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Titolo:
RGS4 inhibits G-protein signaling in cardiomyocytes
Autore:
Tamirisa, P; Blumer, KJ; Muslin, AJ;
Indirizzi:
WashingtonUSAiv, Sch Med, Cardiovasc Res Ctr, Dept Med, St Louis, MO 63110Washington Univ St Louis MO USA 63110 s Ctr, Dept Med, St Louis, MO 63110 Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USAWashington Univ St Louis MO USA 63110 l & Physiol, St Louis, MO 63110 USA
Titolo Testata:
CIRCULATION
fascicolo: 3, volume: 99, anno: 1999,
pagine: 441 - 447
SICI:
0009-7322(19990126)99:3<441:RIGSIC>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
GTPASE-ACTIVATING PROTEINS; RAT MYOCARDIAL-CELLS; CARDIAC MYOCYTES; GENE-EXPRESSION; ANGIOTENSIN-II; DIASTOLIC DYSFUNