, Rochester, MN 55905 USA.
EM harris.peter@mayo.edu
FU NIDDK NIH HHS [R01 DK059597] Funding Source: Medline
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NR 63
TC 46
Z9 54
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
EI 1096-7206
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD FEB
PY 2004
VL 81
IS 2
BP 75
EP 85
DI 10.1016/j.ymgme.2003.10.010
PG 11
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
   Medicine
GA 770JA
UT WOS:000188718400001
PM 14741187
DA 2025-04-10
ER

PT J
AU Braas, KM
   May, V
   Harakall, SA
   Hardwick, JC
   Parsons, RL
AF Braas, KM
   May, V
   Harakall, SA
   Hardwick, JC
   Parsons, RL
TI Pituitary adenylate cyclase-activating polypeptide expression and
   modulation of neuronal excitability in guinea pig cardiac ganglia
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE pituitary adenylate cyclase activating polypeptide; vasoactive
   intestinal peptide; PACAP receptor; cardiac ganglia; parasympathetic
   ganglia; neuropeptide receptors; autonomic nervous system
ID VASOACTIVE INTESTINAL POLYPEPTIDE; DIFFERENTIAL SIGNAL-TRANSDUCTION;
   TERMINAL EXTRACELLULAR DOMAIN; MOLECULAR-CLONING; PACAP RECEPTOR;
   FUNCTIONAL EXPRESSION; NEUROPEPTIDE-Y; PROOPIOMELANOCORTIN EXPRESSION;
   CHOLINE-ACETYLTRANSFERASE; INTRACARDIAC NEURONS
AB Cardiac output is regulated by the coordinate interactions of stimulatory sympathetic and inhibitory parasympathetic signals. Intracardiac parasympathetic ganglia are integrative centers of cardiac regulation, and modulation of the parasympathetic drive on the heart is accomplished by altering intrinsic cardiac ganglion neuron excitability. The pituitary adenylate cyclase-activating polypeptide (PACAP)/vasoactive intestinal peptide (VIP) family of peptides modulates cardiac function, and in guinea pig heart, PACAP appears to act directly on intrinsic parasympathetic cardiac ganglia neurons through PACAP-selective receptors. A multidisciplinary project tested whether cardiac PACAP peptides act through PACAP-selective receptors as excitatory neuromodulators amplifying the parasympathetic inhibition from guinea pig cardiac ganglia. The in vivo sources of regulatory PACAP peptides were localized immunocytochemically to neuronal fibers and a subpopulation of intrinsic postganglionic cardiac neurons. RT-PCR confirmed that cardiac ganglia expressed proPACAP transcripts and have PACAP peptide biosynthetic capabilities. Messenger RNA encoding PACAP-selective PAC1 receptor isoforms were also present in cardiac ganglia. Alternative splicing of PAC1 receptor transcripts produced predominant expression of the very short variant with neither HIP nor HOP cassettes; lower levels of the PAC1HOP2 receptor mRNA were present. Almost all of the parasympathetic neurons expressed membrane-associated PAC1 receptor proteins, localized immunocytochemically, which correlated with the population of cells that responded physiologically to PACAP peptides. PACAP depolarized cardiac ganglia neurons and increased neuronal membrane excitability. The rank order of peptide potency on membrane excitability in response to depolarizing currents was PACAP27>PACAP38>VIP. The PACAP-induced increase in excitability was not a function of membrane depolarization nor was it caused by alterations in action potential configuration. These results support roles for PACAP peptides as integrative modulators amplifying, through PACAP-selective receptors, the parasympathetic cardiac ganglia inhibition of cardiac output.
C1 Univ Vermont, Coll Med, Dept Anat & Neurobiol, Burlington, VT 05405 USA.
C3 University of Vermont
RP Univ Vermont, Coll Med, Dept Anat & Neurobiol, Given Hlth Sci Complex, Burlington, VT 05405 USA.
FU NICHD NIH HHS [HD-27468, R01 HD027468] Funding Source: Medline; NINDS
   NIH HHS [NS-23978, NS-01636] Funding Source: Medline
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NR 68
TC 90
Z9 96
U1 0
U2 3
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD DEC 1
PY 1998
VL 18
IS 23
BP 9766
EP 9779
PG 14
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 141XP
UT WOS:000077169800019
PM 9822736
DA 2025-04-10
ER

PT J
AU Uversky, VN
   Oldfield, CJ
   Midic, U
   Xie, HB
   Xue, B
   Vucetic, S
   Iakoucheva, LM
   Obradovic, Z
   Dunker, AK
AF Uversky, Vladimir N.
   Oldfield, Christopher J.
   Midic, Uros
   Xie, Hongbo
   Xue, Bin
   Vucetic, Slobodan
   Iakoucheva, Lilia M.
   Obradovic, Zoran
   Dunker, A. Keith
TI Unfoldomics of human diseases: linking protein intrinsic disorder with
   diseases
SO BMC GENOMICS
LA English
DT Review
ID NATIVELY UNFOLDED PROTEINS; MOLTEN GLOBULE STATE; RNA-BINDING PROTEIN;
   UNSTRUCTURED PROTEINS; ALPHA-SYNUCLEIN; FUNCTIONAL ANTHOLOGY;
   PARKINSONS-DISEASE; HUB PROTEINS; NEURODEGENERATIVE DISEASES; STRUCTURE
   PREDICTION
AB Background: Intrinsically disordered proteins (IDPs) and intrinsically disordered regions (IDRs) lack stable tertiary and/or secondary structure yet fulfills key biological functions. The recent recognition of IDPs and IDRs is leading to an entire field aimed at their systematic structural characterization and at determination of their mechanisms of action. Bioinformatics studies showed that IDPs and IDRs are highly abundant in different proteomes and carry out mostly regulatory functions related to molecular recognition and signal transduction. These activities complement the functions of structured proteins. IDPs and IDRs were shown to participate in both one-to-many and many-to-one signaling. Alternative splicing and posttranslational modifications are frequently used to tune the IDP functionality. Several individual IDPs were shown to be associated with human diseases, such as cancer, cardiovascular disease, amyloidoses, diabetes, neurodegenerative diseases, and others. This raises questions regarding the involvement of IDPs and IDRs in various diseases.
   Results: IDPs and IDRs were shown to be highly abundant in proteins associated with various human maladies. As the number of IDPs related to various diseases was found to be very large, the concepts of the disease-related unfoldome and unfoldomics were introduced. Novel bioinformatics tools were proposed to populate and characterize the disease-associated unfoldome. Structural characterization of the members of the disease-related unfoldome requires specialized experimental approaches. IDPs possess a number of unique structural and functional features that determine their broad involvement into the pathogenesis of various diseases.
   Conclusion: Proteins associated with various human diseases are enriched in intrinsic disorder. These disease-associated IDPs and IDRs are real, abundant, diversified, vital, and dynamic. These proteins and regions comprise the disease-related unfoldome, which covers a significant part of the human proteome. Profound association between intrinsic disorder and various human diseases is determined by a set of unique structural and functional characteristics of IDPs and IDRs. Unfoldomics of human diseases utilizes unrivaled bioinformatics and experimental techniques, paves the road for better understanding of human diseases, their pathogenesis and molecular mechanisms, and helps develop new strategies for the analysis of disease-related proteins.
C1 [Uversky, Vladimir N.; Oldfield, Christopher J.; Xue, Bin; Dunker, A. Keith] Indiana Univ, Sch Med, Ctr Computat Biol & Bioinformat, Indianapolis, IN 46202 USA.
   [Uversky, Vladimir N.; Xue, Bin] Indiana Univ, Sch Med, Inst Intrinsically Disordered Prot Res, Indianapolis, IN 46202 USA.
   [Uversky, Vladimir N.] Russian Acad Sci, Inst Biol Instrumentat, Pushchino 142290, Moscow Region, Russia.
   [Midic, Uros; Xie, Hongbo; Vucetic, Slobodan; Obradovic, Zoran] Temple Univ, Ctr Informat Sci & Technol, Philadelphia, PA 19122 USA.
   [Iakoucheva, Lilia M.] Rockefeller Univ, Lab Stat Genet, New York, NY 10065 USA.
C3 Indiana University System; Indiana University Indianapolis; Indiana
   University System; Indiana University Indianapolis; Russian Academy of
   Sciences; Pennsylvania Commonwealth System of Higher Education (PCSHE);
   Temple University; Rockefeller University
RP Uversky, VN (corresponding author), Indiana Univ, Sch Med, Ctr Computat Biol & Bioinformat, Indianapolis, IN 46202 USA.
EM vuversky@iupui.edu; cjoldfie@iupui.edu; uros@ist.temple.edu;
   michaelxie@ist.temple.edu; binxue@iupui.edu; vucetic@ist.temple.edu;
   lilia@rockefeller.edu; zoran@ist.temple.edu; kedunker@iupui.edu
RI Uversky, Vladimir/F-4515-2011; xue, bin/E-5617-2011
OI Xie, Hongbo M./0000-0003-2223-0029; Obradovic,
   Zoran/0000-0002-2051-0142; Iakoucheva, Lilia/0000-0002-4542-5219
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   [No title captured]
   [No title captured]
   [No title captured]
NR 115
TC 226
Z9 252
U1 0
U2 44
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2009
VL 10
SU 1
AR S7
DI 10.1186/1471-2164-10-S1-S7
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 479BV
UT WOS:000268634900008
PM 19594884
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Hua, XX
   Sakai, J
   Brown, MS
   Goldstein, JL
AF Hua, XX
   Sakai, J
   Brown, MS
   Goldstein, JL
TI Regulated cleavage of sterol regulatory element binding proteins
   requires sequences on both sides of the endoplasmic reticulum membrane
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LEUCINE ZIPPER PROTEIN; HERPES-SIMPLEX VIRUS; SITE; TRANSCRIPTION; GENE
AB Sterol regulatory element binding proteins (SREBP-1 and SREBP-2) are attached to the endoplasmic reticulum (ER) and nuclear envelope by a hairpin domain consisting of two transmembrane regions connected by a short lumenal loop of similar to 30 hydrophilic amino acids. In sterol-depleted cells, a protease cleaves the protein in the region of the first transmembrane domain, releasing an NH2-terminal fragment of similar to 500 amino acids that activates transcription of genes encoding the low density lipoprotein receptor and enzymes of cholesterol synthesis. In sterol-overloaded cells, proteolysis does not occur, and transcription is repressed. Through mutational analysis in transfected cells, we identify two segments of SREBPs that are required for proteolysis, one on either side of the ER membrane. An arginine in the lumenal loop is essential. A tetrapeptide sequence (DRSR) on the cytosolic face adjacent to the first transmembrane domain is also required for maximal cleavage. Both of these elements are conserved in the human and hamster versions of SREBP-1 and SREBP-2. Sterol-mediated suppression of cleavage of SREBP-1 was found to be dependent on the extreme COOH-terminal region (residue 1034 to the COOH terminus), which exists in two forms as a result of alternative splicing. The form encoded by the ''a'' class exons (exons 18a and 19a) undergoes sterol-regulated cleavage. The form encoded by the ''c'' class exons (18c and 19c) is cleaved less efficiently and is not suppressed by sterols. These studies were made possible through use of a vector that achieves low level expression of epitope-tagged SREBPs under control of the relatively weak thymidine kinase promoter from herpes simplex virus. In contrast to SREBPs overproduced by high level expression vectors, the SREBPs produced at low levels were subject to the same regulated cleavage pattern as the endogenous SREBPs. These results indicate that sterol-regulated proteolysis of SREBPs is a complex process, requiring sequences on both sides of the ER membrane.
RP Hua, XX (corresponding author), UNIV TEXAS,SW MED CTR,DEPT MOLEC GENET,DALLAS,TX 75235, USA.
RI Sakai, Juro/KPY-7126-2024
OI Sakai, Juro/0000-0003-4043-1035
FU NHLBI NIH HHS [HL20948] Funding Source: Medline
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NR 17
TC 176
Z9 206
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 26
PY 1996
VL 271
IS 17
BP 10379
EP 10384
DI 10.1074/jbc.271.17.10379
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA UG257
UT WOS:A1996UG25700082
PM 8626610
OA hybrid
DA 2025-04-10
ER

PT J
AU Seifert, R
   Wenzel-Seifert, K
AF Seifert, R
   Wenzel-Seifert, K
TI Constitutive activity of G-protein-coupled receptors: cause of disease
   and common property of wild-type receptors
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Review
ID INVERSE AGONIST ACTIVITY; LUTEINIZING-HORMONE RECEPTOR;
   GUANINE-NUCLEOTIDE-BINDING; DELTA-OPIOID RECEPTOR; HUMAN
   5-HYDROXYTRYPTAMINE(1A) RECEPTOR; SARCOMA-ASSOCIATED HERPESVIRUS;
   ATYPICAL ANTIPSYCHOTIC-DRUGS; BETA(2) ADRENERGIC-RECEPTOR; ACTIVATING
   POINT MUTATION; AMINO-ACID SUBSTITUTIONS
AB The aim of this review is to provide a systematic overview on constitutively active G-protein-coupled receptors (GPCRs), a rapidly evolving area in signal transduction research. We will discuss mechanisms, pharmacological tools and methodological approaches to analyze constitutive activity. The two-state model defines constitutive activity as the ability of a GPCR to undergo agonist-independent isomerization from an inactive (R) state to an active (R*) state. While the two-state model explains basic concepts of constitutive GPCR activity and inverse agonism, there is increasing evidence for multiple active GPCR conformations with distinct biological activities. As a result of constitutive GPCR activity, basal G-protein activity increases. Until now, constitutive activity has been observed for more than 60 wild-type GPCRs from the families 1-3 and from different species including humans and commonly used laboratory animal species. Additionally, several naturally occurring and disease-causing GPCR mutants with increased constitutive activity relative to wildtype GPCRs have been identified. Alternative splicing, RNA editing, polymorphisms within a given species, species variants and coupling to specific G-proteins all modulate the constitutive activity of GPCRs, providing multiple regulatory switches to fine-tune basal cellular activities. The most important pharmacological tools to analyze constitutive activity are inverse agonists and Na+ that stabilize the R state, and pertussis toxin that uncouples GPCRs from G(i)/G(o)-proteins. Constitutive activity is observed at low and high GPCR expression levels, in native systems and in recombinant systems, and has been reported for GPCRs coupled to G(s)-, G(i)- and G(q)-proteins. Constitutive activity of neurotransmitter GPCRs may provide a tonic support for basal neuronal activity. For the majority of GPCRs known to be constitutively active, inverse agonists have already been identified. Inverse agonists may be useful in the treatment of neuropsychiatric and cardiovascular diseases and of diseases caused by constitutively active GPCR mutants.
C1 Univ Kansas, Dept Pharmacol & Toxicol, Lawrence, KS 66045 USA.
C3 University of Kansas
RP Univ Kansas, Dept Pharmacol & Toxicol, Room 5064,1251 Wescoe Hall Dr,5064 Malott Hall, Lawrence, KS 66045 USA.
EM rseifert@ku.edu
RI Seifert, Roland/G-3189-2013
FU NCRR NIH HHS [1 P20 RR 15563] Funding Source: Medline
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NR 266
TC 502
Z9 583
U1 1
U2 47
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD NOV
PY 2002
VL 366
IS 5
BP 381
EP 416
DI 10.1007/s00210-002-0588-0
PG 36
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 611MN
UT WOS:000179021600001
PM 12382069
DA 2025-04-10
ER

PT J
AU Fukuda, N
   Kishioka, H
   Satoh, C
   Nakayama, T
   Watanabe, Y
   Soma, M
   Izumi, Y
   Kanmatsuse, K
AF Fukuda, N
   Kishioka, H
   Satoh, C
   Nakayama, T
   Watanabe, Y
   Soma, M
   Izumi, Y
   Kanmatsuse, K
TI Role of long-form PDGF A-chain in the growth of vascular smooth muscle
   cells from spontaneously hypertensive rats
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
DE platelet-derived growth factor; vascular smooth muscle cells;
   spontaneously hypertensive rats; antisense DNA; growth
ID FACTOR-BETA; ANGIOTENSIN-II; ANTISENSE OLIGONUCLEOTIDES; GENE
   TRANSCRIPTS; EXPRESSION; RECEPTOR; RNA; MECHANISM; SEQUENCE; CDNA
AB Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) exhibit exaggerated growth relative to cells from normotensive Wistar-Kyoto (WKY) rats. Platelet-derived growth factor (PDGF) A-chain has been implicated in the exaggerated growth of VSMC from SHR. Two isoforms of PDGF A-chain mRNA that either include (long form) or exclude (short form) exon 6 are produced as a result of alternative splicing. The expression of the long-form PDGF A-chain at the mRNA level and its role in the growth of VSMC from SHR have now been investigated with the use of an antisense oligodeoxynucleotide (ODN) complementary to exon 6 of the PDGF A-chain gene. Reverse transcription-polymerase chain reaction (RT-PCR) analysis with primers encompassing exon 6 of PDGF A-chain mRNA revealed bands corresponding to both long-and short-form PDGF A-chain transcripts in quiescent VSMC from both SHR and WKY rats, with the long-form mRNA more abundant in VSMC from SHR than in cells from WKY rats. Expression of the long-form of PDGF A-chain mRNA was enhanced with angiotensin II and transforming growth factor-beta 1 in VSMC from SHR, but not in cells from WKY rats. The antisense ODN significantly inhibited DNA synthesis by VSMC from SHR, but not by cells from WKY rats, in the absence or presence of serum. In addition, the antisense ODN significantly inhibited serum induced proliferation of VSMC from SHR, but not those from WKY rats. The antisense ODN abolished expression of the long-form PDGF A-chain mRNA in VSMC, suggesting that its inhibitory effects on the growth of VSMC from SHR are mediated by depletion of the long-form transcripts. These results indicate that the long-form of PDGF A-chain contributes to the exaggerated growth of VSMC from SHR. (C) 1997 American Journal of Hypertension, Ltd.
RP NIHON UNIV, SCH MED, DEPT INTERNAL MED 2, ITABASHI KU, OOYAGUCHI KAMI 30-1, TOKYO 173, JAPAN.
OI Fukuda, Noboru/0000-0003-0098-054X
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NR 37
TC 28
Z9 31
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0895-7061
EI 1941-7225
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD OCT
PY 1997
VL 10
IS 10
BP 1117
EP 1124
PN 1
PG 8
WC Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA YC214
UT WOS:A1997YC21400006
PM 9370382
DA 2025-04-10
ER

PT J
AU Guo, GL
   Staudinger, J
   Ogura, K
   Klaassen, CD
AF Guo, GL
   Staudinger, J
   Ogura, K
   Klaassen, CD
TI Induction of rat organic anion transporting polypeptide 2 by
   pregnenolone-16α-carbonitrile is via interaction with pregnane X
   receptor
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID MICROSOMAL-ENZYME INDUCERS; GENOMIC ORGANIZATION; BILIARY-EXCRETION;
   TRANSCRIPTIONAL ACTIVATION; PLASMA DISAPPEARANCE; TISSUE DISTRIBUTION;
   MEDIATED TRANSPORT; MOLECULAR-CLONING; GENE-EXPRESSION; LOCALIZATION
AB The rat organic anion transporting polypeptide 2 (oatp2; Slc21a5) is a liver transporter that mediates the uptake of a variety of structurally diverse compounds, and has a high affinity for cardiac glycosides. Treatment of rats with pregnenolone-16alpha- carbonitrile (PCN), a ligand for the rodent pregnane X receptor (PXR), significantly enhances the rat oatp2 gene expression. To understand the molecular mechanism of oatp2 induction by PCN, rat oatp2 gene was cloned. The rat oatp2 gene consists of 16 exons; alternative splicing of the second noncoding exon gives rise to the two published rat oatp2 cDNAs. Approximately 8700 base pairs (bp) of the 5'-flanking region of the rat oatp2 gene were linked to the luciferase reporter gene and used in transient transfection assays in H4IIE cells. Treatment of PCN induced the expression of the reporter gene in a dose-dependent manner. Four potential PXR response elements (PXREs) were identified in the 5'-flanking region of the rat oatp2 gene. One element (DR3-1) is located approximately -5000 bp with three more (DR3-2, DR3-3, and DR3-4) clustered at about -8000 bp. Results from electrophoretic mobility shift assays showed that the PXR-retinoid X receptor alpha heterodimer binds to the DR3-2 with the highest affinity, to the DR3-4 and DR3-1 with a lower affinity, and weakly or not at all to the DR3-3. Furthermore, a series of partial deletions of the 5'-flanking region illustrated that both the proximal and distal clusters of PXREs are required for maximal induction of rat oatp2 by PCN. In conclusion, these data elucidate the molecular mechanism by which PCN treatment induces rat oatp2 gene expression. In addition, this study identifies rat oatp2 as a direct PXR-targeted gene and further supports the hypothesis that activation of PXR affects a network of genes that is involved in either metabolism or transport of drugs, steroids, and bile acids.
C1 Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66160 USA.
C3 University of Kansas; University of Kansas Medical Center
RP Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, 3901 Rainbow Blvd, Kansas City, KS 66160 USA.
EM cklaasse@kumc.edu
FU NIEHS NIH HHS [ES07079, ES09649, ES03192] Funding Source: Medline
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NR 45
TC 116
Z9 131
U1 0
U2 7
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
EI 1521-0111
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD APR
PY 2002
VL 61
IS 4
BP 832
EP 839
AR UNSP 1435/971866
DI 10.1124/mol.61.4.832
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 536ZB
UT WOS:000174730800016
PM 11901222
DA 2025-04-10
ER

PT J
AU Kiss, A
   Farah, K
   Kim, J
   Garriock, RJ
   Drysdale, TA
   Hammond, JR
AF Kiss, A
   Farah, K
   Kim, J
   Garriock, RJ
   Drysdale, TA
   Hammond, JR
TI Molecular cloning and functional characterization of inhibitor-sensitive
   (mENT1) and inhibitor-resistant (mENT2) equilibrative nucleoside
   transporters from mouse brain
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE dipyridamole; nitrobenzylthioinosine; nucleoside transport; transporter
   isoforms; Xenopus oocytes
ID ASCITES-TUMOR-CELLS; PROTEIN-KINASE-C; ADENOSINE TRANSPORT;
   SPECIES-DIFFERENCES; URIDINE-TRANSPORT; MAMMALIAN-CELLS; SH3 DOMAINS;
   ERYTHROCYTES; SYSTEM; RAT
AB Mammalian cells express at least two subtypes of equilibrative nucleoside transporters, i.e. ENT1 and ENT2, which can be distinguished functionally by their sensitivity and resistance respectively to inhibition by nitrobenzylthioinosine. The ENT1 transporters exhibit distinctive species differences in their sensitivities to inhibition by dipyridamole, dilazep and draflazine (human > mouse > rat). A comparison of the ENT1 structures in the three species would facilitate the identification of the regions involved in the actions of these cardioprotective agents. We now report the molecular cloning and functional expression of the murine (m)ENT1 and mENT2 transporters. mENT1 and mENT2 encode proteins containing 458 and 456 residues respectively, with a predicted 11-transmembrane-domain topology. mENT1 has 88 % and 78 % amino acid identity with rat ENT1 and human ENT1 respectively; mENT2 is more highly conserved, with 94 % and 88 % identity with rat ENT2 and human ENT2 respectively. We have also isolated two additional distinct cDNAs that encode proteins similar to mENT1; these probably represent distinct mENT1 isoforms or alternative splicing products. One cDNA encodes a protein with two additional amino acids (designated mENT1b) that adds a potential protein kinase CK2 phosphorylation site in the central intracellular loop of the transporter, and is similar, in this regard, to the human and rat ENT1 orthologues. The other cDNA has a 5'-untranslated region sequence that is distinct from that of full-length mENT1. Microinjection of mENT1, mENT1b or mENT2 cRNA into Xenopus oocytes resulted in enhanced uptake of [H-3]uridine by the oocytes relative to that seen in water-injected controls. mENT1-mediated, but not mENT2-mediated, [H-3]uridine uptake was inhibited by nitrobenzylthioinosine and dilazep. Dipyridamole inhibited both mENT1 and mENT2, but was significantly more effective against mENT1. Adenosine inhibited both systems with a similar potency, as did a range of other purine and pyrimidine nucleosides. These results are compatible with the known characteristics of the native mENT1 and mENT2 transporters.
C1 Univ Western Ontario, Dept Pharmacol & Toxicol, London, ON N6A 5C1, Canada.
   St Josephs Hlth Ctr, Lawson Res Inst, London, ON N6A 4V2, Canada.
C3 Western University (University of Western Ontario); Western University
   (University of Western Ontario); University Western Ontario Hospital
RP Hammond, JR (corresponding author), Univ Western Ontario, Dept Pharmacol & Toxicol, M275 Med Sci Bldg, London, ON N6A 5C1, Canada.
RI Hammond, James/A-4524-2008
OI Drysdale, Thomas/0000-0002-7254-2189
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NR 51
TC 79
Z9 96
U1 0
U2 3
PU PORTLAND PRESS
PI LONDON
PA 59 PORTLAND PLACE, LONDON W1N 3AJ, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD DEC 1
PY 2000
VL 352
BP 363
EP 372
DI 10.1042/0264-6021:3520363
PN 2
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 385VC
UT WOS:000166024400015
PM 11085929
OA Green Published
DA 2025-04-10
ER

PT J
AU Steele, BL
   Alvarez-Veronesi, MC
   Schmidt, TA
AF Steele, B. L.
   Alvarez-Veronesi, M. C.
   Schmidt, T. A.
TI Molecular weight characterization of PRG4 proteins using multi-angle
   laser light scattering (MALLS)
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Article
DE PRG4; Lubricin; MALLS; Superficial zone protein
ID MEGAKARYOCYTE STIMULATING FACTOR; BOVINE SYNOVIAL-FLUID; SUPERFICIAL
   ZONE PROTEIN; BOUNDARY-LUBRICATING ABILITY; VARA-PERICARDITIS SYNDROME;
   SODIUM DODECYL-SULFATE; ARTICULAR-CARTILAGE; GENE-EXPRESSION;
   RECOMBINANT LUBRICIN; PROTEOGLYCAN 4
AB Objectives: Alternative splicing and variable post-translational modifications result in proteoglycan 4 (PRG4) proteins with historically reported apparent molecular weights (Ma) ranging from 150 to 400 kDa. The objectives of this study were to (1) identify and determine the weight averaged molecular weights (M-W's) of PRG4 proteins purified from medium with transforming growth factor-beta 1 (TGF-beta 1) conditioned by mature bovine articular cartilage explants and (2) to examine the effect of reduction and alkylation (RA) on PRG4.
   Methods: Non-reduced (NR) and RA preparations of PRG4 were separated using high performance liquid chromatography-size-exclusion chromatography with an in-line multi-angle laser light scattering (MALLS) detector, which was used for absolute determination of PRG4 M-W. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), immunoblotting, and tandem mass spectrometry (MS/MS) analysis were used to confirm the identity of separated proteins.
   Results: Three putative PRG4 monomers, one with previously uncharacterized M-W, were identified in NR and RA PRG4 preparations of 239 (223,255), 379 (369,389), and 467 (433,501) kDa. Additionally similar to 1 MDa putative PRG4 dimer was identified. Release of a similar to 90 kDa PRG4 fragment was also observed on SDS-PAGE after RA. Western Blotting with anti-PRG4 antibodies detected immunoreactive bands with Ma similar to M-W for all species and excised bands were confirmed to be PRG4 by MS/MS.
   Conclusions: A variety of monomeric PRG4 proteins and a disulfide-bonded dimer/multimer are secreted by chondrocytes in bovine cartilage explants. The observed decrease in Mw's of monomeric PRG4 species upon RA may be due to the release of post-translationally cleaved fragments. Further study of these species will provide insight into the PRG4 molecular structure and function relationship. (C) 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
C1 [Steele, B. L.; Schmidt, T. A.] Univ Calgary, Fac Kinesiol, Calgary, AB T2N 1N4, Canada.
   [Alvarez-Veronesi, M. C.; Schmidt, T. A.] Univ Calgary, Schulich Sch Engn, Ctr Bioengn Res & Educ, Calgary, AB T2N 1N4, Canada.
C3 University of Calgary; University of Calgary
RP Schmidt, TA (corresponding author), Univ Calgary, 2500 Univ Dr NW,KNB 426, Calgary, AB T2N 1N4, Canada.
EM blsteele@ucalgary.ca; cecilia.alvarezveronesi@mail.utoronto.ca;
   tschmidt@ucalgary.ca
RI Schmidt, Tannin/AAE-3830-2019
FU National Science and Engineering Research Council of Canada Discovery
   Grant Programme; Collaborative Research and Training Experience
   Programme; (NSERC-CREATE), Canadian Arthritis Network; Arthritis
   Society; Alberta Innovates Health Solutions OA Team Grant; Faculty of
   Kinesiology and Schulich School of Engineering's Center for
   Bioengineering Research and Education at the University of Calgary
FX We would like to thank Morgan Khan and the Southern Alberta Mass
   Spectrometry Centre for their assistance with MS/MS analysis. We also
   would like to thank Dr M. L. Warman of Harvard Medical School, Boston,
   MA for generously donating anti-sera J108N. This work was supported by
   funding from the National Science and Engineering Research Council of
   Canada Discovery Grant Programme and the Collaborative Research and
   Training Experience Programme. (NSERC-CREATE), Canadian Arthritis
   Network, The Arthritis Society, Alberta Innovates Health Solutions OA
   Team Grant, Faculty of Kinesiology and Schulich School of Engineering's
   Center for Bioengineering Research and Education at the University of
   Calgary.
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NR 44
TC 32
Z9 38
U1 1
U2 19
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1063-4584
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD MAR
PY 2013
VL 21
IS 3
BP 498
EP 504
DI 10.1016/j.joca.2012.12.002
PG 7
WC Orthopedics; Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Orthopedics; Rheumatology
GA 098MA
UT WOS:000315552200012
PM 23257245
OA Bronze
DA 2025-04-10
ER

PT J
AU Scholz, H
   Kirschner, KM
AF Scholz, Holger
   Kirschner, Karin M.
TI Oxygen-dependent gene expression in development and cancer: lessons
   learned from the Wilms' tumor gene, WT1
SO FRONTIERS IN MOLECULAR NEUROSCIENCE
LA English
DT Review
DE hypoxia; Wilms' tumor gene; epithelial-to-mesenchymal transition;
   angiogenesis; epicardium; transcription factor; oncogene; HIF
ID EPITHELIAL-MESENCHYMAL TRANSITION; CORONARY VESSEL DEVELOPMENT; TRKB
   NEUROTROPHIN RECEPTOR; SMOOTH-MUSCLE-CELLS; SUPPRESSOR WT1;
   TRANSCRIPTION FACTOR; MESSENGER-RNA; PROTEIN WT1; RETINOIC ACID;
   TGF-BETA
AB Adequate tissue oxygenation is a prerequisite for normal development of the embryo. Most fetal organs are exquisitely susceptible to hypoxia which occurs when the delivery of oxygen is exceeded by the actual demand. Developmental abnormalities due to insufficient supply with oxygen can result from the impaired expression of genes with essential functions during embryogenesis. As such, the Wilms' tumor gene, WT1, is among the fetal genes that are regulated by the local oxygen tension. WT1 was originally discovered as a tumor suppressor gene owing to loss-of-function mutations in a subset of pediatric renal neoplasias, known as nephroblastomas or Wilms' tumors. Wilms' tumors can arise when pluripotent progenitor cells in the embryonic kidney continue to proliferate rather than differentiating to glomeruli and tubules. WT1 encodes a zinc finger protein, of which multiple isoforms exist due to alternative mRNA splicing in addition to translational and post-translational modifications. While some WT1 isoforms function as transcription factors, other WT1 proteins are presumably involved in post-transcriptional mRNA processing. However, the role of WT1 reaches far beyond that of a tumor suppressor as homozygous disruption of Wt1 in mice caused embryonic lethality with a failure of normal development of the kidneys, gonads, heart, and other tissues. WT1 mutations in humans are associated with malformation of the genitourinary system. A common paradigm of WT1 expressing cells is their capacity to switch between a mesenchymal and epithelial state. Thus, WT1 likely acts as a master switch that enables cells to undergo reciprocal epithelial-to-mesenchymal transition. Impairment of renal precursor cells to differentiate along the epithelial lineage due to WT1 mutations may favor malignant tumor growth. This article shall provide a concise review of the function of WT1 in development and disease with special consideration of its regulation by molecular oxygen.
C1 [Scholz, Holger; Kirschner, Karin M.] Charite, Inst Vegetat Physiol, D-10115 Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin
RP Scholz, H (corresponding author), Charite, Inst Vegetat Physiol, Hess Str 3-4, D-10115 Berlin, Germany.
EM holger.scholz@charite.de
OI Kirschner, Karin/0000-0003-0226-8636
FU Charite - Universitatsmedizin Berlin; Deutsche Forschungsgemeinschaft
FX The authors acknowledge the continued funding of their work by grants
   from the Charite - Universitatsmedizin Berlin and the Deutsche
   Forschungsgemeinschaft.
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NR 157
TC 23
Z9 23
U1 0
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1662-5099
J9 FRONT MOL NEUROSCI
JI Front. Molec. Neurosci.
PY 2011
VL 4
AR 4
DI 10.3389/fnmol.2011.00004
PG 11
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA V38VE
UT WOS:000209370100002
PM 21430823
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Góra-Kupilas, K
   Josko, J
AF Góra-Kupilas, K
   Josko, J
TI The neuroprotective function of vascular endothelial growth factor
   (VEGF)
SO FOLIA NEUROPATHOLOGICA
LA English
DT Review
DE neuroprotection; programmed cell death; neurogenesis; caspase-3;
   VEGFR-2/PI3K/Akt signaling
ID HEME OXYGENASE-1; ANGIOGENIC FACTORS; CEREBRAL-ISCHEMIA; NEURONAL DEATH;
   NITRIC-OXIDE; CELL-DEATH; IN-VITRO; EXPRESSION; HYPOXIA; NEUROGENESIS
AB The vascular endothelial growth factor (VEGF) is known mainly as the potent angiogenic and vascular permeability-enhancing factor. Both processes are very effective in hypoxia. The latest studies show that VEGF has neurotrophic and neuroprotective as well as angiogenic properties. It exerts neuroprotective actions directly through the inhibition of programmed cell death (PCD), or apoptosis and the stimulation of neurogenesis. VEGF is also a mediator of multiple processes including angiogenesis, enhancing blood brain barrier permeability for glucose, antioxidants activation, which indirectly result in neuroprotection. VEGF prevents neurons from death under critical conditions such as hypoxia, glucose deprivation through binding to the specific receptors, which are also expressed on the surface of neuronal cells. The Increased expression of VEGFR-2/flk-1/KDR receptors on neurons subjected to hypoxia, glucose deprivation provides evidence that these receptors are mainly involved in neuroprotective effects of VEGF. Furthermore, binding to these receptors triggers the phosphatidyloinositol 3-kinase (PI3K)/Akt signal transduction system and, in consequence, leads to the inhibition of PCD by activating antiapoptotic proteins through the transcription factor NF kappa B and inhibiting proapoptotic signaling by Bad, caspase-9, caspase-3, and other effectors. Promotion of neuronal cells proliferation by VEGF is also associated with the increased expression of VEGFR-2 receptors and up-regulation of E2F family transcription factors, cyclin D1, cyclin E, and cdc25. It Is known that the amount and types of VEGF isoforms influence Its action. At least six isoforms of VEGF proteins are formed as a result of alternative mRNA splicing and it is unknown which of them and in what proportion occur in the nervous system In physiology and pathophysiology. It seems to be very essential to find out the mechanisms responsible for specific patterns of VEGF isoforms and their receptors expression in different pathologies of the nervous system. Maybe such knowledge will provide new perspectives in VEGF therapy.
C1 Med Univ Silesia, Dept Environm Med & Epidemiol, PL-41808 Zabrze, Poland.
C3 Medical University Silesia
RP Med Univ Silesia, Dept Environm Med & Epidemiol, Jordana 19, PL-41808 Zabrze, Poland.
EM medsrod@infomed.slam.katowice.pl
OI Josko - Ochojska, Jadwiga/0000-0001-9310-9088
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NR 55
TC 135
Z9 158
U1 0
U2 9
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA ST 2, POZNAN, 61-615, POLAND
SN 1641-4640
EI 1509-572X
J9 FOLIA NEUROPATHOL
JI Folia Neuropathol.
PY 2005
VL 43
IS 1
BP 31
EP 39
PG 9
WC Neurosciences; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Pathology
GA 933XZ
UT WOS:000229667500005
PM 15827888
DA 2025-04-10
ER

PT J
AU Luo, YE
   Villani, KR
   Lei, HQ
   Kuo, LY
   Imery, I
   Stoker, BE
   Fatima, N
   Noles, SM
   Moore, CM
   Barton, ER
AF Luo, Yangyi E.
   Villani, Katelyn R.
   Lei, Hanqin
   Kuo, Li-Ying
   Imery, Ian
   Stoker, Bradley E.
   Fatima, Naureen
   Noles, Steven M.
   Moore, Cara M.
   Barton, Elisabeth R.
TI Ablation of specific insulin-like growth factor I forms reveals the
   importance of cleavage for regenerative capacity and glycosylation for
   skeletal muscle storage
SO FASEB JOURNAL
LA English
DT Article
DE anabolic signaling; muscle injury; postnatal growth; post-translational
   processing; proprotein convertase
ID (IGF)-I E-PEPTIDES; IGF-I; BODY GROWTH; EXPRESSION; HYPERTROPHY;
   INSULIN-LIKE-GROWTH-FACTOR-1; OVEREXPRESSION; SEQUENCES; GENE
AB Insulin-like growth factor-I (IGF-I) facilitates mitotic and anabolic actions in all tissues. In skeletal muscle, IGF-I can promote growth and resolution of damage by promoting satellite cell proliferation and differentiation, suppressing inflammation, and enhancing fiber formation. While the most well-characterized form of IGF-I is the mature protein, alternative splicing and post-translational modification complexity lead to several additional forms of IGF-I. Previous studies showed muscle efficiently stores glycosylated pro-IGF-I. However, non-glycosylated forms display more efficient IGF-I receptor activation in vitro, suggesting that the removal of the glycosylated C terminus is a necessary step to enable increased activity. We employed CRISPR-Cas9 gene editing to ablate IGF-I glycosylation sites (2ND) or its cleavage site (3RA) in mice to determine the necessity of glycosylation or cleavage for IGF-I function in postnatal growth and during muscle regeneration. 3RA mice had the highest circulating and muscle IGF-I content, whereas 2ND mice had the lowest levels compared to wild-type mice. After weaning, 4-week-old 2ND mice exhibited higher body and skeletal muscle mass than other strains. However, by 16 weeks of age, muscle and body size differences disappeared. Even though 3RA mice had more IGF-I stored in muscle in homeostatic conditions, regeneration was delayed after cardiotoxin-induced injury, with prolonged necrosis most evident at 5 days post injury (dpi). In contrast, 2ND displayed improved regeneration with reduced necrosis, and greater fiber size and muscle mass at 11 and 21 dpi. Overall, these results demonstrate that while IGF-I glycosylation may be important for storage, cleavage is needed to enable IGF-I to be used for efficient activity in postnatal growth and following acute injury.
   CRISPR-Cas9 gene editing to ablate IGF-I glycosylation sites or its cleavage site in mice shows that glycosylation improves accumulation of IGF-I, but that the absence of glycosylation improves postnatal growth and muscle regeneration.image
C1 [Luo, Yangyi E.; Villani, Katelyn R.; Lei, Hanqin; Kuo, Li-Ying; Imery, Ian; Stoker, Bradley E.; Fatima, Naureen; Noles, Steven M.; Barton, Elisabeth R.] Univ Florida, Coll Hlth & Human Performance, Appl Physiol & Kinesiol, 202G Florida Gym,1864 Stadium Rd, Gainesville, FL 32611 USA.
   [Luo, Yangyi E.; Villani, Katelyn R.; Barton, Elisabeth R.] Univ Florida, Myol Inst, Gainesville, FL USA.
   [Moore, Cara M.] Univ Florida, Anim Care Serv, Gainesville, FL USA.
C3 State University System of Florida; University of Florida; State
   University System of Florida; University of Florida; State University
   System of Florida; University of Florida
RP Barton, ER (corresponding author), Univ Florida, Coll Hlth & Human Performance, Appl Physiol & Kinesiol, 202G Florida Gym,1864 Stadium Rd, Gainesville, FL 32611 USA.
EM erbarton@ufl.edu
RI Barton, Elisabeth/LMO-8319-2024
OI Barton, Elisabeth/0000-0002-7401-4398; Luo, Yangyi/0000-0001-7418-0030
FU HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin
   Diseases (NIAMS) [P50 AR052646]; NIH
FX This study is supported by NIH P50 AR052646 Wellstone Physiological
   Assessment Core, and we are grateful for technical assistance from Mr.
   C.S. Henley-Beasley and Mr. J. Herr. Genetically engineered mice were
   generated with the assistance of Northwestern University Transgenic and
   Targeted Mutagenesis Lab.
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NR 60
TC 1
Z9 1
U1 1
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD MAY 15
PY 2024
VL 38
IS 9
AR e23634
DI 10.1096/fj.202302512RR
PG 16
WC Biochemistry & Molecular Biology; Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics; Cell Biology
GA OY6A2
UT WOS:001210865200001
PM 38679876
OA hybrid
DA 2025-04-10
ER

PT J
AU Brazert, M
   Pawelczyk, LA
AF Brazert, Maciej
   Pawelczyk, Leszek A.
TI Insulin-like growth factor-1 isoforms in human ovary Preliminary report
   on the expression of the IGF-1 gene in PCOS patients and healthy
   controls
SO GINEKOLOGIA POLSKA
LA English
DT Article
DE IGF-1; isoforms; PCOS; insulin-like growth factor-1; ovary; alternative
   splicing
ID WOMEN; PREVALENCE; MECHANISMS; RESISTANCE; PEPTIDES; CRITERIA
AB Insulin-like growth factor 1 (IGF-1), produced and secreted locally may affect the mechanisms of folliculogenesis and cause ovarian dysfunction, characteristic of PCOS. The expression of the IGF-1 gene gives rise to three different isoforms of the original molecule. Until now, the role of IGF-1 isoforms has been documented in the repair processes of damaged muscle fibers, cardiomyocytes, hepatocytes, and neurons. The literature offers no reports on the presence and role of IGF-1 isoforms in the ovary
   Objectives: The aim of the study was to assess the IGF-1A, B and C isoforms at the level of IGF-1 gene transcription in the ovaries of PCOS women and healthy controls.
   Material and methods: Serum samples and ovarian tissues from PCOS women, treated and non-treated with metformin (PCOS M(+);n=12 and PODS M(-),n=37, respectively), and controls (n=21) were obtained. The expression of mRNA species of IGF-1 in the ovaries was determined by quantitative RT-PCR.
   Results: The presence of transcripts of three types of IGF-1 isoforms was observed in healthy controls and PODS patients, regardless of metformin treatment. Total expression of all isoforms was higher in the M(-)(Me-26640) group as compared to the M(+)(Me-13470) group, as well as controls (Me-17030)-(not significant, p=0.061). Similar results for IGF-1A were obtained in all groups. The relative expression of IGF-1A was lower in the M(-)(86.02%) group and differed statistically from controls (91.38%) (p=0.011).
   Conclusions: We detected the presence of mRNA for three IGF-1 isoforms in human ovary To the best of our knowledge, this has been the first report on the presence of mRNA for three IGF-1 isoforms in human ovary We found differences in the relative expression of IGF-1A isoforms between the investigated groups.
C1 [Brazert, Maciej; Pawelczyk, Leszek A.] Poznan Univ Med Sci, Dept Infertil & Reprod Endocrinol, Poznan, Poland.
C3 Poznan University of Medical Sciences
RP Brazert, M (corresponding author), Univ Med Sci, Dept Infertil & Reprod Endocrinol Poznan, Ul Polna 33, PL-60535 Poznan, Poland.
EM maciejbrazert@interia.pl
OI Pawelczyk, Leszek/0000-0003-3309-3269; Brazert,
   Maciej/0000-0002-2423-8238
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NR 34
TC 6
Z9 7
U1 0
U2 3
PU VIA MEDICA
PI GDANSK
PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND
SN 0017-0011
EI 2543-6767
J9 GINEKOL POL
JI Ginekol. Pol.
PY 2015
VL 86
IS 12
BP 890
EP 895
DI 10.17772/gp/60708
PG 6
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA CZ2QB
UT WOS:000366948600002
PM 26995937
OA Green Submitted, gold
DA 2025-04-10
ER

PT J
AU Tharp, WG
   Lee, YH
   Greene, SM
   Vincellete, E
   Beach, TG
   Pratley, RE
AF Tharp, William G.
   Lee, Yong-Ho
   Greene, Shane M.
   Vincellete, Elise
   Beach, Thomas G.
   Pratley, Richard E.
TI Measurement of Altered AβPP Isoform Expression in Frontal Cortex of
   Patients with Alzheimer's Disease by Absolute Quantification Real-Time
   PCR
SO JOURNAL OF ALZHEIMERS DISEASE
LA English
DT Article
DE Alternative splicing; Alzheimer's disease (AD); amyloid-beta (A beta);
   amyloid-beta protein precursor (A beta PP); dementia; kunitz; polymerase
   chain reaction
ID AMYLOID PRECURSOR PROTEIN; CEREBRAL THROMBOSIS; BRAIN; APP; DEPOSITION;
   ADIPOCYTES; RELEVANCE; CELLS
AB Enzymatic cleavage of amyloid-beta protein precursor (A beta PP) produces amyloid-beta (A beta) peptides which form the insoluble cortical plaques characteristic of Alzheimer's disease (AD). A beta PP is post-transcriptionally processed into three major isoforms with differential cellular and tissue expression patterns. Changes in A beta PP isoform expression may be indicative of disease pathogenesis in AD, but accurately measuring A beta PP gene isoforms has been difficult to standardize, reproduce, and interpret. In light of this, we developed a set of isoform specific absolute quantification real time PCR standards that allow for quantification of transcript copy numbers for total A beta PP and all three major isoforms (A beta PP695, A beta PP751, and A beta PP770) in addition to glyceraldehyde-3-dehydrogenase (GAPDH) and examined expression patterns in superior frontal gyrus (SFG) and cerebellar samples from patients with (n = 12) and without AD (n = 10). Both total A beta PP and A beta PP695 transcripts were significantly decreased in SFG of patients with AD compared to control (p = 0.037 and p = 0.034, respectively). A beta PP751 and A beta PP770 transcripts numbers were not significantly different between AD and control (p > 0.15). There was trend for decreased percentage A beta PP695 (p = 0.051) and increased percentage A beta PP770 (p = 0.013) expression in SFG of patients with AD. GAPDH transcripts levels were also decreased significantly in the SFG of patients with AD compared to control (p = 0.005). Decreasing total A beta PP and A beta PP695 copy number was associated with increased plaque burden and decreased cognitive function. In this study we describe a simple procedure for measuring A beta PP isoform transcripts by real-time PCR and confirm previous studies showing altered A beta PP isoform expression patterns in AD.
C1 [Pratley, Richard E.] Florida Hosp, Inst Diabet, Orlando, FL 32804 USA.
   [Pratley, Richard E.] Sanford Burnham Res Inst, Orlando, FL USA.
   [Tharp, William G.; Greene, Shane M.; Vincellete, Elise; Pratley, Richard E.] Univ Vermont, Dept Med, Burlington, VT USA.
   [Lee, Yong-Ho] Catholic Univ, Dept Biomed Sci, Taegu, South Korea.
   [Beach, Thomas G.] Banner Sun Hlth Res Inst, Phoenix, AZ USA.
C3 Adventist Health Services; AdventHealth; Sanford Burnham Prebys Medical
   Discovery Institute; University of Vermont; Catholic University of
   Korea; Banner Research; Banner Health; Banner Sun Health Research
   Institute
RP Pratley, RE (corresponding author), Florida Hosp, Inst Diabet, 2415 N Orange Ave, Orlando, FL 32804 USA.
EM Richard.Pratley@flhosp.org
RI Lee, Youngil/AAX-2787-2021
FU National Institute of Neurological Disorders and Stroke [U24 NS072026];
   National Institute on Aging (Arizona Alzheimer's Disease Core Center)
   [P30 AGI9610]; Arizona Department of Health Services (Arizona
   Alzheimer's Research Center) [211002]; Arizona Biomedical Research
   Commission (Arizona Parkinson's Disease Consortium) [4001, 0011, 05-901,
   1001]; Michael J. Fox Foundation for Parkinson's Research
FX The Brain and Body Donation Program is supported by the National
   Institute of Neurological Disorders and Stroke (U24 NS072026 National
   Brain and Tissue Resource for Parkinson's Disease and Related
   Disorders), the National Institute on Aging (P30 AGI9610 Arizona
   Alzheimer's Disease Core Center), the Arizona Department of Health
   Services (contract 211002, Arizona Alzheimer's Research Center), the
   Arizona Biomedical Research Commission (contracts 4001, 0011, 05-901 and
   1001 to the Arizona Parkinson's Disease Consortium) and the Michael J.
   Fox Foundation for Parkinson's Research.
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NR 30
TC 13
Z9 13
U1 0
U2 3
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1387-2877
EI 1875-8908
J9 J ALZHEIMERS DIS
JI J. Alzheimers Dis.
PY 2012
VL 29
IS 2
BP 449
EP 457
DI 10.3233/JAD-2011-111337
PG 9
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 916SV
UT WOS:000302124400018
PM 22258516
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Cao, X
   Kambe, F
   Miyazaki, T
   Sarkar, D
   Ohmori, S
   Seo, H
AF Cao, X
   Kambe, F
   Miyazaki, T
   Sarkar, D
   Ohmori, S
   Seo, H
TI Novel human ZAKI-4 isoforms: hormonal and tissue-specific regulation and
   function as calcineurin inhibitors
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE chromosome 6; DSCR1L1; RNA-ligase-mediated 5 '-RACE; thyroid hormone
ID DEPENDENT PROTEIN PHOSPHATASE; SYNDROME CANDIDATE REGION-1;
   DOWN-SYNDROME; INSITU HYBRIDIZATION; CARDIAC-HYPERTROPHY; STRIATED
   MUSCLES; CYCLOSPORINE-A; GENE FAMILY; DATABASE; CALCIUM
AB We identified a thyroid hormone [3,5,3'-tri-iodothyronine (T-3)]-responsive gene, ZAKI-4, in cultured human skin fibroblasts. It belongs to a family of genes that encode proteins containing a conserved motif. The motif binds to calcineurin and inhibits its phosphatase activity. In the present study, we have demonstrated three different ZAKI-4 transcripts, alpha, beta1 and beta2, in human brain by 5'- and 3'-RACE (rapid amplification of cDNA ends). The a transcript was identical with the one that we originally cloned from human fibroblasts and the other two are novel. The three transcripts are generated by alternative initiation and splicing from a single gene on the short arm of chromosome 6. It is predicted that beta1 and beta2 encode an identical protein product, beta, which differs from alpha in its N-terminus. Since alpha and beta contain an identical C-terminal region harbouring the conserved motif, both isoforms are suggested to inhibit calcineurin activity. Indeed, each isoform associates with calcineurin A and inhibits its activity in a similar manner, suggesting that the difference in N-terminus of each isoform does not affect the inhibitory function on calcineurin. An examination of the expression profile of the three transcripts in 12 human tissues revealed that the alpha transcript is expressed exclusively in the brain, whereas beta transcripts are expressed ubiquitously, most abundantly in brain, heart, skeletal muscle and kidney. It was also demonstrated that human skin fibroblasts express both alpha and beta transcripts, raising the question of which transcript is up-regulated by T-3. It was revealed that T-3 markedly induced the expression of alpha isoform but not of beta. This T-3-mediated increase in the alpha isoform was associated with a significant decrease in endogenous calcineurin activity. These results suggest that the expression of ZAKI-4 isoforms is subjected to distinct hormonal as well as tissue-specific regulation, constituting a complex signalling network through inhibition of calcineurin.
C1 Nagoya Univ, Res Inst Environm Med, Div Mol & Cellular Adaptat, Dept Endocrinol & Metab, Nagoya, Aichi 4648601, Japan.
C3 Nagoya University
RP Seo, H (corresponding author), Nagoya Univ, Res Inst Environm Med, Div Mol & Cellular Adaptat, Dept Endocrinol & Metab, Nagoya, Aichi 4648601, Japan.
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NR 44
TC 47
Z9 49
U1 0
U2 0
PU PORTLAND PRESS
PI LONDON
PA 59 PORTLAND PLACE, LONDON W1N 3AJ, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD OCT 15
PY 2002
VL 367
BP 459
EP 466
DI 10.1042/BJ20011797
PN 2
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 607EN
UT WOS:000178778800016
PM 12102656
OA Green Published
DA 2025-04-10
ER

PT J
AU Chen, YR
   Hsiao, NW
   Lee, YZ
   Huang, SS
   Chang, CC
   Tsai, JR
   Lin, HC
   Toullec, JY
   Lee, CY
   Lyu, PC
AF Chen, Yun-Ru
   Hsiao, Nai-Wan
   Lee, Yi-Zong
   Huang, Shiau-Shan
   Chang, Chih-Chun
   Tsai, Jyuan-Ru
   Lin, Hui-Chen
   Toullec, Jean-Yves
   Lee, Chi-Ying
   Lyu, Ping-Chiang
TI Structure-Based Functional Analysis of a Hormone Belonging to an
   Ecdysozoan Peptide Superfamily: Revelation of a Common Molecular
   Architecture and Residues Possibly for Receptor Interaction
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE neuropeptide; peptide hormone; structure-function; <p>Na+/K+-ATPase</p>;
   osmoregulation; tertiary structure; mutant; brachyuran
ID CRUSTACEAN HYPERGLYCEMIC HORMONE; MOLT-INHIBITING HORMONE;
   SCYLLA-SERRATA FORSKAL; AMINO-ACID-SEQUENCE; GREEN SHORE CRAB;
   ION-TRANSPORT; CARCINUS-MAENAS; MUTATIONAL ANALYSIS;
   SECONDARY-STRUCTURE; BIOLOGICAL-ACTIVITY
AB A neuropeptide (Sco-CHH-L), belonging to the crustacean hyperglycemic hormone (CHH) superfamily and preferentially expressed in the pericardial organs (POs) of the mud crab Scylla olivacea, was functionally and structurally studied. Its expression levels were significantly higher than the alternative splice form (Sco-CHH) in the POs, and increased significantly after the animals were subjected to a hypo-osmotic stress. Sco-CHH-L, but not Sco-CHH, significantly stimulated in vitro the Na+, K+-ATPase activity in the posterior (6th) gills. Furthermore, the solution structure of Sco-CHH-L was resolved using nuclear magnetic resonance spectroscopy, revealing that it has an N-terminal tail, three alpha-helices (alpha 2, Gly(9)-Asn(28); alpha 3, His(34)-Gly(38); and alpha 5, Glu(62)-Arg(72)), and a pi-helix (pi 4, Cys(43)-Tyr(54)), and is structurally constrained by a pattern of disulfide bonds (Cys(7)-Cys(43), Cys(23)-Cys(39), and Cys(26)-Cys(52)), which is characteristic of the CHH superfamily-peptides. Sco-CHH-L is topologically most similar to the molt-inhibiting hormone from the Kuruma prawn Marsupenaeus japonicus with a backbone root-mean-square-deviation of 3.12 angstrom. Ten residues of Sco-CHH-L were chosen for alanine-substitution, and the resulting mutants were functionally tested using the gill Na+, K+-ATPase activity assay, showing that the functionally important residues (I2, F3, E45, D69, I71, and G73) are located at either end of the sequence, which are sterically close to each other and presumably constitute the receptor binding sites. Sco-CHH-L was compared with other members of the superfamily, revealing a folding pattern, which is suggested to be common for the crustacean members of the superfamily, with the properties of the residues constituting the presumed receptor binding sites being the major factors dictating the ligand-receptor binding specificity.
C1 [Chen, Yun-Ru; Lee, Yi-Zong; Lyu, Ping-Chiang] Natl Tsing Hua Univ, Inst Bioinformat & Struct Biol, Hsinchu 300044, Taiwan.
   [Hsiao, Nai-Wan; Huang, Shiau-Shan; Chang, Chih-Chun; Lee, Chi-Ying] Natl Changhua Univ Educ, Dept Biol, Changhua 500207, Taiwan.
   [Lee, Yi-Zong] Natl Tsing Hua Univ, Instrument Ctr, Hsinchu 300044, Taiwan.
   [Tsai, Jyuan-Ru; Lin, Hui-Chen] Tunghai Univ, Dept Life Sci, Taichung 407224, Taiwan.
   [Toullec, Jean-Yves] Sorbonne Univ, Fac Sci, Adaptat & Div Milieu Marin AD2M, CNRS UMR 7144,Stn Biol Roscoff, F-29682 Roscoff, France.
   [Lyu, Ping-Chiang] Natl Tsing Hua Univ, Dept Med Sci, Hsinchu 300044, Taiwan.
C3 National Tsing Hua University; National Changhua University of
   Education; National Tsing Hua University; Tunghai University; Centre
   National de la Recherche Scientifique (CNRS); CNRS - Institute of
   Ecology & Environment (INEE); Sorbonne Universite; National Tsing Hua
   University
RP Lyu, PC (corresponding author), Natl Tsing Hua Univ, Inst Bioinformat & Struct Biol, Hsinchu 300044, Taiwan.; Lee, CY (corresponding author), Natl Changhua Univ Educ, Dept Biol, Changhua 500207, Taiwan.; Lyu, PC (corresponding author), Natl Tsing Hua Univ, Dept Med Sci, Hsinchu 300044, Taiwan.
EM chenyrusa@gmail.com; nady@cc.ncue.edu.tw; s942545@go.thu.edu.tw;
   hss.33333@gmail.com; u9120037@imss.hshs.tyc.edu.tw;
   jrtsaibio@thu.edu.tw; hclin@thu.edu.tw; jean-yves.toullec@sb-roscoff.fr;
   bicylee@cc.ncue.edu.tw; pclyu@mx.nthu.edu.tw
RI LIN, HUI-CHEN/AGH-9182-2022
OI Lyu, Ping-Chiang/0000-0002-6824-543X; Lee, Chi-Ying/0000-0002-9591-1370;
   Lin, Hui-Chen/0000-0001-7932-3045; LEE, YI-ZONG/0000-0002-5651-863X;
   TOULLEC, Jean-Yves/0009-0007-5764-9969
FU Ministry of Science and Technology (MOST), Taiwan [AS-CFII-108-112,
   109-2311-B-007-004-MY3, 109-2311-B-018-001];  [108-2311-B-018-001]
FX This research was funded by the Ministry of Science and Technology
   (MOST), Taiwan (109-2311-B-007-004-MY3 to P.-C.L.; 108-2311-B-018-001
   and 109-2311-B-018-001 to C.-Y.L.).
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NR 68
TC 2
Z9 2
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2021
VL 22
IS 20
AR 11142
DI 10.3390/ijms222011142
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA WS6CZ
UT WOS:000715268100001
PM 34681803
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Tang, TT
   Cheng, X
   Truong, B
   Sun, LZ
   Yang, XF
   Wang, H
AF Tang, TingTing
   Cheng, Xiang
   Truong, Billy
   Sun, LiZhe
   Yang, XiaoFeng
   Wang, Hong
TI Molecular basis and therapeutic implications of CD40/CD40L immune
   checkpoint
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE CD40/CD40L; immune checkpoint; molecular basis; effector function;
   therapeutic implications
ID NF-KAPPA-B; ANTI-CD40 MONOCLONAL-ANTIBODY; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
   CD8(+) T-CELLS; PERIPHERAL-BLOOD MONOCYTES; GERMINAL CENTER FORMATION;
   MYELOID DENDRITIC CELLS; NECROSIS-FACTOR-ALPHA; HUMAN CD40 LIGAND;
   PHASE-I
AB The CD40 receptor and its ligand CD40L is one of the most critical molecular pairs of the stimulatory immune checkpoints. Both CD40 and CD40L have a membrane form and a soluble form generated by proteolytic cleavage or alternative splicing. CD40 and CD40L are widely expressed in various types of cells, among which B cells and myeloid cells constitutively express high levels of CD40, and T cells and platelets express high levels of CD40L upon activation. CD40L self-assembles into functional trimers which induce CD40 trimerization and downstream signaling. The canonical CD40/CD40L signaling is mediated by recruitment of TRAFs and NF-kappa B activation, which is supplemented by signal pathways such as PI3K/AKT, MAPKs and JAK3/STATs. CD40/CD40L immune checkpoint leads to activation of both innate and adaptive immune cells via two-way signaling. CD40/CD40L interaction also participates in regulating thrombosis, tissue inflammation, hematopoiesis and tumor cell fate. Because of its essential role in immune activation, CD40/CD40L interaction has been regarded as an attractive immunotherapy target. In recent years, significant advance has been made in CD40/CD40L-targeted therapy. Various types of agents, including agonistic/antagonistic monoclonal antibodies, cellular vaccines, adenoviral vectors and protein antagonist, have been developed and evaluated in early-stage clinical trials for treating malignancies, autoimmune diseases and allograft rejection. In general, these agents have demonstrated favorable safety and some of them show promising clinical efficacy. The mechanisms of benefits include immune cell activation and tumor cell lysis/apoptosis in malignancies, or immune cell inactivation in autoimmune diseases and allograft rejection. This review provides a comprehensive overview of the structure, processing, cellular expression pattern, signaling and effector function of CD40/CD40L checkpoint molecules. In addition, we summarize the progress, targeted diseases and outcomes of current ongoing and completed clinical trials of CD40/CD40L-targeted therapy. (C) 2020 Elsevier Inc. All rights reserved.
C1 [Tang, TingTing; Cheng, Xiang] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Cardiol, Wuhan, Peoples R China.
   [Tang, TingTing; Truong, Billy; Sun, LiZhe; Yang, XiaoFeng; Wang, Hong] Temple Univ, Ctr Metab Dis Res, Lewis Katz Sch Med, Philadelphia, PA 19122 USA.
   [Sun, LiZhe] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Cardiovasc Med, Xian, Peoples R China.
   [Truong, Billy; Yang, XiaoFeng; Wang, Hong] Temple Univ, Lewis Katz Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19122 USA.
C3 Huazhong University of Science & Technology; Pennsylvania Commonwealth
   System of Higher Education (PCSHE); Temple University; Xi'an Jiaotong
   University; Pennsylvania Commonwealth System of Higher Education
   (PCSHE); Temple University
RP Wang, H (corresponding author), Med Educ & Res Bldg,Room 1060 3500 N Broad St, Philadelphia, PA 19140 USA.
EM hong.wang@temple.edu
FU National Institutes of Health (NIH) [HL82774, HL110764, HL130233,
   HL131460, DK104114, DK113775]; National Institute of Diabetes and
   Digestive and Kidney Diseases [R01DK113775] Funding Source: NIH RePORTER
FX This work is supported in part by the National Institutes of Health
   (NIH) grants HL82774, HL110764, HL130233, HL131460, DK104114, DK113775
   and HL131460 to HW.
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NR 224
TC 144
Z9 155
U1 18
U2 91
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
EI 1879-016X
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD MAR
PY 2021
VL 219
AR 107709
DI 10.1016/j.pharmthera.2020.107709
EA FEB 2021
PG 20
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QJ4PT
UT WOS:000619674700002
PM 33091428
OA Green Accepted
DA 2025-04-10
ER

PT J
AU Pretorius, E
   Wallner, B
   Marx, J
AF Pretorius, E.
   Wallner, B.
   Marx, J.
TI Cortisol resistance in conditions such as asthma and the involvement of
   11 β-HSD-2:: A hypothesis
SO HORMONE AND METABOLIC RESEARCH
LA English
DT Review
DE glucocorticoid receptors; mineralocorticoid receptors; cortisol
   resistance; 11 beta-HSD enzyme isoforms
ID HUMAN GLUCOCORTICOID-RECEPTOR; NF-KAPPA-B; PITUITARY-ADRENAL AXIS;
   BETA-HYDROXYSTEROID DEHYDROGENASE; HEAT-SHOCK-PROTEIN; HUMAN
   MINERALOCORTICOID RECEPTOR; 11-BETA-HYDROXYSTEROID DEHYDROGENASE;
   MULTIPLE-SCLEROSIS; MESSENGER-RNA; TRANSCRIPTIONAL ACTIVATION
AB The two types of corticosteroid hormones, the mineralocorticoids and glucocorticoids, act in a complementary manner and are functionally closely linked. Alclosterone and glucocorticoids express their functions through the glucocorticoid receptors (GRs; GR alpha and GR beta) and the mineralocorticoid receptors (MRs). Commercially available steroidal drugs used in conditions such as asthma may act on both GR and MR receptors; although glucocorticoid-receptor agonists play a fundamental role in the treatment of inflammatory conditions, prolonged exposure may have adverse effects such as the development of resistance. Glucocorticoid resistance in such conditions has been observed to be accompanied by a downregulation of GR alpha., a twofold decrease in GR protein half-life, downregulation of GRa mRNA expression, and enhanced expression of GR beta. Other suggestions for glucocorticoid resistance include alternative splicing of the GR gene with subsequent expression of the GR beta protein isoform, defective regulation of gene transcription of the GR gene or GR mutations, defective DNA binding and transactivating domains of the GR. In addition, we would like to suggest that dysregulation of the MR enzyme 11 beta-HSD-2 may be one of the causes of resistance. When expressed in cells with MRs, this enzyme's major role is to prevent permanent. occupancy of MR by glucocorticoid hormones, allowing concentration-dependent binding of aldosterone to MR. However, deficiency of the 11 beta-HSD isoforms (particularly 11 beta-HSD-2) leads to the activation of MRs by glucocorticoids rather than the glucocorticoids interacting With its "normal" receptors, the GRs. We will substantiate on support for our hypothesis in the dysregulation of this enzyme, which is typically associated with significantly higher levels of circulating plasma cortisol and elevated levels of cholesterol, little or no response to systemic glucocorticoids, and problems associated with homeostasis primarily in the distal nephron and distal colon. These are some of the symptoms typically noted in cortisol resistance.
C1 Univ Pretoria, Fac Hlth Sci, Sch Hlth Sci, Dept Anat, ZA-0001 Pretoria, South Africa.
   Univ Vienna, Dept Anthropol, A-1010 Vienna, Austria.
C3 University of Pretoria; University of Vienna
RP Pretorius, E (corresponding author), Univ Pretoria, Fac Hlth Sci, Sch Hlth Sci, Dept Anat, BMW Bldg,POB 2034, ZA-0001 Pretoria, South Africa.
EM resia.pretorius@up.ac.za
RI Wallner, Bernard/B-1089-2009; Pretorius, Etheresia/P-2978-2016
OI Pretorius, Etheresia/0000-0002-9108-2384; wallner,
   bernard/0000-0002-1089-7443
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NR 116
TC 17
Z9 17
U1 0
U2 2
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0018-5043
J9 HORM METAB RES
JI Horm. Metab. Res.
PD JUN
PY 2006
VL 38
IS 6
BP 368
EP 376
DI 10.1055/s-2006-944530
PG 9
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 062SR
UT WOS:000238965300002
PM 16823718
DA 2025-04-10
ER

PT J
AU Fang, SM
   Wang, HX
   Qiu, KH
   Pang, YY
   Li, C
   Liang, XL
AF Fang, Shumei
   Wang, Hanxin
   Qiu, Kaihua
   Pang, Yuanyuan
   Li, Chen
   Liang, Xilong
TI The fungicide pyraclostrobin affects gene expression by altering the DNA
   methylation pattern in Magnaporthe oryzae
SO FRONTIERS IN PLANT SCIENCE
LA English
DT Article
DE Magnaporthe oryzae; pyraclostrobin; gene expression; cytosine
   methylation; adenine methylation
ID MITOCHONDRIAL FISSION; MOLECULAR CHAPERONES; BODY METHYLATION;
   CARDIOLIPIN; RESISTANCE; COMPLEX; HEART; TRYPANOTHIONE; N-6-ADENINE;
   METABOLISM
AB Introduction: Rice blast disease caused by Magnaporthe oryzae has long been the main cause of rice (Oryza sativa L.) yield reduction worldwide. The quinone external inhibitor pyraclostrobin is widely used as a fungicide to effectively control the spread of pathogenic fungi, including M. oryzae. However, M. oryzae can develop resistance through multiple levels of mutation, such as target protein cytb mutation G143A/S, leading to a decrease in the effectiveness of the biocide after a period of application. Therefore, uncovering the possible mutational mechanisms from multiple perspectives will further provide feasible targets for drug development. Methods: In this work, we determined the gene expression changes in M. oryzae in response to pyraclostrobin stress and their relationship with DNA methylation by transcriptome and methylome. Results: The results showed that under pyraclostrobin treatment, endoplasmic reticulum (ER)-associated and ubiquitin-mediated proteolysis were enhanced, suggesting that more aberrant proteins may be generated that need to be cleared. DNA replication and repair processes were inhibited. Glutathione metabolism was enhanced, while lipid metabolism was impaired. The number of alternative splicing events increased. These changes may be related to the elevated methylation levels of cytosine and adenine in gene bodies. Both hypermethylation and hypomethylation of differentially methylated genes (DMGs) mainly occurred in exons and promoters. Some DMGs and differentially expressed genes (DEGs) were annotated to the same pathways by GO and KEGG, including protein processing in the ER, ubiquitin-mediated proteolysis, RNA transport and glutathione metabolism, suggesting that pyraclostrobin may affect gene expression by altering the methylation patterns of cytosine and adenine. Discussion: Our results revealed that 5mC and 6mA in the gene body are associated with gene expression and contribute to adversity adaptation in M. oryzae. This enriched the understanding for potential mechanism of quinone inhibitor resistance, which will facilitate the development of feasible strategies for maintaining the high efficacy of this kind of fungicide.
C1 [Fang, Shumei; Qiu, Kaihua; Li, Chen; Liang, Xilong] Heilongjiang Bayi Agr Univ, Coll Agr, Heilongjiang Plant Growth Regulator Engn Technol R, Daqing, Peoples R China.
   [Fang, Shumei; Wang, Hanxin; Pang, Yuanyuan] Heilongjiang Bayi Agr Univ, Coll Life Sci & Biotechnol, Heilongjiang Prov Key Lab Environm Microbiol & Rec, Daqing, Peoples R China.
C3 Heilongjiang Bayi Agricultural University; Heilongjiang Bayi
   Agricultural University
RP Liang, XL (corresponding author), Heilongjiang Bayi Agr Univ, Coll Agr, Heilongjiang Plant Growth Regulator Engn Technol R, Daqing, Peoples R China.
EM xilongliang@126.com
RI Liang, Xilong/AAD-1326-2022
FU Incubation Subjects of Heilongjiang Bayi Agricultural University
   [XZR2014-01]; Provincial and Natural Science Foundation of Heilongjiang,
   China [C2016047]; PhD research startup foundation of Heilongjiang Bayi
   Agricultural University [XDB-2016-01]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by Incubation Subjects of Heilongjiang Bayi Agricultural University
   [grant number XZR2014-01], the Provincial and Natural Science Foundation
   of Heilongjiang, China [grant number C2016047] and PhD research startup
   foundation of Heilongjiang Bayi Agricultural University [XDB-2016-01].
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   Zhu QH, 2016, MOL PLANT MICROBE IN, V29, P187, DOI 10.1094/MPMI-08-15-0194-FI
   Zilberman D, 2017, GENOME BIOL, V18, DOI 10.1186/s13059-017-1230-2
NR 94
TC 2
Z9 2
U1 10
U2 20
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-462X
J9 FRONT PLANT SCI
JI Front. Plant Sci.
PD APR 30
PY 2024
VL 15
AR 1391900
DI 10.3389/fpls.2024.1391900
PG 16
WC Plant Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences
GA QN6L3
UT WOS:001221589500001
PM 38745924
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Lee, J
   Jefcoate, C
AF Lee, Jinwoo
   Jefcoate, Colin
TI Monitoring of Dual crisPr/cas9Mediated steroidogenic acute regulatory
   Protein gene Deletion and cholesterol accumulation Using high-resolution
   Fluorescence In Situ hybridization in a single cell
SO FRONTIERS IN ENDOCRINOLOGY
LA English
DT Article
DE steroidogenic acute regulatory protein; CRIS PR; fluorescence in situ
   hybridization; cholesterol; lipid droplets
ID HORMONE-SENSITIVE LIPASE; LEYDIG TUMOR-CELLS; LIPOID
   ADRENAL-HYPERPLASIA; STAR EXPRESSION; CONTACT SITES; STIMULATION;
   MECHANISMS; CAS9; RNA; PROKARYOTES
AB Recent advances in fluorescence microscopy, coupled with CRISPR/Cas9 gene editing technology, provide opportunities for understanding gene regulation at the single-cell level. The application of direct imaging shown here provides an in situ side-by-side comparison of CRISPR/Cas9-edited cells and adjacent unedited cells. We apply this methodology to the steroidogenic acute regulatory protein (StAR) gene in Y-1 adrenal cells and MA-10 testis cells. StAR is a gatekeeper protein that controls the access of cholesterol from the cytoplasm to the inner mitochondria. The loss of this mitochondrial cholesterol transfer mediator rapidly increases lipid droplets in cells, as seen in StAR-/-mice. Here, we describe a dual CRISPR/Cas9 strategy marked by GFP/mCherry expression that deletes StAR activity within 12 h. We used single-molecule fluorescence in situ hybridization (sm-FISH) imaging to directly monitor the time course of gene editing in single cells. We achieved StAR gene deletion at high efficiency dual gRNA targeting to the proximal promoter and exon 2. Seventy percent of transfected cells showed a slow DNA deletion as measured by PCR, and loss of Br-cAMP stimulated transcription. This DNA deletion was seen by sm-FISH in both loci of individual cells relative to non-target Cyp11a1 and StAR exon 7. sm-FISH also distinguishes two effects on stimulated StAR expression without this deletion. Br-cAMP stimulation of primary and spliced StAR RNA at the gene loci were removed within 4 h in this dual CRISPR/Cas9 strategy before any effect on cytoplasmic mRNA and protein occurred. StAR mRNA disappeared between 12 and 24 h in parallel with this deletion, while cholesterol ester droplets increased fourfold. These alternative changes match distinct StAR expression processes. This dual gRNA and sm-FISH approach to CRISPR/Cas9 editing facilitates rapid testing of editing strategies and immediate assessment of single-cell adaptation responses without the perturbation of clonal expansion procedures.
C1 [Lee, Jinwoo; Jefcoate, Colin] Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI 53706 USA.
   [Lee, Jinwoo; Jefcoate, Colin] Univ Wisconsin, Endocrinol & Reprod Physiol Program, Madison, WI 53706 USA.
   [Jefcoate, Colin] Univ Wisconsin, Mol & Environm Toxicol Ctr, Madison, WI 53706 USA.
   [Jefcoate, Colin] Univ Wisconsin, Mol & Cellular Pharmacol, Madison, WI 53706 USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison
RP Lee, J; Jefcoate, C (corresponding author), Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI 53706 USA.; Lee, J; Jefcoate, C (corresponding author), Univ Wisconsin, Endocrinol & Reprod Physiol Program, Madison, WI 53706 USA.; Jefcoate, C (corresponding author), Univ Wisconsin, Mol & Environm Toxicol Ctr, Madison, WI 53706 USA.; Jefcoate, C (corresponding author), Univ Wisconsin, Mol & Cellular Pharmacol, Madison, WI 53706 USA.
EM jwlee7@wisc.edu; jefcoate@wisc.edu
FU NIH [RO1 DK074819, RO1 DK090249]; University of Wisconsin School of
   Medicine and Public Health Department of Cell and Regenerative Biology
FX This study was financially supported by NIH (RO1 DK074819, RO1
   DK090249). This research was also supported by funding from the
   University of Wisconsin School of Medicine and Public Health Department
   of Cell and Regenerative Biology.
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NR 56
TC 5
Z9 5
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
   SWITZERLAND
SN 1664-2392
J9 FRONT ENDOCRINOL
JI Front. Endocrinol.
PD OCT 25
PY 2017
VL 8
AR 289
DI 10.3389/fendo.2017.00289
PG 18
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA FK6SB
UT WOS:000413634400001
PM 29118738
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Shimano, H
   Horton, JD
   Shimomura, I
   Hammer, RE
   Brown, MS
   Goldstein, JL
AF Shimano, H
   Horton, JD
   Shimomura, I
   Hammer, RE
   Brown, MS
   Goldstein, JL
TI Isoform 1c of sterol regulatory element binding protein is less active
   than isoform 1a in livers of transgenic mice and in cultured cells
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE SREBP-1; alternative splicing; cholesterol; fatty acids; transgenic mice
ID LIPOPROTEIN RECEPTOR PROMOTER; LEUCINE ZIPPER PROTEIN;
   MOLECULAR-CLONING; SYNTHASE GENE; TRANSCRIPTION; ACID; IDENTIFICATION;
   SREBP-1; ACTIVATION; EXPRESSION
AB We have produced transgenic mice whose livers express a dominant positive NH2-terminal fragment of sterol regulatory element binding protein-1c (SREBP-1c). Unlike full-length SREBP-1c, the NH2-terminal fragment enters the nucleus without a requirement for proteolytic release from cell membranes, and hence it is immune to downregulation by sterols, We compared SREBP-1c transgenic mice with a line of transgenic mice that produces an equal amount of the NH2-terminal fragment of SREBP-1a. SREBP-1a and -1c are alternate transcripts from a single gene that differ in the first exon, which encodes part of an acidic activation domain. The 1a protein contains a long activation domain with 12 negatively charged amino acids, whereas the 1c protein contains a short activation domain with only 6 such amino acids. As previously reported, livers of the SREBP-1a transgenic mice were massively enlarged, owing to accumulation of triglycerides and cholesterol, SREBP-1c transgenic livers were only slightly enlarged with only a moderate increase in triglycerides, but not cholesterol, The mRNAs for the LDL receptor and several cholesterol biosynthetic enzymes were elevated in SREBP-1a transgenic mice, but not in 1c transgenic mice. The mRNAs for fatty acid synthase and acetyl CoA carboxylase were elevated 9- and 16-fold in 1a animals, but only 2- and 4-fold in 1c animals. Experiments with transfected cells confirmed that SREBP-1c is a much weaker activator of transcription than SREBP-1a when both are expressed at levels approximating those found in nontransfected cells, SREBP-1c became a strong activator only when expressed at supraphysiologic levels, We conclude that SREBP-1a is the most active form of SREBP-1 and that SREBP-1c may be produced when cells require a lower rate of transcription of genes regulating cholesterol and fatty acid metabolism.
C1 UNIV TEXAS,SW MED CTR,DEPT MOL GENET,DALLAS,TX 75235.
   UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235.
   UNIV TEXAS,SW MED CTR,HOWARD HUGHES MED INST,DALLAS,TX 75235.
C3 University of Texas System; University of Texas Dallas; University of
   Texas Southwestern Medical Center Dallas; University of Texas System;
   University of Texas Southwestern Medical Center Dallas; University of
   Texas Dallas; University of Texas System; University of Texas Dallas;
   Howard Hughes Medical Institute; University of Texas Southwestern
   Medical Center Dallas
RI Shimano, Hitoshi/V-1761-2019
OI Shimano, Hitoshi/0000-0002-5562-5572; Hammer, Robert
   E./0000-0001-5487-7551
FU NHLBI NIH HHS [HL-20948] Funding Source: Medline
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NR 33
TC 697
Z9 807
U1 2
U2 31
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD MAR 1
PY 1997
VL 99
IS 5
BP 846
EP 854
DI 10.1172/JCI119248
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA WN152
UT WOS:A1997WN15200007
PM 9062341
OA Green Published, Bronze
DA 2025-04-10
ER

PT J
AU Shaw, JB
   Cai, Q
   Mtshali, C
   Myles, EL
   Washington, B
AF Shaw, J. B.
   Cai, Q.
   Mtshali, C.
   Myles, E. L.
   Washington, B.
TI Heterogeneity of histamine H3 receptor genomic expression in
   the cerebral cortex of spontaneously hypertensive rat
SO CELLULAR AND MOLECULAR BIOLOGY
LA English
DT Article
DE alternative splicing; gene expression; histamine H-3 receptor; third
   intracellular loop; RT-PCR
ID PHARMACOLOGICAL CHARACTERIZATION; BINDING SITES; MESSENGER-RNA; CLONING;
   ISOFORMS; BRAIN; ORGANIZATION; IDENTIFICATION; PROFILES; GENE
AB Specific binding of [3H]-N-alpha-methylhistamine to homogenates from cerebral cortex tissue was analyzed in aged Wistar Kyoto (WKY) and Spontaneously Hypertensive rats (SHR). Scatchard plot analysis of [3H]-N-alpha-methylhistamine binding of the H-3 receptor in the cerebral cortex from aged ( 6, 9, 12, and 16 week) SHR animals indicated that Bmax increased, respectively, 38.05 +/- 1.58, 59.63 +/- 2.48, 79.17 +/- 5.02, and 84.41 +/- 3.72 fmol/mg of protein. Binding studies using tissue from WKY rats indicated that maximal binding ( Bmax) of the ligand to the receptor was not significantly altered. The analyses also yielded Kd values of 5, 7.2, 6.3 and 3.8 nM in SHR tissue respectively. Primers based on the sequence of the third intracellular loop of the H3 receptor were amplified at 35 cycles yielding several amplicons. These amplicons expressed sizes 875, 485, and 280 bp in 6 and 9 week cortical tissue from WKY animals where as in cortical tissue from 6 and 9 week SHR animals only two amplicons were expressed, 485 and 280 bp, respectively. Differences in gene expression for 12 and 16 week WKY and SHR rats were also compared using identical primers. Five amplicons were expressed in cortical tissue from 12 and 16 week WKY rats with 1000, 900, 821, 485, and 430 bp where as in 12 and 16 week SHR animals only one amplicon was expressed at 485 bp. The present results imply ( 1) that H3 receptor density in cortical tissue of SHR animals increases with age where as the number of the expressed amplicons of the detected H3 receptor decreases; and ( 2) even though a decrease in number of expressed amplicons of the H3 receptor were observed, an increase in expression of the larger amplicon (similar to 500 bp) is evident.
C1 Tennessee State Univ, Dept Biol Sci, Nashville, TN 37209 USA.
C3 Tennessee State University
RP Washington, B (corresponding author), Tennessee State Univ, Dept Biol Sci, Nashville, TN 37209 USA.
EM bwashington@tnstate.edu
FU NCRR NIH HHS [RR11808] Funding Source: Medline
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NR 28
TC 2
Z9 2
U1 0
U2 0
PU C M B  ASSOC
PI POITIERS
PA 40 AVENUE  RECTEUR PINEAU,  BAT MECANIQUE, 86022 POITIERS, FRANCE
SN 0145-5680
J9 CELL MOL BIOL
JI Cell. Mol. Biol.
PY 2007
VL 53
IS 4
BP 45
EP 50
DI 10.1170/T807
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 197JH
UT WOS:000248550400008
PM 17531160
DA 2025-04-10
ER

PT J
AU Fleck, D
   Garratt, AN
   Haass, C
   Willem, M
AF Fleck, Daniel
   Garratt, Alistair N.
   Haass, Christian
   Willem, Michael
TI BACE1 Dependent Neuregulin Processing: Review
SO CURRENT ALZHEIMER RESEARCH
LA English
DT Article
DE Alzheimer's disease; A beta; APP; BACE1; neuregulin; schizophrenia;
   secretase
ID AMYLOID PRECURSOR PROTEIN; ALPHA-CONVERTING-ENZYME; PERIPHERAL
   NERVOUS-SYSTEM; MELTRIN-BETA ADAM19; ALZHEIMERS-DISEASE; HEART
   DEVELOPMENT; CARDIAC DEVELOPMENT; SECRETASE CLEAVAGE; GAMMA-SECRETASE;
   SCHWANN-CELL
AB Neuregulin-1 (NRG1), known also as heregulin, acetylcholine receptor inducing activity (ARIA), glial growth factor (GGF), or sensory and motor neuron derived factor (SMDF), plays essential roles in several developmental processes, and is required also later in life. Many variants of NRG1 are produced via alternative splicing and usage of distinct promoters. All contain an epidermal growth factor (EGF)-like domain, which alone is sufficient to bind and activate the cognate receptors, members of the ErbB family. NRG1 mediated signaling is crucial for cardiogenesis and the development of the mammary gland and ErbB2 (HER2), an orphan co-receptor for NRG1 is the target of the drug Herceptin (R) (trastuzumab) used for treatment of metastatic breast cancer. In the nervous system, NRG1 controls the early development of subpopulations of neural crest cells. In particular, NRG1 acts as an essential paracrine signaling molecule expressed on the axonal surface, where it signals to Schwann cells throughout development and regulates the thickness of the myelin sheath. NRG1 is required also by other cell types in the nervous system, for instance as an axonal signal released by proprioceptive afferents to induce development of the muscle spindle, and it controls aspects of cortical interneuron development as well as the formation of thalamocortical projections. Work from several laboratories implicates dysregulation of NRG1/ErbB4 signaling in the etiology of schizophrenia. Biochemical studies have shown that the precursor proteins of NRG1 can be released from the membrane through limited proteolysis. In addition, most NRG1 isoforms contain a transmembrane domain, which is processed by gamma-secretase after shedding. Thereby the intracellular domain is released into the cytoplasm. Despite this, the importance of NRG1 cleavage for its functions in vivo remained unclear until recently. beta-Secretase (beta-site amyloid precursor protein cleaving enzyme 1, BACE1) was first identified through its function as the rate limiting enzyme of amyloid-beta-peptide (A beta) production. A beta is the major component of amyloid plaques in Alzheimer's disease (AD). More recently it was shown that Neuregulin-1 is a major physiological substrate of BACE1 during early postnatal development. Mutant mice lacking BACE1 display severe hypomyelination of peripheral nerves similar to that seen in mice lacking NRG1/ErbB signaling in Schwann cells, and a BACE1-dependent activation of NRG1 in the process of peripheral myelination was proposed. Here we summarize the current knowledge about the role of NRG1 proteolysis for ErbB receptor mediated signaling during development and in Alzheimer's disease.
C1 [Fleck, Daniel; Haass, Christian; Willem, Michael] Univ Munich, German Ctr Neurodegenert Dis DZNE, D-80336 Munich, Germany.
   [Fleck, Daniel; Haass, Christian; Willem, Michael] Univ Munich, Adolf Butenandt Inst, D-80336 Munich, Germany.
   [Garratt, Alistair N.] Max Delbruck Ctr Mol Med, D-13125 Berlin, Germany.
C3 Helmholtz Association; German Center for Neurodegenerative Diseases
   (DZNE); University of Munich; University of Munich; Helmholtz
   Association; Max Delbruck Center for Molecular Medicine
RP Willem, M (corresponding author), Univ Munich, German Ctr Neurodegenert Dis DZNE, D-80336 Munich, Germany.
EM Michael.Willem@med.uni-muenchen.de
RI Garratt, Alistair/HGC-0774-2022; Haass, Christian/ADX-5077-2022;
   Garratt, Alistair/D-9893-2013
OI Willem, Michael/0000-0001-8829-3802; Garratt,
   Alistair/0000-0001-9631-3041
FU Deutsche Forschungsgemeinschaft (DFG); Leibniz Award; National Genome
   Research Network (NGFNplus); Helmholtz Alliance for Mental Health and
   Ageing (HELMA); Virtual Institute Neurodegeneration Ageing; Breuer
   foundation; Forschungsprofessur of the Ludwig-Maximilians-University; 
   [SFB596];  [A9]
FX The authors thank Dr. Sven Lammich for comments on the manuscript. This
   work was supported by the Deutsche Forschungsgemeinschaft (DFG), the
   Leibniz Award (to C. H.), the SFB596 (Project A9, to C. H. and M. W.),
   the National Genome Research Network (NGFNplus, to C. H. and A.N.G.),
   the Helmholtz Alliance for Mental Health and Ageing (HELMA, to C. H. and
   M. W.) and the Virtual Institute Neurodegeneration & Ageing (to C. H.),
   the Breuer foundation (stipendium to D. F.). C. H. is supported by a
   Forschungsprofessur of the Ludwig-Maximilians-University.
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NR 82
TC 58
Z9 66
U1 0
U2 19
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1567-2050
J9 CURR ALZHEIMER RES
JI Curr. Alzheimer Res.
PD FEB
PY 2012
VL 9
IS 2
BP 178
EP 183
DI 10.2174/156720512799361637
PG 6
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 941YX
UT WOS:000304006900005
PM 22455478
DA 2025-04-10
ER

PT J
AU Andreae, EA
   Warejcka, DJ
   Twining, SS
AF Andreae, Emily A.
   Warejcka, Debra J.
   Twining, Sally S.
TI Thrombin alters the synthesis and processing of CYR61/CCN1 in human
   corneal stromal fibroblasts and myofibroblasts through multiple distinct
   mechanisms
SO MOLECULAR VISION
LA English
DT Article
ID MATRICELLULAR PROTEIN CCN1; TISSUE GROWTH-FACTOR;
   MATRIX-METALLOPROTEINASE; PLASMINOGEN-ACTIVATOR; CELL-ADHESION;
   CATHEPSIN S; EXPRESSION; RECEPTOR; MIGRATION; GENE
AB Purpose: Previous research in our laboratory indicated that prothrombin and other coagulation enzymes required to activate prothrombin to thrombin are synthesized by the cornea and that apoptotic human corneal stromal cells can provide a surface for prothrombin activation through the intrinsic and extrinsic coagulation pathways. The purpose of the work reported here is to study the role of thrombin activity in the regulation of matricellular protein Cyr61 (CCN1) produced by wounded phenotype human corneal stromal fibroblasts and myofibroblasts.
   Methods: Stromal cells from human donor corneas were converted to defined wounded phenotype fibroblasts and myofibroblasts with fetal bovine serum, followed by basic fibroblast growth factor (bFGF) and transforming growth factor beta-1 (TGF beta-1), respectively, and stimulated with varying concentrations (0-10.0 units (U)/ml) of thrombin from 1-7 h. Cyr61 transcript levels were determined using reverse transcriptase-PCR (RT-PCR) and quantitative PCR (qPCR) while protein forms were analyzed using western blot data. Protease activities were characterized via protease class- specific inhibitors and western blot analysis. Thrombin activity was quantified using the fluorogenic peptide Phe-Pro-Arg-AFC. Protease-activated receptor (PAR) agonist peptides-1 and -4 were used to determine whether cells increased Cyr61 through PAR signaling pathways. The PAR-1 antagonist SCH 79797 was used to block the thrombin cleavage of the receptor. PCR data were analyzed using MxPro software and western blot data were analyzed using Image Lab (TM) and Image J software. Student t test and one- and two-way ANOVA (with or without ranking, depending on sample distribution), together with Dunnett's test or Tukey comparison tests for post-hoc analysis, were used to determine statistical significance.
   Results: Full-length Cyr61 is expressed by human corneal stromal fibroblasts and myofibroblasts and is significantly upregulated by active thrombin stimulation at the message (p<0.03) and protein (p<0.03) levels for fibroblasts and myofibroblasts. Inhibition by the allosteric thrombin-specific inhibitor hirudin prevented the thrombin-associated increase in the Cyr61 protein expression, indicating that the proteolytic activity of thrombin is required for the increase of the Cyr61 protein level. PAR-1 agonist stimulation of fibroblasts and myofibroblasts significantly increased cell-associated Cyr61 protein levels (p<0.04), and PAR-1 antagonist SCH 79797 significantly inhibited the thrombin stimulated increase of Cyr61 in fibroblasts but not in myofibroblasts. In the fibroblast and myofibroblast conditioned media, Cyr61 was detected as the full-length 40 kDa protein in the absence of thrombin, and mainly at 24 kDa in the presence of thrombin at >= 0.5 U/ml, using an antibody directed toward the internal linker region between the von Willebrand factor type C and thrombospondin type-1 domains. Although known to undergo alternative splicing, Cyr61 that is synthesized by corneal fibroblasts and myofibroblasts is not alternatively spliced in response to thrombin stimulation nor is Cyr61 directly cleaved by thrombin to generate its 24 kDa form; instead, Cyr61 is proteolytically processed into 24 kDa N- and 16 kDa C-terminal fragments by a thrombin activated leupeptin-sensitive protease present in conditioned media with activity distinct from the proteolytic activity of thrombin.
   Conclusions: In cultured human corneal stromal fibroblasts and myofibroblasts, thrombin regulates Cyr61 through two mechanisms: 1) thrombin increases the Cyr61 expression at the message and protein levels, and 2) thrombin increases the activation of a leupeptin-sensitive protease that stimulates the cleavage of Cyr61 into N- and C-terminal domain populations in or near the thrombospondin type-1 domain. Generation of Cyr61 peptides during corneal injury stimulation may reveal additional functions of the protein, which modulate corneal wound healing activities or decrease activities of the full-length Cyr61 form.
C1 [Andreae, Emily A.; Warejcka, Debra J.; Twining, Sally S.] Med Coll Wisconsin, Dept Biochem, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
   [Andreae, Emily A.] Marshfield Clin Res Inst, Marshfield, WI USA.
   [Twining, Sally S.] Med Coll Wisconsin, Dept Ophthalmol, Milwaukee, WI 53226 USA.
C3 Medical College of Wisconsin; Medical College of Wisconsin
RP Twining, SS (corresponding author), Med Coll Wisconsin, Dept Biochem, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM stwining@mcw.edu
FU National Institutes of Health (NIH) [R0EY012731, R0EY021152, P3EY001931,
   T32EY014537]; Research for the Prevention of Blindness (RPB), Inc.;
   National Eye Institute [T32EY014537] Funding Source: NIH RePORTER
FX Funding for this study was provided by National Institutes of Health
   (NIH) Grant R0EY012731 and R0EY021152, P3EY001931, and T32EY014537, and
   an unrestricted grant from Research for the Prevention of Blindness
   (RPB), Inc. Conflict of Interest Disclosure: The authors have no
   personal or financial conflicts of interest to disclose. Presentations:
   Portions of this work were presented at the Association for Research in
   Vision and Ophthalmology (ARVO) Annual Meeting years 2009 and 2013 and
   at the 2009 Medical College of Wisconsin Annual Research Day in
   Milwaukee, Wisconsin.
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NR 86
TC 1
Z9 1
U1 0
U2 5
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
   ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD JUL 29
PY 2020
VL 26
BP 540
EP 562
PG 23
WC Biochemistry & Molecular Biology; Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Ophthalmology
GA MT5CO
UT WOS:000554990000001
PM 32818017
DA 2025-04-10
ER

PT J
AU Solís, C
   Thompson, WC
   Peña, JR
   McDermott-Roe, C
   Langa, P
   Warren, CM
   Chrzanowska, M
   Wolska, BM
   Solaro, RJ
   Detombe, P
   Goldspink, PH
AF Solis, Christopher
   Thompson, Walter C. C.
   Pena, James R. R.
   McDermott-Roe, Christopher
   Langa, Paulina
   Warren, Chad M. M.
   Chrzanowska, Magdalena
   Wolska, Beata M. M.
   Solaro, R. John
   Detombe, Pieter H.
   Goldspink, Paul
TI Mechano-growth factor E-domain modulates cardiac contractile function
   through 14-3-3 protein interactomes
SO FRONTIERS IN PHYSIOLOGY
LA English
DT Article
DE mechano-growth factor; E-domain peptide; 14-3-3 protein; contractile
   function of the heart; protein-protein interaction (PPI)
ID ORPHAN NUCLEAR RECEPTOR; SKELETAL-MUSCLE CELLS; BINDING-PROTEIN;
   INHIBITORY INTERACTION; STRUCTURAL BASIS; GENE-EXPRESSION; E-PEPTIDES;
   IGF-I; INSULIN; PHOSPHORYLATION
AB In the heart, alternative splicing of the igf-I gene produces two isoforms: IGF-IEa and IGF-IEc, (Mechano-growth factor, MGF). The sequence divergence between their E-domain regions suggests differential isoform function. To define the biological actions of MGF's E-domain, we performed in silico analysis of the unique C-terminal sequence and identified a phosphorylation consensus site residing within a putative 14-3-3 binding motif. To test the functional significance of Ser 18 phosphorylation, phospho-mimetic (S/E-18) and phospho-null (S/A(18)) peptides were delivered to mice at different doses for 2 weeks. Cardiovascular function was measured using echocardiography and a pressure-volume catheter. At the lowest (2.25 mg/kg/day) and highest (9 mg/kg/day) doses, the peptides produced a depression in systolic and diastolic parameters. However, at 4.5 mg/kg/day the peptides produced opposing effects on cardiac function. Fractional shortening analysis also showed a similar trend, but with no significant change in cardiac geometry. Microarray analysis discovered 21 genes (FDR p < 0.01), that were expressed accordant with the opposing effects on contractile function at 4.5 mg/kg/day, with the nuclear receptor subfamily 4 group A member 2 (Nr4a2) identified as a potential target of peptide regulation. Testing the regulation of the Nr4a family, showed the E-domain peptides modulate Nr4a gene expression following membrane depolarization with KCl in vitro. To determine the potential role of 14-3-3 proteins, we examined 14-3-3 isoform expression and distribution. 14-3-3 gamma localized to the myofilaments in neonatal cardiac myocytes, the cardiac myocytes and myofilament extracts from the adult heart. Thermal shift analysis of recombinant 14-3-3 gamma protein showed the S/A(18) peptide destabilized 14-3-3 gamma folding. Also, the S/A(18) peptide significantly inhibited 14-3-3 gamma's ability to interact with myosin binding protein C (MYPC3) and phospholamban (PLN) in heart lysates from dobutamine injected mice. Conversely, the S/E-18 peptide showed no effect on 14-3-3 gamma stability, did not inhibit 14-3-3 gamma's interaction with PLN but did inhibit the interaction with MYPC3. Replacing the glutamic acid with a phosphate group on Ser 18 (pSer(18)), significantly increased 14-3-3 gamma protein stability. We conclude that the state of Ser 18 phosphorylation within the 14-3-3 binding motif of MGF's E-domain, modulates protein-protein interactions within the 14-3-3 gamma interactome, which includes proteins involved in the regulation of contractile function.
C1 [Solis, Christopher; Thompson, Walter C. C.; Langa, Paulina; Warren, Chad M. M.; Solaro, R. John; Detombe, Pieter H.; Goldspink, Paul] Univ Illinois, Dept Physiol & Biophys, Chicago, IL 60607 USA.
   [Pena, James R. R.; Solaro, R. John; Goldspink, Paul] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA.
   [McDermott-Roe, Christopher] Univ Penn, Perelman Sch Med, Cardiovasc Inst, Dept Med, Philadelphia, PA USA.
   [McDermott-Roe, Christopher] Univ Penn, Perelman Sch Med, Cardiovasc Inst, Dept Genet, Philadelphia, PA USA.
   [Langa, Paulina; Warren, Chad M. M.; Wolska, Beata M. M.] Univ Illinois, Ctr Cardiovasc Res, Chicago, IL USA.
   [Chrzanowska, Magdalena] Med Coll Wisconsin, Blood Res Inst, Cardiovasc Ctr, Dept Pharmacol & Toxicol,Versiti, Milwaukee, WI USA.
   [Wolska, Beata M. M.] Univ Illinois, Dept Med, Div Cardiol, Chicago, IL USA.
   [Detombe, Pieter H.] Univ Montpellier, Phymedexp, Inserm, CNRS, Montpellier, France.
C3 University of Illinois System; University of Illinois Chicago;
   University of Illinois Chicago Hospital; Medical College of Wisconsin;
   University of Pennsylvania; University of Pennsylvania; University of
   Illinois System; University of Illinois Chicago; University of Illinois
   Chicago Hospital; Medical College of Wisconsin; Versiti Blood Center of
   Wisconsin; University of Illinois System; University of Illinois
   Chicago; University of Illinois Chicago Hospital; Institut National de
   la Sante et de la Recherche Medicale (Inserm); Universite de
   Montpellier; Centre National de la Recherche Scientifique (CNRS)
RP Goldspink, PH (corresponding author), Univ Illinois, Dept Physiol & Biophys, Chicago, IL 60607 USA.; Goldspink, PH (corresponding author), Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA.
EM pgolds@uic.edu
RI Solis-Ocampo, Chrisopher/Q-3252-2019
OI Solis-Ocampo, Chrisopher/0000-0003-4584-7363
FU National Institutes Health K99; American Heart Association Postdoctoral
   Fellowship [HL151825];  [AHA834691];  [P01 HL062426];  [R01 HL158634]; 
   [R01 HL157893]
FX Funding This work was supported National Institutes Health K99 HL151825
   (CS), American Heart Association Postdoctoral Fellowship, AHA834691
   (PL), P01 HL062426 (PdT, RJS), R01 HL158634 (BW, RJS, PG) and R01
   HL157893 (MC, PG).
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NR 71
TC 0
Z9 0
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-042X
J9 FRONT PHYSIOL
JI Front. Physiol.
PD NOV 16
PY 2022
VL 13
AR 1028345
DI 10.3389/fphys.2022.1028345
PG 24
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 6R6TP
UT WOS:000892433700001
PM 36467694
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU García-Fernández, M
   Gutiérrez-Gil, B
   Garcia-Gámez, E
   Arranz, JJ
AF Garcia-Fernandez, Marta
   Gutierrez-Gil, Beatriz
   Garcia-Gamez, Elsa
   Arranz, Juan J.
TI Identification of single nucleotide polymorphisms in the ovine
   acetyl-CoA carboxylase-alpha gene
SO SMALL RUMINANT RESEARCH
LA English
DT Article
DE Sheep; Acetyl-CoA carboxylase; Single nucleotide polymorphisms; Genetic
   variability
ID FATTY-ACID-COMPOSITION; PROMOTER-I; PHOSPHORYLATION; ASSOCIATION;
   EXPRESSION; UPSTREAM; SEQUENCE; MOTIF; GOAT; AMP
AB Acetyl-CoA carboxylase (ACACA) is the rate-limiting enzyme in the biosynthesis of palmitic acid and long-chain fatty acids. The dietary intake of palmitic acid, which represents approximately 22% of sheep milk fatty acids, increases low-density lipoprotein (LDL) levels and the risk of developing human cardiovascular diseases. Following the candidate gene approach for improving sheep milk composition, and as a first step in assessing the possible influence of the ovine ACACA gene on milk fatty acid composition and its potential use as an animal genetic model of human atherosclerosis disease, we present here an investigation into the genetic variability of the ovine ACACA gene. We sequenced approximately 6.6 kb of ovine ACACA cDNA, including most of the coding sequence of the protein (except 348 bp), in Spanish Churra sheep. A total of 22 synonymous single nucleotide polymorphisms (SNPs) were identified in the analysed sequence, which were genotyped in a set of eight sheep breeds with different productive aptitudes (dairy, meat and double aptitudes). Two of the SNPs identified, SNP03 (c.1450T>C) and SNP15 (c.5134T>C), which appeared to be breed-specific variations, were situated in the gene sequence coding for the biotin-carboxylase (BC) and acetyl-CoA carboxyltransferase (ACCT) domains of the protein, respectively. Particularly interesting is SNP12 (c.4579G>A), which displayed higher frequencies in the dairy-specialised breeds relative to the meat-producing breeds. Moreover, in the dairy breeds studied, the frequency of this SNP showed a positive correlation with the degree of dairy specialisation. A previously described alternative splicing site (Ser-1200) affecting an important regulatory region of the enzyme was observed in one of the Churra animals. Despite the high genetic variability observed in this gene, none of the identified SNPs caused an amino acid change. However, these polymorphisms could be in linkage disequilibrium with other mutations showing a functional effect on the ACACA enzyme. Hence, the characterisations of the allelic variants reported herein lay the groundwork for evaluation of the potential use of these SNPs as genetic markers of fat content and fatty acid composition in sheep dairy products. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Garcia-Fernandez, Marta; Gutierrez-Gil, Beatriz; Garcia-Gamez, Elsa; Arranz, Juan J.] Univ Leon, Fac Vet, Dept Anim Prod, E-24071 Leon, Spain.
C3 Universidad de Leon
RP Arranz, JJ (corresponding author), Univ Leon, Fac Vet, Dept Anim Prod, Campus Vegazana, E-24071 Leon, Spain.
EM jjarrs@unileon.es
RI Garcia-Gamez, Elsa/D-9158-2011; Gutierrez, Beatriz/AAU-1711-2021;
   /H-1225-2015
OI Gutierrez-Gil, Beatriz/0000-0001-7990-5723; /0000-0001-9058-131X
FU Spanish Ministry of Science [AGL2005-04321]; Castilla and Leon regional
   government (junta de Castilla y Leon) [GR43]; Spanish Ministry of
   Education
FX This work was supported by the Spanish Ministry of Science (Project
   AGL2005-04321) and the Castilla and Leon regional government (junta de
   Castilla y Leon) by a grant for research groups of excellence (Project
   GR43). Marta Garcia-Fernandez is funded by an FPI contract from the
   Spanish Ministry of Science. Beatriz Gutierrez-Gil is funded by the
   "Juan de la Cierva Program" of the Spanish Ministry of Science. Elsa
   Garcia-Gamez is funded by an FPU contract from Spanish Ministry of
   Education.
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NR 34
TC 9
Z9 11
U1 0
U2 11
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0921-4488
EI 1879-0941
J9 SMALL RUMINANT RES
JI Small Ruminant Res.
PD MAY
PY 2010
VL 90
IS 1-3
BP 34
EP 40
DI 10.1016/j.smallrumres.2009.12.010
PG 7
WC Agriculture, Dairy & Animal Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture
GA 599AP
UT WOS:000277882500005
DA 2025-04-10
ER

PT J
AU Yue, YL
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   Li, T
   Nian, H
   Jiang, BJ
AF Yue, Yanlei
   Jiang, Ze
   Sapey, Enoch
   Wu, Tingting
   Sun, Shi
   Cao, Mengxue
   Han, Tianfu
   Li, Tao
   Nian, Hai
   Jiang, Bingjun
TI Transcriptomal dissection of soybean circadian rhythmicity in two
   geographically, phenotypically and genetically distinct cultivars
SO BMC GENOMICS
LA English
DT Article
DE Soybean; Circadian rhythmicity; Time-series transcriptome; J; GmELF3a;
   GmFT family
ID FLOWERING-LOCUS-T; MAP-BASED CLONING; GENE-EXPRESSION; MATURITY LOCUS;
   CLOCK; HOMOLOGS; TIME; IDENTIFICATION; ORGANIZATION; REDUNDANCY
AB BackgroundIn soybean, some circadian clock genes have been identified as loci for maturity traits. However, the effects of these genes on soybean circadian rhythmicity and their impacts on maturity are unclear.ResultsWe used two geographically, phenotypically and genetically distinct cultivars, conventional juvenile Zhonghuang 24 (with functional J/GmELF3a, a homolog of the circadian clock indispensable component EARLY FLOWERING 3) and long juvenile Huaxia 3 (with dysfunctional j/Gmelf3a) to dissect the soybean circadian clock with time-series transcriptomal RNA-Seq analysis of unifoliate leaves on a day scale. The results showed that several known circadian clock components, including RVE1, GI, LUX and TOC1, phase differently in soybean than in Arabidopsis, demonstrating that the soybean circadian clock is obviously different from the canonical model in Arabidopsis. In contrast to the observation that ELF3 dysfunction results in clock arrhythmia in Arabidopsis, the circadian clock is conserved in soybean regardless of the functional status of J/GmELF3a. Soybean exhibits a circadian rhythmicity in both gene expression and alternative splicing. Genes can be grouped into six clusters, C1-C6, with different expression profiles. Many more genes are grouped into the night clusters (C4-C6) than in the day cluster (C2), showing that night is essential for gene expression and regulation. Moreover, soybean chromosomes are activated with a circadian rhythmicity, indicating that high-order chromosome structure might impact circadian rhythmicity. Interestingly, night time points were clustered in one group, while day time points were separated into two groups, morning and afternoon, demonstrating that morning and afternoon are representative of different environments for soybean growth and development. However, no genes were consistently differentially expressed over different time-points, indicating that it is necessary to perform a circadian rhythmicity analysis to more thoroughly dissect the function of a gene. Moreover, the analysis of the circadian rhythmicity of the GmFT family showed that GmELF3a might phase- and amplitude-modulate the GmFT family to regulate the juvenility and maturity traits of soybean.ConclusionsThese results and the resultant RNA-seq data should be helpful in understanding the soybean circadian clock and elucidating the connection between the circadian clock and soybean maturity.
C1 [Yue, Yanlei; Cao, Mengxue; Li, Tao] Henan Agr Univ, Coll Life Sci, Zhengzhou 450002, Peoples R China.
   [Jiang, Ze; Nian, Hai] South China Agr Univ, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Peoples R China.
   [Sapey, Enoch; Wu, Tingting; Sun, Shi; Han, Tianfu; Jiang, Bingjun] Chinese Acad Agr Sci, Inst Crop Sci, MARA Key Lab Soybean Biol Beijing, Beijing 100081, Peoples R China.
C3 Henan Agricultural University; South China Agricultural University;
   Chinese Academy of Agricultural Sciences; Institute of Crop Sciences,
   CAAS
RP Li, T (corresponding author), Henan Agr Univ, Coll Life Sci, Zhengzhou 450002, Peoples R China.; Nian, H (corresponding author), South China Agr Univ, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Peoples R China.; Jiang, BJ (corresponding author), Chinese Acad Agr Sci, Inst Crop Sci, MARA Key Lab Soybean Biol Beijing, Beijing 100081, Peoples R China.
EM litao0504@henau.edu.cr; hnian@scau.edu.cn; jlangbingjun@caas.cn
RI Jiang, Bingjun/GWQ-4354-2022
OI li, tao/0000-0002-6422-608X
FU Key Area Research and Development Program of Guangdong Province
   [2020B020220008]; Key R&D and Promotion projects in Henan
   [192102110019]; National Key R&D Program of China [2017YFD0101400];
   China Agriculture Research System [CARS-04]
FX This work was supported by grants from the Key Area Research and
   Development Program of Guangdong Province (2020B020220008), the Key R&D
   and Promotion projects in Henan (192102110019), the National Key R&D
   Program of China (2017YFD0101400) and the China Agriculture Research
   System (CARS-04). The funding bodies played no role in the design of the
   study and collection, analysis, and interpretation of data and in
   writing the manuscript.
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NR 60
TC 2
Z9 2
U1 3
U2 27
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD JUL 10
PY 2021
VL 22
IS 1
AR 529
DI 10.1186/s12864-021-07869-8
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA TK9YT
UT WOS:000674512500004
PM 34246232
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Piras, R
   Iatropoulos, P
   Bresin, E
   Todeschini, M
   Gastoldi, S
   Valoti, E
   Alberti, M
   Mele, C
   Galbusera, M
   Cuccarolo, P
   Benigni, A
   Remuzzi, G
   Noris, M
AF Piras, Rossella
   Iatropoulos, Paraskevas
   Bresin, Elena
   Todeschini, Marta
   Gastoldi, Sara
   Valoti, Elisabetta
   Alberti, Marta
   Mele, Caterina
   Galbusera, Miriam
   Cuccarolo, Paola
   Benigni, Ariela
   Remuzzi, Giuseppe
   Noris, Marina
TI Molecular Studies and an ex vivo Complement Assay on Endothelium
   Highlight the Genetic Complexity of Atypical Hemolytic Uremic Syndrome:
   The Case of a Pedigree With a Null CD46 Variant
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE atypical hemolytic uremic syndrome; complement; membrane cofactor
   protein; incomplete penetrance; splicing; CD46 expression; ex-vivo
   assay; rare variants
ID MEMBRANE COFACTOR PROTEIN; FACTOR-H; MUTATIONS; ACTIVATION; AHUS; HUS;
   MCP; IMPACT; CFH
AB Atypical hemolytic uremic syndrome (aHUS) is an ultra-rare disease characterized by microangiopathic hemolysis, thrombocytopenia, and renal impairment and is associated with dysregulation of the alternative complement pathway on the microvascular endothelium. Outcomes have improved greatly with pharmacologic complement C5 blockade. Abnormalities in complement genes (CFH, CD46, CFI, CFB, C3, and THBD), CFH-CFHR genomic rearrangements, and anti-FH antibodies have been reported in 40-60% of cases. The penetrance of aHUS is incomplete in carriers of complement gene abnormalities; and multiple hits, including the CFH-H3 and CD46(GGAAC) risk haplotypes and the CFHR1*B risk allele, as well as environmental factors, contribute to disease development. Here, we investigated the determinants of penetrance of aHUS associated with CD46 genetic abnormalities. We studied 485 aHUS patients and found CD46 rare variants (RVs) in about 10%. The c.286+2T>G RV was the most prevalent (13/485) and was associated with G RV who experienced a severe form of aHUS and developed end-stage renal failure. The father and paternal uncle with the same variant in homozygosity and six heterozygous relatives are unaffected. Flow cytometry analysis showed about 50% reduction of CD46 expression on blood mononuclear cells from the heterozygous proband and over 90% reduction in cells from the proband's unaffected homozygous father and aunt. Further genetic studies did not reveal RVs in known aHUS-associated genes or common genetic modifiers that segregated with the disease. Importantly, a specific ex vivo test showed excessive complement deposition on endothelial cells exposed to sera from the proband, and also from his mother and maternal uncle, who do not carry the c.286+2T>G RV, indicating that they share a circulating defect that results in complement dysregulation on the endothelium. These results highlight the complexity of the genetics of aHUS and indicate that CD46 deficiency may not be enough to induce aHUS. We hypothesize that the proband inherited from his mother a genetic abnormality in a complement circulating factor that has not been identified yet, which synergized with the CD46 RV in predisposing him to the aHUS phenotype.
C1 [Piras, Rossella; Iatropoulos, Paraskevas; Bresin, Elena; Todeschini, Marta; Gastoldi, Sara; Valoti, Elisabetta; Alberti, Marta; Mele, Caterina; Galbusera, Miriam; Cuccarolo, Paola; Benigni, Ariela; Remuzzi, Giuseppe; Noris, Marina] Ist Ric Farmacol Mario Negri IRCCS, Clin Res Ctr Rare Dis Aldo & Cele Dacco, Bergamo, Italy.
C3 Istituto di Ricerche Farmacologiche Mario Negri IRCCS
RP Noris, M (corresponding author), Ist Ric Farmacol Mario Negri IRCCS, Clin Res Ctr Rare Dis Aldo & Cele Dacco, Bergamo, Italy.
EM marina.noris@marionegri.it
RI Todeschini, Marta/ABF-4705-2020; Ariela, Benigni/ABH-3492-2020; Mele,
   Caterina/ABF-3728-2020; Remuzzi, Giuseppe/V-9766-2017; Piras,
   Rossella/AAZ-1122-2020; Gastoldi, Sara/ABG-7604-2020; Valoti,
   Elisabetta/ABG-8444-2020; NORIS, MARINA/ABG-2219-2020; Alberti,
   Marta/ABG-8825-2020; Bresin, Elena/ABG-2409-2020
OI Piras, Rossella/0000-0002-0218-0901; Bresin, Elena/0000-0003-4198-2891;
   Benigni, Ariela/0000-0002-4721-5485; Todeschini,
   Marta/0000-0003-3422-8815; Iatropoulos, Paraskevas/0000-0001-9406-5734;
   Alberti, Marta/0000-0001-8011-9586; Mele, Caterina/0000-0002-9536-3474;
   Valoti, Elisabetta/0000-0002-9997-3800
FU European Union [305608]; Italian Ministero della Salute
   [RF-2016-02361720]; Progetto DDD Onlus-Associazione per la lotta alla
   DDD (Milan, Italy); Cassa di Sovvenzioni e Risparmio fra il Personale
   della Banca D'Italia (Rome, Italy); Fondazione Aiuti per la Ricerca
   sulle Malattie Rare ARMR ONLUS (Bergamo, Italy)
FX This work was partially supported by the European Union Framework
   Programme 7 (FP7)-EURenOmics project 305608 and by the Italian Ministero
   della Salute (RF-2016-02361720). RP and EV are recipients of a research
   contract from Progetto DDD Onlus-Associazione per la lotta alla DDD
   (Milan, Italy) and Cassa di Sovvenzioni e Risparmio fra il Personale
   della Banca D'Italia (Rome, Italy). PC is recipient of a fellowship from
   Fondazione Aiuti per la Ricerca sulle Malattie Rare ARMR ONLUS (Bergamo,
   Italy). The funding sources had no role in study design or in the
   collection, analysis, and interpretation of data, nor in the writing of
   the report or in the decision to submit the paper for publication.
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NR 47
TC 8
Z9 9
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD NOV 3
PY 2020
VL 7
AR 579418
DI 10.3389/fmed.2020.579418
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OR8CZ
UT WOS:000589696200001
PM 33224962
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Azakie, A
   Larkin, SB
   Farrance, IK
   Grenningloh, G
   Ordahl, CP
AF Azakie, A
   Larkin, SB
   Farrance, IK
   Grenningloh, G
   Ordahl, CP
TI DTEF-1, a novel member of the transcription enhancer factor-1 (TEF-1)
   multigene family
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CAT BINDING-FACTOR; FACTOR-I TEF-1; GENE-EXPRESSION; MYOD FAMILY;
   ACTIVATION; ELEMENT; MOUSE; SEQUENCE; HOMOLOGY; PROMOTER
AB M-CAT motifs mediate muscle-specific transcriptional activity via interaction with binding factors that are antigenically and biochemically related to vertebrate transcription enhancer factor-1 (TEF-1), a member of the TEA/ATTS domain family of transcription factors. M-CAT binding activities present in cardiac and skeletal muscle tissues cannot be fully accounted for by existing cloned isoforms of TEF-1. TEF-1-related cDNAs isolated from heart libraries indicate that at least three classes of TEF-1-related cDNAs are expressed in these and other tissues. One class are homologues of the human TEF-1 originally cloned from HeLa cells (Xiao, J. H., Davidson, I., Matthes, H., Garnier, J. M., and Chambon, P. (1991) Cell 65, 551-568). A second class represents homologues of the avian TEF-1-related gene previously isolated (Stewart, A. F., Larkin, S. B., Farrance, I. K., Mar, J. H., Hall, D. E., and Ordahl, C. P. (1994) J. Biol. Chem. 269, 3147-3150). The third class consists of a novel, divergent TEF-1 cDNA, named DTEF-1, and its preliminary characterization is described here. Two isoforms of DTEF-1 (DTEF-1A and DTEF-1B) were isolated as 1.9-kilobase pair clones with putative open reading frames of 433 and 432 amino acids whose differences are attributable to alternative splicing at the C terminus of the TEA DNA binding domain. Cardiac muscle contains high levels of DTEF-1 transcripts, but unexpectedly low levels are detected in skeletal muscle, DTEF-1 transcripts are present at intermediate levels in gizzard and lung, and at low levels in kidney. DTEF-1A is a sequence-specific M-CAT-binding factor. The distinct spatial pattern of expression, and unusual amino acid sequence in its DNA binding domain, may indicate a particular role for DTEF-1 in cell-specific gene regulation. Recent work also suggests that at least one more TEF-1-related gene exists in vertebrates. We propose a naming system for the four TEF-1 gene family members identified to date that preserves existing nomenclature and provides a means for extending that nomenclature as additional family members may be identified.
C1 UNIV CALIF SAN DIEGO, CARDIOVASC RES INST, DEPT ANAT, SAN FRANCISCO, CA 94143 USA.
   UNIV CALIF SAN DIEGO, CARDIOVASC RES INST, DEPT SURG, SAN FRANCISCO, CA 94143 USA.
   GLAXO INST MOLEC BIOL SA, CH-1211 GENEVA, SWITZERLAND.
C3 University of California System; University of California San Diego;
   University of California System; University of California San Diego;
   GlaxoSmithKline; GlaxoSmithKline Switzerland
FU NHLBI NIH HHS [HL-35561, HL-43821] Funding Source: Medline; PHS HHS [FO5
   24892] Funding Source: Medline
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NR 32
TC 46
Z9 49
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 5
PY 1996
VL 271
IS 14
BP 8260
EP 8265
DI 10.1074/jbc.271.14.8260
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA UD600
UT WOS:A1996UD60000060
PM 8626520
OA hybrid
DA 2025-04-10
ER

PT J
AU Bianchi, L
   Wible, B
   Arcangeli, A
   Taglialatela, M
   Morra, F
   Castaldo, P
   Crociani, O
   Rosati, B
   Faravelli, L
   Olivotto, M
   Wanke, E
AF Bianchi, L
   Wible, B
   Arcangeli, A
   Taglialatela, M
   Morra, F
   Castaldo, P
   Crociani, O
   Rosati, B
   Faravelli, L
   Olivotto, M
   Wanke, E
TI herg encodes a K<SUP>+</SUP> current highly conserved in tumors
   of different histogenesis:: A selective advantage for cancer cells?
SO CANCER RESEARCH
LA English
DT Article
ID POTASSIUM CHANNEL; NEUROBLASTOMA-CELLS; INWARD RECTIFIER; OXYGEN;
   DROSOPHILA; ACTIVATION; DEPENDENCE; FAMILY; BLOCK; LINE
AB The human ether a-go-go-related gene (herg) encodes a K+ currnt (I-HERG) that plays a fundamental role in heart excitability by regulating the action potential repolarization (I-Kr); mutations of this gene are responsible for the chromosome 7-linked long QT syndrome (LQT2). In this report, we show that in a variety (n = 17) of tumor cell lines of different species (human and murine) and distinct histogenesis (neuroblastoma, rhabdomyosarcoma, adenocarcinoma, lung microcytoma, pituitary tumors, insulinoma beta-cells, and monoblastic leukemia), a novel K+ inward-rectifier current (I-IR), which is biophysically and pharmacologically similar to I-HERG, can be recorded with the patch-clamp technique. Northern blot experiments with a human herg cDNA probe revealed that both in human and murine clones the very high expression of herg transcripts can be quantified in at least three clearly identifiable bands, suggesting an alternative splicing of HERG mRNA. Moreover, se cloned a cDNA encoding for I-IR the SH-SY5Y human neuroblastoma, The sequence of this cDNA result was practically identical to that already reported for herg, indicating a high conservation of this gene in tumors. Consistently, the expression of this clone in Xenopus oocytes showed that the encoded K+ channel had substantially all of the biophysical and pharmacological properties of the native I(IR)ibed for tumor cells. In addition, in the tumor clones studied, I-IR governs the resting potential, whereas it could not be detected either by the patch clamp or the Northern blot techniques in cells obtained from primary cell cultures of parental tissues (sensory neurons and myotubes), whose resting potential is controlled by the classical K+ anomalous rectifier current, This current substitution had a profound impact on the resting potential, which was markedly depolarized in tumors as compared with normal cells. These results suggest that I, is normally only expressed during the early stages of cell differentiation frozen by neoplastic transformation, playing an important pathophysiological role in the regulatory mechanisms of neoplastic cell survival, In fact, because of its biophysical features, I-IR,s keeping the resting potential within the depolarized values required for unlimited tumor growth, could also appear suitable to afford a selective advantage in an ischemic environment.
C1 Univ Milan, Dipartimento Fisiol & Biochim Gen, I-20133 Milan, Italy.
   Case Western Reserve Univ, Rammelkamp Ctr Educ & Res, Cleveland, OH 44109 USA.
   Univ Florence, Ist Patol Gen, Florence, Italy.
   Univ Naples Federico II, Dipartimento Neurosci, Sez Farmacol, Naples, Italy.
C3 University of Milan; University System of Ohio; Case Western Reserve
   University; MetroHealth System; University of Florence; University of
   Naples Federico II
RP Wanke, E (corresponding author), Univ Milan, Dipartimento Fisiol & Biochim Gen, Via Celoria 26, I-20133 Milan, Italy.
RI Taglialatela, Maurizio/ABH-4262-2020; Taglialatela, Maurizio/K-1840-2013
OI Bianchi, Laura/0000-0003-2615-5345; Taglialatela,
   Maurizio/0000-0002-8202-0560; Crociani, Olivia/0000-0003-3485-2132
FU NHLBI NIH HHS [HL36930] Funding Source: Medline
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NR 32
TC 239
Z9 268
U1 0
U2 14
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD FEB 15
PY 1998
VL 58
IS 4
BP 815
EP 822
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YX289
UT WOS:000072025300041
PM 9485040
DA 2025-04-10
ER

PT J
AU Patel, PD
   Kodati, B
   Clark, AF
AF Patel, Pinkal D.
   Kodati, Bindu
   Clark, Abbot F.
TI Role of Glucocorticoids and Glucocorticoid Receptors in Glaucoma
   Pathogenesis
SO CELLS
LA English
DT Review
DE glucocorticoid receptor; glaucoma; animal models; anti-inflammatory
   steroids; primary open-angle glaucoma; steroid glaucoma; ocular
   hypertension; eye; corticosteroids
ID INDUCED OCULAR HYPERTENSION; OPEN-ANGLE GLAUCOMA; TRABECULAR MESHWORK
   CELLS; LINKED ACTIN NETWORKS; INTRAOCULAR-PRESSURE; PLASMA-CORTISOL;
   AQUEOUS-HUMOR; NONINVASIVE MEASUREMENT; PROTEOMIC ANALYSIS;
   GENE-EXPRESSION
AB The glucocorticoid receptor (GR), including both alternative spliced isoforms (GR alpha and GR beta), has been implicated in the development of primary open-angle glaucoma (POAG) and iatrogenic glucocorticoid-induced glaucoma (GIG). POAG is the most common form of glaucoma, which is the leading cause of irreversible vision loss and blindness in the world. Glucocorticoids (GCs) are commonly used therapeutically for ocular and numerous other diseases/conditions. One serious side effect of prolonged GC therapy is the development of iatrogenic secondary ocular hypertension (OHT) and OAG (i.e., GC-induced glaucoma (GIG)) that clinically and pathologically mimics POAG. GC-induced OHT is caused by pathogenic damage to the trabecular meshwork (TM), a tissue involved in regulating aqueous humor outflow and intraocular pressure. TM cells derived from POAG eyes (GTM cells) have a lower expression of GR beta, a dominant negative regulator of GC activity, compared to TM cells from age-matched control eyes. Therefore, GTM cells have a greater pathogenic response to GCs. Almost all POAG patients develop GC-OHT when treated with GCs, in contrast to a GC responder rate of 40% in the normal population. An increased expression of GR beta can block GC-induced pathogenic changes in TM cells and reverse GC-OHT in mice. The endogenous expression of GR beta in the TM may relate to differences in the development of GC-OHT in the normal population. A number of studies have suggested increased levels of endogenous cortisol in POAG patients as well as differences in cortisol metabolism, suggesting that GCs may be involved in the development of POAG. Additional studies are warranted to better understand the molecular mechanisms involved in POAG and GIG in order to develop new disease-modifying therapies to better treat these two sight threatening forms of glaucoma. The purpose of this timely review is to highlight the pathological and clinical features of GC-OHT and GIG, mechanisms responsible for GC responsiveness, potential therapeutic options, as well as to compare the similar features of GIG with POAG.
C1 [Patel, Pinkal D.; Kodati, Bindu; Clark, Abbot F.] Univ North Texas Hlth Sci Ctr, North Texas Eye Res Inst, Dept Pharmacol & Neurosci, Ft Worth, TX 76107 USA.
RP Clark, AF (corresponding author), Univ North Texas Hlth Sci Ctr, North Texas Eye Res Inst, Dept Pharmacol & Neurosci, Ft Worth, TX 76107 USA.
EM pinkal.patel@unthsc.edu; bindu.kodati@unthsc.edu; abe.clark@unthsc.edu
RI Patel, Pinkal/GQP-2308-2022; kodati, bindu/ABD-4569-2021; Patel,
   Pinkal/GQP-2130-2022
OI Clark, Abbot/0000-0003-3594-6560; Patel, Pinkal/0000-0002-7704-4381;
   Kodati, Bindu/0000-0002-4956-841X
FU NIH [EY016242, EY030967]
FX This research was supported by NIH grants EY016242 and EY030967. We also
   would like to thank research collaborators, as well as former graduate
   students and postdoctoral fellows from the Clark lab.
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NR 103
TC 11
Z9 13
U1 2
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD OCT
PY 2023
VL 12
IS 20
AR 2452
DI 10.3390/cells12202452
PG 20
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA W8OX8
UT WOS:001094177900001
PM 37887296
OA Green Published, Green Submitted, gold
DA 2025-04-10
ER

PT J
AU Chaabane, M
   Andreeva, K
   Hwang, JY
   Kook, TL
   Park, JW
   Cooper, NGF
AF Chaabane, Mohamed
   Andreeva, Kalina
   Hwang, Jae Yeon
   Kook, Tae Lim
   Park, Juw Won
   Cooper, Nigel G. F.
TI seekCRIT: Detecting and characterizing differentially expressed circular
   RNAs using high-throughput sequencing data
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID RETINAL ISCHEMIA; GENE-EXPRESSION; SEQ; COVERAGE; DEPTH; QUANTIFICATION;
   IDENTIFICATION; BIOGENESIS; ABUNDANT; REVEALS
AB Over the past two decades, researchers have discovered a special form of alternative splicing that produces a circular form of RNA. Although these circular RNAs (circRNAs) have garnered considerable attention in the scientific community for their biogenesis and functions, the focus of current studies has been on the tissue-specific circRNAs that exist only in one tissue but not in other tissues or on the disease-specific circRNAs that exist in certain disease conditions, such as cancer, but not under normal conditions. This approach was conducted in the relative absence of methods that analyze a group of common circRNAs that exist in both conditions, but are more abundant in one condition relative to another (differentially expressed). Studies of differentially expressed circRNAs (DECs) between two conditions would serve as a significant first step in filling this void. Here, we introduce a novel computational tool, seekCRIT (seek for differentially expressed CircRNAs In Transcriptome), that identifies the DECs between two conditions from high-throughput sequencing data. Using rat retina RNA-seq data from ischemic and normal conditions, we show that over 74% of identifiable circRNAs are expressed in both conditions and over 40 circRNAs are differentially expressed between two conditions. We also obtain a high qPCR validation rate of 90% for DECs with a FDR of < 5%. Our results demonstrate that seekCRIT is a novel and efficient approach to detect DECs using rRNA depleted RNA-seq data. seekCRIT is freely downloadable at. The source code is licensed under the MIT License. seekCRIT is developed and tested on Linux CentOS-7.
   Author summary The focus of circRNA studies has been on condition-specific circRNAs, however, there are situations in which circRNAs exist in both conditions with different abundance. Here, we introduce a new and robust analytic software, seekCRIT (seekfor differentially expressedCircRNAsInTranscriptome), that identifies the differentially expressed circRNAs (DECs) between two conditions from high-throughput sequencing data. seekCRIT provides a straightforward normalized quantification of circRNAs and statistical measures by adapting a junction-count-based estimation approach. Using publicly available ribosomal RNA depleted RNA-seq data and our own rat retina RNA-seq data, we show that seekCRIT can efficiently detect circRNAs and identify DECs. We also obtain a high qPCR validation rate of 90% for DECs with a FDR of < 5%. Our results demonstrate that seekCRIT is a novel and efficient software to detect DECs using rRNA depleted RNA-seq data.
C1 [Chaabane, Mohamed; Hwang, Jae Yeon; Kook, Tae Lim; Park, Juw Won] Univ Louisville, Dept Comp Sci & Engn, Louisville, KY 40292 USA.
   [Andreeva, Kalina; Cooper, Nigel G. F.] Univ Louisville, Dept Anat Sci & Neurobiol, Louisville, KY 40292 USA.
   [Park, Juw Won; Cooper, Nigel G. F.] Univ Louisville, KBRIN Bioinformat Core, Louisville, KY 40292 USA.
   [Chaabane, Mohamed] Colorado State Univ, Dept Comp Sci, Ft Collins, CO 80523 USA.
C3 University of Louisville; University of Louisville; University of
   Louisville; Colorado State University System; Colorado State University
   Fort Collins
RP Park, JW (corresponding author), Univ Louisville, Dept Comp Sci & Engn, Louisville, KY 40292 USA.; Cooper, NGF (corresponding author), Univ Louisville, Dept Anat Sci & Neurobiol, Louisville, KY 40292 USA.; Park, JW; Cooper, NGF (corresponding author), Univ Louisville, KBRIN Bioinformat Core, Louisville, KY 40292 USA.
EM juw.park@louisville.edu; nigel.cooper@louisville.edu
OI Andreeva, Kalina/0000-0002-5206-532X; Hwang, Jae
   Yeon/0000-0002-7247-0146
FU National Institute of General Medical Sciences (NIGMS) of the National
   Institute of Health (NIH) [P20GM103436, R15GM126446]
FX NC is supported by P20GM103436 from the National Institute of General
   Medical Sciences (NIGMS, https://www.nigms.nih.gov/) of the National
   Institute of Health (NIH). JP, JH are supported by R15GM126446 from the
   National Institute of General Medical Sciences (NIGMS) of the National
   Institute of Health (NIH). The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 54
TC 15
Z9 16
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-734X
EI 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD OCT
PY 2020
VL 16
IS 10
AR e1008338
DI 10.1371/journal.pcbi.1008338
PG 13
WC Biochemical Research Methods; Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA OL2IH
UT WOS:000585164300001
PM 33079938
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Durocher, M
   Ander, BP
   Jickling, G
   Hamade, F
   Hull, H
   Knepp, B
   Liu, DZ
   Zhan, XH
   Tran, A
   Cheng, XY
   Ng, K
   Yee, A
   Sharp, FR
   Stamova, B
AF Durocher, Marc
   Ander, Bradley P.
   Jickling, Glen
   Hamade, Farah
   Hull, Heather
   Knepp, Bodie
   Liu, Da Zhi
   Zhan, Xinhua
   Anh Tran
   Cheng, Xiyuan
   Ng, Kwan
   Yee, Alan
   Sharp, Frank R.
   Stamova, Boryana
TI Inflammatory, regulatory, and autophagy co-expression modules and hub
   genes underlie the peripheral immune response to human intracerebral
   hemorrhage
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
DE Intracerebral hemorrhage; ICH; NRF2; Autophagy; Hematoma; Hematoma
   clearance; Src kinase inhibitors; Gene expression; Co-expression
   networks; Gene networks
ID ISCHEMIC-STROKE; BRAIN-INJURY; SUBARACHNOID HEMORRHAGE; T-LYMPHOCYTES;
   BLOOD; ACTIVATION; PATHWAY; EXPRESSION; APOPTOSIS; RECEPTOR
AB BackgroundIntracerebral hemorrhage (ICH) has a high morbidity and mortality. The peripheral immune system and cross-talk between peripheral blood and brain have been implicated in the ICH immune response. Thus, we delineated the gene networks associated with human ICH in the peripheral blood transcriptome. We also compared the differentially expressed genes in blood following ICH to a prior human study of perihematomal brain tissue.MethodsWe performed peripheral blood whole-transcriptome analysis of ICH and matched vascular risk factor control subjects (n=66). Gene co-expression network analysis identified groups of co-expressed genes (modules) associated with ICH and their most interconnected genes (hubs). Mixed-effects regression identified differentially expressed genes in ICH compared to controls.ResultsOf seven ICH-associated modules, six were enriched with cell-specific genes: one neutrophil module, one neutrophil plus monocyte module, one T cell module, one Natural Killer cell module, and two erythroblast modules. The neutrophil/monocyte modules were enriched in inflammatory/immune pathways; the T cell module in T cell receptor signaling genes; and the Natural Killer cell module in genes regulating alternative splicing, epigenetic, and post-translational modifications. One erythroblast module was enriched in autophagy pathways implicated in experimental ICH, and NRF2 signaling implicated in hematoma clearance. Many hub genes or module members, such as IARS, mTOR, S1PR1, LCK, FYN, SKAP1, ITK, AMBRA1, NLRC4, IL6R, IL17RA, GAB2, MXD1, PIK3CD, NUMB, MAPK14, DDX24, EVL, TDP1, ATG3, WDFY3, GSK3B, STAT3, STX3, CSF3R, PIP4K2A, ANXA3, DGAT2, LRP10, FLOT2, ANK1, CR1, SLC4A1, and DYSF, have been implicated in neuroinflammation, cell death, transcriptional regulation, and some as experimental ICH therapeutic targets. Gene-level analysis revealed 1225 genes (FDR p<0.05, fold-change > |1.2|) have altered expression in ICH in peripheral blood. There was significant overlap of the 1225 genes with dysregulated genes in human perihematomal brain tissue (p=7x10(-3)). Overlapping genes were enriched for neutrophil-specific genes (p=6.4x10(-08)) involved in interleukin, neuroinflammation, apoptosis, and PPAR signaling.ConclusionsThis study delineates key processes underlying ICH pathophysiology, complements experimental ICH findings, and the hub genes significantly expand the list of novel ICH therapeutic targets. The overlap between blood and brain gene responses underscores the importance of examining blood-brain interactions in human ICH.
C1 [Durocher, Marc; Ander, Bradley P.; Jickling, Glen; Hamade, Farah; Hull, Heather; Knepp, Bodie; Liu, Da Zhi; Zhan, Xinhua; Anh Tran; Cheng, Xiyuan; Ng, Kwan; Yee, Alan; Sharp, Frank R.; Stamova, Boryana] Univ Calif Davis, Dept Neurol, Sch Med, Sacramento, CA 95817 USA.
   [Stamova, Boryana] MIND Inst Biosci Bldg, 2805 50th St, Sacramento, CA 95817 USA.
C3 University of California System; University of California Davis
RP Stamova, B (corresponding author), Univ Calif Davis, Dept Neurol, Sch Med, Sacramento, CA 95817 USA.; Stamova, B (corresponding author), MIND Inst Biosci Bldg, 2805 50th St, Sacramento, CA 95817 USA.
EM bsstamova@ucdavis.edu
RI Jickling, Glen/J-8790-2019; Stamova, Boryana/ABA-2981-2020; Yee,
   Alan/AAH-4604-2019; Liu, DaZhi/B-6850-2011; Tran, Anh/KCY-8639-2024
OI Jickling, Glen/0000-0003-3543-0820; Knepp, Bodie/0000-0002-0761-8060;
   Stamova, Boryana/0000-0002-5440-8816
FU NIH NINDS (National Institute of Neurological Disorders and Stroke)
   [R01NS079153, R01NS075035, R01NS097000, R01NS101718]; American Heart
   Association [16BGIA27250263]; American Heart Association (AHA)
   [16BGIA27250263] Funding Source: American Heart Association (AHA)
FX This study was funded by the NIH NINDS (National Institute of
   Neurological Disorders and Stroke) (R01NS079153, R01NS075035,
   R01NS097000 and R01NS101718), and by the American Heart Association
   (16BGIA27250263).
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NR 122
TC 46
Z9 49
U1 1
U2 15
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD MAR 5
PY 2019
VL 16
AR 56
DI 10.1186/s12974-019-1433-4
PG 21
WC Immunology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Neurosciences & Neurology
GA HN8RA
UT WOS:000460461800001
PM 30836997
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Rahimi, N
AF Rahimi, Nader
TI C-type Lectin CD209L/L-SIGN and CD209/DC-SIGN: Cell Adhesion Molecules
   Turned to Pathogen Recognition Receptors
SO BIOLOGY-BASEL
LA English
DT Review
DE CD209; L-SIGN; CD209L; DC-SIGN; C-type lectin; cell adhesion molecule;
   C-type lectin domain family 4 member M; CLEC4M; LSECtin; CLEC4G;
   SARS-CoV-2; COVID-19
ID ACUTE RESPIRATORY SYNDROME; HUMAN-IMMUNODEFICIENCY-VIRUS; SIGN-MEDIATED
   INTERNALIZATION; CD209L L-SIGN; DC-SIGN; DENDRITIC CELLS;
   ENDOTHELIAL-CELLS; SYNDROME CORONAVIRUS; FUNCTIONAL RECEPTOR; SARS
   CORONAVIRUS
AB Simple Summary
   COVID-19 pandemic continues to pose a serious threat to global public health with overwhelming worldwide socio-economic disruption. SARS-CoV-2, the viral agent of COVID-19, uses its surface glycoprotein Spike (S) for host cell attachment and entry. The emerging picture of pathogenesis of SARS-CoV-2 demonstrates that S protein, in addition, to ACE2, interacts with the carbohydrate recognition domain (CRD) of C-type lectin receptors, CD209L and CD209. Recognition of CD209L and CD209 which are widely expressed in SARS-CoV-2 target organs can facilitate entry and transmission leading to dysregulation of the host immune response and other major organs including, cardiovascular system. Establishing a comprehensive map of the SARS-CoV-2 interaction with CD209 family proteins, and their roles in transmission and pathogenesis can provide new insights into host-pathogen interaction with implications in therapies and vaccine development.
   C-type lectin CD209/DC-SIGN and CD209L/L-SIGN proteins are distinct cell adhesion and pathogen recognition receptors that mediate cellular interactions and recognize a wide range of pathogens, including viruses such as SARS, SARS-CoV-2, bacteria, fungi and parasites. Pathogens exploit CD209 family proteins to promote infection and evade the immune recognition system. CD209L and CD209 are widely expressed in SARS-CoV-2 target organs and can contribute to infection and pathogenesis. CD209 family receptors are highly susceptible to alternative splicing and genomic polymorphism, which may influence virus tropism and transmission in vivo. The carbohydrate recognition domain (CRD) and the neck/repeat region represent the key features of CD209 family proteins that are also central to facilitating cellular ligand interactions and pathogen recognition. While the neck/repeat region is involved in oligomeric dimerization, the CRD recognizes the mannose-containing structures present on specific glycoproteins such as those found on the SARS-CoV-2 spike protein. Considering the role of CD209L and related proteins in diverse pathogen recognition, this review article discusses the recent advances in the cellular and biochemical characterization of CD209 and CD209L and their roles in viral uptake, which has important implications in understanding the host-pathogen interaction, the viral pathobiology and driving vaccine development of SARS-CoV-2.
C1 [Rahimi, Nader] Boston Univ, Sch Med, Dept Pathol, Med Campus, Boston, MA 02118 USA.
C3 Boston University
RP Rahimi, N (corresponding author), Boston Univ, Sch Med, Dept Pathol, Med Campus, Boston, MA 02118 USA.
EM nrahimi@bu.edu
OI Rahimi, Nader/0000-0002-6745-1725
FU CTSI grant [UL1 TR001430]; Department of Pathology, Boston University;
   Evans Center for Interdisciplinary Biomedical Research ARC on COVID-19
FX This work was supported in part through grants from CTSI grant UL1
   TR001430, Malory Fund, Department of Pathology, Boston University and a
   grant from The Evans Center for Interdisciplinary Biomedical Research
   ARC on COVID-19.
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NR 121
TC 57
Z9 60
U1 1
U2 20
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2079-7737
J9 BIOLOGY-BASEL
JI Biology-Basel
PD JAN
PY 2021
VL 10
IS 1
AR 1
DI 10.3390/biology10010001
PG 15
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA PV1FD
UT WOS:000609738900001
PM 33375175
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Zhao, ZD
   Tian, HS
   Shi, BG
   Jiang, YY
   Liu, X
   Hu, J
AF Zhao, Zhidong
   Tian, Hongshan
   Shi, Bingang
   Jiang, Yanyan
   Liu, Xiu
   Hu, Jiang
TI Transcriptional Regulation of the Bovine Fatty Acid Transport Protein 1
   Gene by Kruppel-Like Factors 15
SO ANIMALS
LA English
DT Article
DE bovine; Kruppel-like factors 15; unsaturated fatty acid; 5 ' RACE
ID II CORE PROMOTER; SKELETAL-MUSCLE; FATP1 GENE; EXPRESSION;
   IDENTIFICATION; KLF15
AB Simple Summary The nutritional value and qualities of beef are enhanced when the unsaturated fatty acid content is increased. Fatty acid transport protein 1 (FATP1), also called SLC27A1, an integral membrane protein that facilitates long-chain fatty acid influx, is involved in the genetic network for oleic acid synthesis in beef. Polymorphisms in bovine SLC27A1 gene are most significantly associated with oleic acid. Its expression exhibits significant positive correlations with bovine intramuscular fat content in the longissimus thoracis muscle. However, the transcription factors that contribute to the control and regulation of its expression have not been characterized extensively. In this study, we determined the tissue distribution of SLC27A1 mRNA and found that bovine SLC27A1 was highly expressed in subcutaneous adipose tissue and the longissimus thoracis muscle. Furthermore, we analyzed the molecular mechanisms involved in SLC27A1 regulation and found that the transcriptional activity of SLC27A1 gene was dependent on KLF15 transcription factor. These results may lead to an enhanced understanding of the regulation of SLC27A1 expression in other models, as well as provide new insights into the regulatory mechanism and biological functions of the SLC27A1 gene in determining the lipid composition in beef. Oleic acid is a major monounsaturated fatty acid, which accounts for about 33% of the fatty acid content in beef and is considered to have the least negative effect on serum cholesterol levels. Fatty acid transport protein 1 (FATP1), an integral membrane protein that facilitates long-chain fatty acid (LCFA) influx, is involved in the genetic network for oleic acid synthesis in beef. Its expression exhibits significant positive correlations with intramuscular fat (IMF) content in the longissimus thoracis. However, the expression mechanism of SLC27A1 or FATP1 is still unclear. To elucidate the molecular mechanisms involved in bovine SLC27A1 regulation, we cloned and characterized the promoter region of SLC27A1. By applying 5 '-rapid amplification of cDNA end analysis, we identified two alternative splice variants of this gene. Using a series of 5 ' deletion promoter plasmids in luciferase reporter assays, we found that the core promoter was 96 base pairs upstream from the transcription initiation site. Electrophoretic mobility shift assay combined with a site-directed mutation experiment demonstrated that KLF15 binding to the promoter region drives the SLC27A1 transcription. KLF15 plays an essential role in adipogenesis and skeletal muscle lipid flux. Thus, these results might provide further information on the regulatory roles of SLC27A1 gene in mediating the lipid composition in beef.
C1 [Hu, Jiang] Gansu Agr Univ, Coll Anim Sci & Technol, Lanzhou 730070, Gansu, Peoples R China.
   Gansu Agr Univ, Gansu Key Lab Herbivorous Anim Biotechnol, Lanzhou 730070, Gansu, Peoples R China.
C3 Gansu Agricultural University; Gansu Agricultural University
RP Hu, J (corresponding author), Gansu Agr Univ, Coll Anim Sci & Technol, Lanzhou 730070, Gansu, Peoples R China.
EM huj@gsau.edu.cn
RI Tian, Hongshan/LKM-5157-2024
OI zhao, zhidong/0000-0003-4672-7873
FU Gansu Youth Science and Technology Fund [17JR5RA140]; Sheng Tongsheng
   innovation funds [GSAU-STS-1726]; Basic Research Innovation Group
   Project of Gansu Province [17JR5RA137]; Scientific research start-up
   funds for openly-recruited doctors [GSAU-RCZX201711]
FX This research was supported by the Gansu Youth Science and Technology
   Fund (17JR5RA140), Scientific research start-up funds for
   openly-recruited doctors (GSAU-RCZX201711), Sheng Tongsheng innovation
   funds (GSAU-STS-1726), and The Basic Research Innovation Group Project
   of Gansu Province (17JR5RA137).
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NR 34
TC 8
Z9 12
U1 2
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2076-2615
J9 ANIMALS-BASEL
JI Animals
PD SEP
PY 2019
VL 9
IS 9
AR 654
DI 10.3390/ani9090654
PG 11
WC Agriculture, Dairy & Animal Science; Veterinary Sciences; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture; Veterinary Sciences; Zoology
GA JA6VC
UT WOS:000487978900084
PM 31491871
OA gold, Green Published
DA 2025-04-10
ER

PT J
AU Chao, E
   Kim, HW
   Mykles, DL
AF Chao, Erica
   Kim, Hyun-Woo
   Mykles, Donald L.
TI Cloning and tissue expression of eleven troponin-C isoforms in the
   American lobster, Homarus americanus
SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR
   BIOLOGY
LA English
DT Article
DE Troponin-C; Isoform; Lobster; Crustacea; Muscle; Homarus americanus;
   Myofibrillar protein; Fiber type; cDNA; Cloning; Tissue distribution
ID AMINO-ACID-SEQUENCES; FRESH-WATER CRUSTACEAN; SKELETAL-MUSCLE FIBERS; 2
   MAJOR ISOFORMS; CARDIAC TROPONIN; MYOFIBRILLAR PROTEINS; ACTIVATION
   PROPERTIES; GECARCINUS-LATERALIS; INVERTEBRATE MUSCLES; BINDING
   PROPERTIES
AB Troponin-C is the Ca2+-binding subunit of the troponin regulatory complex in striated muscles. As TnC isoforms can influence the Ca2+-activation properties of fiber phenotypes, the diversity and tissue distribution of TnC cDNAs were assessed in the American lobster, Homarus americanus. We cloned ten full-length cDNAs and one partial cDNA coding for distinct TnC isoforms. Five were sequenced from expressed sequence tag clones and were designated Ha-TnC(2b ') (2094 nt, 141 aa and 15.9 kDa), -C-4 ' (1667 nt, 155 aa and 17.3 kDa), -C-5 (2884 nt, 149 aa and 17.3 kDa), -C-6 (2439 nt, 155 nt and 17.4 kDa) and -C-6x (2171 nt. 154 aa and 16.9 kDa). The remainder were cloned using a combination of reverse transcription-polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends: five full-length cDNAs, designated Ha-TnC(1) (814 nt, 150 aa and 17.1 kDa), -C-2a(639 nt, 152 aa and 17.2 kDa), -C-2b'. (2136 nt, 155 aa and 17.5 kDa), -C-3 (1046 nt, 150 aa and 16.9 kDa), -C-4'. (842 nt, 108 aa and 12.1 kDa) and one partial (3 ') cDNA, designated Ha-TnC4 ', (563 nt and 57 aa). Ha-TnC(1), -C-2a, and -C-2b ' corresponded to lobster TnC sequences in the GenBank protein database (Ha-TnC(1), -C-2a, and -C-2b). Alternative splicing appeared responsible for TnC(2b ') and -C-2b ''; TnC(4 '), -C-4 ''; and-C-4 ''; and TnC(6) and -C-6x. The deduced amino acid sequences differed primarily in the terminal regions and EF-hands land III. Ha-TnC(6x) had a highly divergent 76 aa proline-rich N-terminal sequence. Tissue expression of the Ha-TnC isoforms was analyzed qualitatively by endpoint PCR. Ha-TnC(1), -C-2a, -C-2b ', -C-2b '' and - C-3 were expressed primarily in skeletal muscles; Ha-TnC(5) was expressed in heart: and Ha-TnC(4) and -C-6 variants were expressed in muscles and other tissues. The number and diversity of TnC sequences suggest the potential for varying the Ca2+-activated properties of the troponin-tropomyosin regulatory complex through differential expression of TnC isoforms. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Chao, Erica; Mykles, Donald L.] Colorado State Univ, Dept Biol, Ft Collins, CO 80523 USA.
   [Kim, Hyun-Woo] Pukyong Natl Univ, Dept Marine Biol, Pusan 608737, South Korea.
C3 Colorado State University System; Colorado State University Fort
   Collins; Pukyong National University
RP Mykles, DL (corresponding author), Colorado State Univ, Dept Biol, Ft Collins, CO 80523 USA.
EM don@lamar.colostate.edu
RI Kim, Hyun-Woo/AFN-9184-2022
OI Mykles, Donald/0000-0003-4030-2575
FU NSF [IOS-0618203]
FX We thank Dr. Ernest S. Chang, University of California-Davis Bodega
   Marine Laboratory, for providing animals; Dr. David Towle, Mount Desert
   Island Biological Laboratory, for providing EST clones of lobster TnC
   and EF2; and Matt Thompson for technical assistance. This research was
   supported by a grant from NSF (IOS-0618203).
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NR 52
TC 20
Z9 22
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1096-4959
EI 1879-1107
J9 COMP BIOCHEM PHYS B
JI Comp. Biochem. Physiol. B-Biochem. Mol. Biol.
PD SEP
PY 2010
VL 157
IS 1
BP 88
EP 101
DI 10.1016/j.cbpb.2010.05.007
PG 14
WC Biochemistry & Molecular Biology; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Zoology
GA 627GK
UT WOS:000280027300013
PM 20546913
DA 2025-04-10
ER

PT J
AU Gemmati, D
   D'Aversa, E
   Antonica, B
   Grisafi, M
   Salvatori, F
   Pizzicotti, S
   Pellegatti, P
   Ciccone, M
   Moratelli, S
   Serino, ML
   Tisato, V
AF Gemmati, Donato
   D'Aversa, Elisabetta
   Antonica, Bianca
   Grisafi, Miriana
   Salvatori, Francesca
   Pizzicotti, Stefano
   Pellegatti, Patrizia
   Ciccone, Maria
   Moratelli, Stefano
   Serino, Maria Luisa
   Tisato, Veronica
TI Gene Dosage of F5 c.3481C&gt;T Stop-Codon (p.R1161Ter) Switches
   the Clinical Phenotype from Severe Thrombosis to Recurrent Haemorrhage:
   Novel Hypotheses for Readthrough Strategy
SO GENES
LA English
DT Article
DE premature stop-codon (PTC); FV Leiden; cis-segregation; inherited
   thrombophilia; blood coagulation; readthrough
ID COAGULATION-FACTOR-V; ACTIVATED PROTEIN-C; MISSENSE MUTATION; LEIDEN
   MUTATION; MOLECULAR CHARACTERIZATION; ANTICOAGULANT RESPONSE; CATALYZED
   ACTIVATION; NONSENSE MUTATION; INHERITED DEFECTS; SYSTEMS BIOLOGY
AB Inherited defects in the genes of blood coagulation essentially express the severity of the clinical phenotype that is directly correlated to the number of mutated alleles of the candidate leader gene (e.g., heterozygote vs. homozygote) and of possible additional coinherited traits. The F5 gene, which codes for coagulation factor V (FV), plays a two-faced role in the coagulation cascade, exhibiting both procoagulant and anticoagulant functions. Thus, defects in this gene can be predisposed to either bleeding or thrombosis. A Sanger sequence analysis detected a premature stop-codon in exon 13 of the F5 gene (c.3481C>T; p.R1161Ter) in several members of a family characterised by low circulating FV levels and contrasting clinical phenotypes. The propositus, a 29 y.o. male affected by recurrent haemorrhages, was homozygous for the F5 stop-codon and for the F5 c.1691G>A (p.R506Q; FV-Leiden) inherited from the heterozygous parents, which is suggestive of combined cis-segregation. The homozygous condition of the stop-codon completely abolished the F5 gene expression in the propositus (FV:Ag < 1%; FV:C < 1%; assessed by ELISA and PT-based one-stage clotting assay respectively), removing, in turn, any chance for FV-Leiden to act as a prothrombotic molecule. His father (57 y.o.), characterised by severe recurrent venous thromboses, underwent a complete molecular thrombophilic screening, revealing a heterozygous F2 G20210A defect, while his mother (56 y.o.), who was negative for further common coagulation defects, reported fully asymptomatic anamnesis. To dissect these conflicting phenotypes, we performed the ProC (R) Global (Siemens Helthineers) coagulation test aimed at assessing the global pro- and anticoagulant balance of each family member, investigating the responses to the activated protein C (APC) by means of an APC-sensitivity ratio (APC-sr). The propositus had an unexpectedly poor response to APC (APC-sr: 1.09; n.v. > 2.25), and his father and mother had an APC-sr of 1.5 and 2.0, respectively. Although ProC (R) Global prevalently detects the anticoagulant side of FV, the exceptionally low APC-sr of the propositus and his discordant severe-moderate haemorrhagic phenotype could suggest a residual expression of mutated FV p.506QQ through a natural readthrough or possible alternative splicing mechanisms. The coagulation pathway may be physiologically rebalanced through natural and induced strategies, and the described insights might be able to track the design of novel treatment approaches and rebalancing molecules.
C1 [Gemmati, Donato; D'Aversa, Elisabetta; Antonica, Bianca; Grisafi, Miriana; Salvatori, Francesca; Tisato, Veronica] Univ Ferrara, Dept Translat Med, I-44121 Ferrara, Italy.
   [Gemmati, Donato; Tisato, Veronica] Univ Ferrara, Univ Strateg Ctr Studies Gender Med, I-44121 Ferrara, Italy.
   [Gemmati, Donato; Moratelli, Stefano; Serino, Maria Luisa] Univ Ferrara, Ctr Haemostasis & Thrombosis, I-44121 Ferrara, Italy.
   [Pizzicotti, Stefano; Pellegatti, Patrizia] Hosp Univ Ferrara, I-44121 Ferrara, Italy.
   [Ciccone, Maria] Hosp Univ Ferrara, Haematol Unit, I-44121 Ferrara, Italy.
   [Tisato, Veronica] Univ Ferrara, Lab Technol Adv Therapies LTTA Ctr, I-44121 Ferrara, Italy.
C3 University of Ferrara; University of Ferrara; University of Ferrara;
   University of Ferrara; Arcispedale Sant'Anna; University of Ferrara;
   Arcispedale Sant'Anna; University of Ferrara
RP Gemmati, D (corresponding author), Univ Ferrara, Dept Translat Med, I-44121 Ferrara, Italy.; Gemmati, D (corresponding author), Univ Ferrara, Univ Strateg Ctr Studies Gender Med, I-44121 Ferrara, Italy.; Gemmati, D (corresponding author), Univ Ferrara, Ctr Haemostasis & Thrombosis, I-44121 Ferrara, Italy.
EM d.gemmati@unife.it
RI Serino, Maria/AAC-7368-2022; Tisato, Veronica/K-4525-2016; Pellegatti,
   Patrizia/A-1891-2011; Salvatori, Francesca/C-5501-2016
OI D'Aversa, Elisabetta/0000-0003-3058-5866; Gemmati,
   Donato/0000-0001-6213-6120; Antonica, Bianca/0009-0003-1153-2643;
   Salvatori, Francesca/0000-0001-8950-9978
FU University of Ferrara
FX No Statement Available
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NR 72
TC 0
Z9 0
U1 1
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4425
J9 GENES-BASEL
JI Genes
PD APR
PY 2024
VL 15
IS 4
AR 432
DI 10.3390/genes15040432
PG 14
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA PA2B5
UT WOS:001211283000001
PM 38674367
OA Green Published, gold
DA 2025-04-10
ER

PT J
AU Xiao, P
   Goodarzi, P
   Pezeshki, A
   Hagen, DE
AF Xiao, Ping
   Goodarzi, Parniyan
   Pezeshki, Adel
   Hagen, Darren E.
TI RNA-seq reveals insights into molecular mechanisms of metabolic
   restoration via tryptophan supplementation in low birth weight piglet
   model
SO JOURNAL OF ANIMAL SCIENCE
LA English
DT Article
DE lipid metabolism; low birth weight; piglets; RNA sequencing; tryptophan
ID INTRAUTERINE GROWTH RESTRICTION; DIFFERENTIAL EXPRESSION; DEVELOPMENTAL
   ORIGINS; INSULIN SENSITIVITY; BINDING PROTEINS; AMINO-ACID; LIVER;
   PREDISPOSES; ADIPONECTIN; RESISTANCE
AB Low birth weight (LBW) is associated with metabolic disorders in early life. While dietary L-tryptophan (Trp) can ameliorate postprandial plasma triglycerides (TG) disposal in LBW piglets, the genetic and biological basis underlying Trp-caused alterations in lipid metabolism is poorly understood. In this study, we collected 24 liver samples from 1-mo-old LBW and normal birth weight (NBW) piglets supplemented with different concentrations of dietary Trp (NBW with 0% Trp, NO; LBW with 0% Trp, LO; LBW with 0.4% Trp, L4; LBW with 0.8% Trp, L8; N = 6 in each group.) and conducted systematic, transcriptome-wide analysis using RNA sequencing (RNA-seq). We identified 39 differentially expressed genes (DEG) between NO and LO, and genes within "increased dose effect" clusters based on dose-series expression profile analysis, enriched in fatty acid response of gene ontology (GO) biological process (BP). We then identified RNA-binding proteins including SRSF1, DAZAP1, PUM2, PCBP3, IGF2BP2, and IGF2BP3 significantly (P < 0.05) enriched in alternative splicing events (ASE) in comparison with LO as control. There were significant positive and negative relationships between candidate genes from co-expression networks (including PID1, ANKRD44, RUSC1, and CYP2J34) and postprandial plasma TG concentration. Further, we determined whether these candidate hub genes were also significantly associated with metabolic and cardiovascular traits in humans via human phenome-wide association study (Phe-WAS), and analysis of mammalian orthologs suggests a functional conservation between human and pig. Our work demonstrates that transcriptomic changes during dietary Trp supplementation in LBW piglets. We detected candidate genes and related BP that may play roles on lipid metabolism restoration. These findings will help to better understand the amino acid support in LBW metabolic complications.
   Lay Summary
   Low birth weight (LBW) has been associated with higher rate of mortality and morbidity and the development of metabolic complications, leaving burdens on livestock production and human health care. The feasibility of LBW metabolic restoration via postnatal nutrition compensation has been verified and the role of one of essential amino acids, i-tryptophan (Trp), on rescuing lipid metabolism in LBW was determined, while the underlying molecular mechanism and key gene regulation is little known. Our study was conducted to identify the unique molecular mechanisms between LBW and normal birth weight (NBW), and to identify the metabolic restoration related genes and biological processes after dietary Trp supplementation in LBW piglet model. We found that differentially expressed genes (DEG) between LBW and NBW were related to fatty acid response based on gene ontology enrichment analysis, and LBW piglets supplemented withTrp showed lower postprandial plasma triglycerides (TG) level as NBW, with similar expression feature of lipid metabolism related genes.
C1 [Xiao, Ping; Goodarzi, Parniyan; Pezeshki, Adel; Hagen, Darren E.] Oklahoma State Univ, Dept Anim & Food Sci, Stillwater, OK 74078 USA.
C3 Oklahoma State University System; Oklahoma State University - Stillwater
RP Hagen, DE (corresponding author), Oklahoma State Univ, Dept Anim & Food Sci, Stillwater, OK 74078 USA.
EM darren.hagen@okstate.edu
OI Xiao, Ping/0000-0001-5678-501X; Hagen, Darren/0000-0001-8295-020X
FU USDA National Institute of Food and Agriculture (NIFA)
   [2021-67016-33399, 1016157, 1012889]; USDA National Institute of Food
   and Agriculture
FX The authors thank Mohammad Habibi, Kennedy Roberts, Julia Sutton, and
   Cedrick N. Shili for their invaluable assistance in animal husbandry and
   Dr Andrew Foote for reviewing this manuscript. This work is supported by
   Animal Health and Production and Animal Products: Improved Nutritional
   Performance, Growth, and Lactation of Animals program from the USDA
   National Institute of Food and Agriculture (NIFA) grant no.
   2021-67016-33399 (AP) and Hatch project accession no. 1016157 (DEH) and
   1012889 (AP) from the USDA National Institute of Food and Agriculture.
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NR 65
TC 2
Z9 2
U1 1
U2 19
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0021-8812
EI 1525-3163
J9 J ANIM SCI
JI J. Anim. Sci.
PD MAY 1
PY 2022
VL 100
IS 5
DI 10.1093/jas/skac156
EA MAY 2022
PG 10
WC Agriculture, Dairy & Animal Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture
GA 1T1YS
UT WOS:000804533600009
PM 35552417
OA hybrid, Green Published
DA 2025-04-10
ER

PT J
AU Cohn, RD
   Mayer, U
   Saher, G
   Herrmann, R
   van der Flier, A
   Sonnenberg, A
   Sorokin, L
   Voit, T
AF Cohn, RD
   Mayer, U
   Saher, G
   Herrmann, R
   van der Flier, A
   Sonnenberg, A
   Sorokin, L
   Voit, T
TI Secondary reduction of α7B integrin in laminin α2 deficient congenital
   muscular dystrophy supports an additional transmembrane link in skeletal
   muscle
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article
DE extracellular matrix; alpha 7 integrin; muscle function; muscular
   dystrophy
ID EXTRACELLULAR-MATRIX; CYTOPLASMIC DOMAINS; CELL-ADHESION; GLYCOPROTEIN
   COMPLEX; MOUSE DEVELOPMENT; BETA-1D INTEGRIN; CARDIAC-MUSCLE;
   EXPRESSION; CHAIN; DYSTROGLYCAN
AB The integrins are a large family of heterodimeric transmembrane cellular receptors which mediate the association between the extracellular matrix (ECM) and cytoskeletal proteins. The alpha 7 beta 1 integrin is a major laminin binding integrin in skeletal and cardiac muscle and is thought to be involved in myogenic differentiation and migration processes. The main binding partners of the alpha 7 integrin are laminin-l (alpha 1-beta 1-gamma 1), laminin-2 (alpha 2-beta 1-gamma 1) and laminin-4 (alpha 2-beta 2-gamma 1). Targeted deletion of the gene for the alpha 7 integrin subunit (ITGA7) in mice leads to a novel form of muscular dystrophy. In the present study we have investigated the expression of two alternative splice variants, the alpha 7B and beta 1D integrin subunits, in normal human skeletal muscle, as well as in various forms of muscular dystrophy. In normal human skeletal muscle the expression of the alpha 7 integrin subunit appeared to be developmentally regulated: it was first detected at 2 years of age. Ln contrast, the beta 1D integrin could be detected in immature and mature muscle in the sarcolemma of normal fetal skeletal muscle at 18 weeks gestation. The expression of alpha 7B integrin was significantly reduced at the sarcolemma in six patients with laminin alpha 2 chain deficient congenital muscular dystrophy (CMD) (age >2 years). However, this reduction was not correlated with the amount of laminin alpha 2 chain expressed. In contrast, the expression of the laminin a2 chain was not altered in the skeletal muscle of the alpha 7 knock-out mice. These data argue in favor that there is not a tight correlation between the expression of the alpha 7 integrin subunit and that of the laminin alpha 2 chain in either human or murine dystrophic muscle. Interestingly, in dystrophinopathies (Duchenne and Becker muscular dystrophy; DMD/BMD) expression of alpha 7B was upregulated irrespective of the level of dystrophin expression as shown by a strong sarcolemmal staining pattern even in young boys (age <2 years). The expression of the beta 1D integrin subunit was not altered in any of our patients with different types of muscular dystrophy. In contrast, sarcolemmal expression of beta 1D integrin was significantly reduced in the alpha 7 integrin knock-out mice, whereas the expression of the components of the DGC was not altered. The secondary loss of alpha 7B in laminin alpha 2 chain deficiency defines a biochemical change in the composition of the plasma membrane resulting from a primary protein deficiency in the basal lamina. These findings, in addition to the occurrence of a muscular dystrophy in alpha 7 deficient mice, implies that the alpha 7B integrin is an important laminin receptor within the plasma membrane which plays a significant role in skeletal muscle function and stability. (C) 1999 Elsevier Science B.V. All rights reserved.
C1 Univ Essen Gesamthsch, Dept Pediat, D-45122 Essen, Germany.
   Univ Essen Gesamthsch, Dept Pediat Neurol, D-45122 Essen, Germany.
   Max Planck Inst Biochem, D-82152 Martinsried, Germany.
   Netherlands Canc Inst, Div Cell Biol, Amsterdam, Netherlands.
   Univ Erlangen Nurnberg, Inst Expt Med, D-8520 Erlangen, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen; Max Planck
   Society; Netherlands Cancer Institute; University of Erlangen Nuremberg
RP Voit, T (corresponding author), Univ Essen Gesamthsch, Dept Pediat, Hufelandstr 55, D-45122 Essen, Germany.
EM thomas.voit@uni-essen.de
RI Cohn, Ronald/AAC-5835-2021; Sorokin, Lev/C-2662-2014; Saher,
   Gesine/AAH-1826-2021
OI van der Flier, Arjan/0000-0002-6911-9291; Saher,
   Gesine/0000-0003-3507-9604; Sorokin, Lydia/0000-0001-7704-7921
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NR 53
TC 62
Z9 75
U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD MAR 1
PY 1999
VL 163
IS 2
BP 140
EP 152
DI 10.1016/S0022-510X(99)00012-X
PG 13
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 196DJ
UT WOS:000080293500006
PM 10371075
DA 2025-04-10
ER

PT J
AU Alberti, C
AF Alberti, C.
TI Hereditary/familial versus sporadic prostate cancer: few indisputable
   genetic differences and many similar clinicopathological features
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE Inheritance; Prostate cancer; Microenvironment; Tumors; Urology
ID D-RECEPTOR GENE; CLINICAL CHARACTERISTICS; SUSCEPTIBILITY GENE;
   MOLECULAR MARKERS; RISK; POLYMORPHISMS; ASSOCIATION; EXPRESSION;
   VARIANTS; ANDROGEN
AB Genetic factors and their interactions with environmental conditions and internal microenvironment influence the prostate cancer (PC) development, so that gene expression couldn't strictly occur on the basis of reductionist determinisms of DNA causality but should also conform to multifactorial and stochastic events, moreover, considering the preRNA alternative splicing-mediated multi-protein assemblying mechanisms. Nevertheless, after age and ethnic background, the strongest epidemiological risk factor for PC is a positive family history. However, apart from RNaseL-, ElaC2-, MSR1-genes, there are not other identified high-risk genetic variants which might be considered responsible for hereditary PC, moreover suggesting that familial PC is a genetically heterogeneous disease, many gene loci rather than a specific major susceptibility gene predisposing to it. Gene-environment interactions play a crucial role in cancer development especially when low penetrance genes, such as in case of genetic polymorphisms, are the major players. Several epidemiological studies show, in some families, a possible, either syncronous or metachronous, association of other tumors (breast, brain, gastrointestinal tumors, lymphomas) with PC, thus suggesting a common genetic background. As far as the role of androgen metabolism and androgen receptor (AR)-related genes in the development of familial PC is concerned, a small number of either guanine-guanine-cytosine (<16) or cytosine-adenine-guanine (<18) repeats appears to increase the AR activity, resulting in a raising PC risk. Regarding the expression of both androgen and estrogen receptor-related genes in sporadic and hereditary PC, the immunohistochemistry findings show that the percentage of AR-positive cancer cells is higher in hereditary PC than in sporadic forms, whereas the mean number of estrogen-a-receptor-positive stromal cells is higher in sporadic PC rather than in that hereditary. As for 5-alpha-steroid-reductase-2 gene, the dinucleoticle thymine-adenine repeated 18 times on the last exon, confers an increased PC predisposition, as it is mainly shown in African-American populations. Also VDR gene, that is a component of ligand (steroid)-dependent nuclear transcription factor superfamily, shows various polymorphisms which appear to be associated with PC risk. Except an earlier age of onset, no anatomo-clinical and tumor progression peculiarities between hereditary and sporadic PC have been generally identified. Indeed, tumor progression and metastasis, both in hereditary and sporadic PC, are mainly influenced by a variety of biochemical and immune-mediated tumor microenvironmental conditions rather than by the hereditary genetic factors, thus gene expression associated with invasive ability representing a newly acquired genetic variant rather than a selection of pre-existent gene abnormalities in PC cells. It's questionable whether genetic testing of unaffected men of hereditary PC families might be actually useful. Nevertheless a suitable counselling must be proposed. Family history and/or gene profiling-guided preventive strategies for men at high risk of familial PC, range from dietary to drug measures. Cancer chemopreventive approaches may include 5-alpha-reductase inhibitors, histone deacetylase inhibitors, antioxidans, non-steroidal anti-inflammatory drugs, cholesterol-lowering statins, vitamin D analogues.
C1 Univ Parma, LD Surg Semeiot, I-43100 Parma, Italy.
C3 University of Parma
RP Alberti, C (corresponding author), Univ Parma, LD Surg Semeiot, I-43100 Parma, Italy.
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NR 74
TC 23
Z9 25
U1 0
U2 6
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PD JAN
PY 2010
VL 14
IS 1
BP 31
EP 41
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 554DM
UT WOS:000274415700004
PM 20184087
DA 2025-04-10
ER

PT J
AU Cooper, AJL
AF Cooper, AJL
TI The role of glutamine transaminase K (GTK) in sulfur and α-keto acid
   metabolism in the brain, and in the possible bioactivation of
   neurotoxicants
SO NEUROCHEMISTRY INTERNATIONAL
LA English
DT Review
DE glutamine transaminase K; sulfur metabolism; alpha-keto acid metabolism;
   kynurenine aminotransferase; bioactivation of neurotoxicants
ID CONJUGATE BETA-LYASE; KYNURENINE AMINOTRANSFERASE-I; METHIONINE SALVAGE
   PATHWAY; KIDNEY-SELECTIVE PRODRUGS; KETIMINE DECARBOXYLATED DIMER; LIVER
   OMEGA-AMIDASE; RAT-BRAIN; AMINOETHYLCYSTEINE KETIMINE; AMINO-ACIDS;
   L-CYSTATHIONINE
AB Glutamine transaminase K (GTK), which is a freely reversible glutamine (methionine) aromatic amino acid aminotransferase, is present in most mammalian tissues, including brain. Quantitatively, the most important amine donor in vivo is glutamine. The product of glutamine transamination (i.e., alpha-ketoglutaramate; alphaKGM) is rapidly removed by cyclization and/or conversion to alpha-ketoglutarate. Transamination is therefore "pulled" in the direction of glutamine utilization. Major biological roles of GTK are to maintain low levels of phenylpyruvate and to close the methionine salvage pathway. GTK also catalyzes the transamination of cystathionine, lanthionine, and thialysine to the corresponding alpha-keto acids, which cyclize to ketimines. The cyclic ketimines and several metabolites derived there from are found in brain. It is not clear whether these compounds have a biological function or are metabolic dead-ends. However, high-affinity binding of lanthionine ketimine (LK) to brain membranes has been reported.
   Mammalian tissues possess several enzymes capable of catalyzing transamination of kynurenine in vitro. Two of these kynurenine aminotransferases (KATs), namely KAT I and KAT II, are present in brain and have been extensively studied. KAT I and KAT II are identical to GTK and alpha-aminoadipate aminotransferase, respectively. GTK/KAT I is largely cytosolic in kidney, but mostly mitochondrial in brain. The same gene codes for both forms, but alternative splicing dictates whether a 32-amino acid mitochondrial-targeting sequence is present in the expressed protein. The activity of KAT I is altered by a missense mutation (E61G) in the spontaneously hypertensive rat. The symptoms may be due in part to alteration of kynurenine transamination. However, owing to strong competition from other amino acid substrates, the turnover of kynurenine to kynurenate by GTK/KAT I in nervous tissue must be slow unless kynurenine and GTK are sequestered in a compartment distinct from the major amino acid pools. The possibility is discussed that the spontaneous hypertension in rats carrying the GTK/KAT I mutation may be due in part to disruption of glutamine transamination.
   GTK is one of several pyridoxal 5'-phosphate (PLP)-containing enzymes that can catalyze non-physiological beta-elimination reactions with cysteine S-conjugates containing a good leaving group attached at the sulfur. These elimination reactions may contribute to the bioactivation of certain electrophiles, resulting in toxicity to kidney, liver, brain, and possibly other organs. On the other hand, the beta-lyase reaction catalyzed by GTK may be useful in the conversion of some cysteine S-conjugate prodrugs to active components in vivo.
   The roles of GTK in (a) brain nitrogen, sulfur, and aromatic amino acid/kynurenine metabolism, (b) brain alpha-keto acid metabolism, (c) bioactivation of certain electrophiles in brain, (d) prodrug targeting, and (e) maintenance of normal blood pressure deserve further study. (C) 2004 Elsevier Ltd. All rights reserved.
C1 Cornell Univ, Weill Med Coll, Burke Med Res Inst, Dept Biochem, White Plains, NY 10605 USA.
   Cornell Univ, Weill Med Coll, Burke Med Res Inst, Dept Neurol & Neurosci, White Plains, NY 10605 USA.
C3 Cornell University; Weill Cornell Medicine; Cornell University; Weill
   Cornell Medicine
RP Cornell Univ, Weill Med Coll, Burke Med Res Inst, Dept Biochem, 785 Mamaroneck Ave, White Plains, NY 10605 USA.
EM acooper@burke.org
RI Cooper, Arthur/H-5171-2016
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NR 186
TC 98
Z9 106
U1 0
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0197-0186
EI 1872-9754
J9 NEUROCHEM INT
JI Neurochem. Int.
PD JUN
PY 2004
VL 44
IS 8
BP 557
EP 577
DI 10.1016/j.neuint.2003.12.002
PG 21
WC Biochemistry & Molecular Biology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 805TG
UT WOS:000220388000001
PM 15016471
DA 2025-04-10
ER

PT J
AU Hai, J
   Li, ST
   Lin, Q
   Pan, QG
   Gao, F
   Ding, MX
AF Hai, J
   Li, ST
   Lin, Q
   Pan, QG
   Gao, F
   Ding, MX
TI Vascular endothelial growth factor expression and angiogenesis induced
   by chronic cerebral hypoperfusion in rat brain
SO NEUROSURGERY
LA English
DT Article
DE angiogenesis; animal model; carotid artery-jugular vein fistula;
   cerebral arteriovenous malformations; vascular endothelial growth factor
ID FACTOR MESSENGER-RNA; ARTERIOVENOUS-MALFORMATIONS; UP-REGULATION;
   STRUCTURAL PROTEINS; HYPOXIA; ISCHEMIA; MODEL; OCCLUSION; RECEPTORS;
   VEGF
AB OBJECTIVE: In a rat model, we studied the time courses of vascular endothelial growth factor (VEGF) expression and angiogenesis induced by chronic cerebral hypoperfusion in the brain, and we investigated the histological bases of normal-perfusion pressure breakthrough.
   METHODS: Twenty-one Sprague-Dawley rats were randomly divided into a control group ( n = 3) and a model group assessed at various time points after the creation of a carotid artery-jugular vein fistula (12 h, n = 3; 24 h, n = 3; 72 h, n = 3; 7 d, n = 3; 21 d, n = 3; 90 d, n = 3). The time courses of the expression of VEGF messenger ribonucleic acid (mRNA) and protein in rat brain were analyzed with semiquantitative reverse transcriptase-polymerase chain reaction and Western blot assays, respectively. Immunohistochemical techniques were used to evaluate VEGF protein localization with rabbit polyclonal anti-rat VEGF, VEGF receptor (VEGFR) expression with rabbit polyclonal antibodies to VEGFR-1 and -2, microvascular density with mouse monoclonal anti-rat CD31, and astrocytic reactivity with polyclonal anti-glial fibrillary acidic protein, in cerebral cortical tissue of the right middle cerebral artery territory.
   RESULTS: Three alternative splicing forms, i.e., VEGF(188), VEGF(164), and VEGF(120), were observed in cerebral coritcal tissue of the right middle cerebral artery territory in semiquantitative reverse transcriptase-polymerase chain reaction analyses. VEGF(164) mRNA was the predominant isoform expressed in rat brain. VEGF(188) mRNA and VEGF(120) mRNA were also detected but at very low levels (not statistically significant). Low levels of VEGF(164) mRNA were observed in the control brains. However, VEGF(164) mRNA levels were significantly increased in the model brains at 24 hours postoperatively, peaked by 7 days, decreased by 21 days, and returned to basal levels by 90 days after fistula formation. VEGF protein expression, as measured in Western blot assays, was also increased in rat brains in the model group from 24 hours to 21 days postoperatively but returned to control levels by 90 days after fistula formation. VEGF immunohistochemical analyses indicated that this increased expression was mostly associated with endothelial cells. Consistent with the VEGF protein expression findings, up-regulation of VEGFR-1 but not VEGFR-2 expression on endothelial cells in the model brains was observed. Microvascular density in the rat brains began to increase significantly 7 days after fistula formation in the model group, as assessed immunohistochemically, and the increase was maintained for 90 days. Although no prominent astrocytic reactivity was observed in the rat brains throughout the experiments, there was an absence of astrocytic foot processes surrounding some cerebral capillaries 90 days after fistula formation in the model group.
   CONCLUSION: These results demonstrated that chronic cerebral hypoperfusion could induced sustained up-regulation of VEGF mRNA and protein expression in rat brain, which was correlated with angiogenesis. An absence of corresponding astrocytic reactivity during angiogenesis may be an important factor accounting for structural deficits of the blood-brain barrier and the occurrence of normal-perfusion pressure breakthrough.
C1 Tongji Univ, Tongji Hosp, Dept Neurosurg, Shanghai 200065, Peoples R China.
   Shanghai Med Univ 2, Dept Chem, Shanghai, Peoples R China.
   Shanghai Med Univ 2, Dept Cytobiol, Shanghai, Peoples R China.
   Shanghai Med Univ 2, Peoples Hosp 9, Dept Neurosurg, Shanghai, Peoples R China.
C3 Tongji University; Shanghai Jiao Tong University; Shanghai Jiao Tong
   University; Shanghai Jiao Tong University
RP Hai, J (corresponding author), Tongji Univ, Tongji Hosp, Dept Neurosurg, 389 XinCun Rd, Shanghai 200065, Peoples R China.
RI LI, SHUTING/LTZ-8022-2024; Friedlander, Robert/A-2845-2016
OI Friedlander, Robert/0000-0003-4423-9219
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NR 39
TC 67
Z9 87
U1 0
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD OCT
PY 2003
VL 53
IS 4
BP 963
EP 970
DI 10.1227/01.NEU.0000083594.10117.7A
PG 8
WC Clinical Neurology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Surgery
GA 731QP
UT WOS:000185898200052
PM 14519228
DA 2025-04-10
ER

EF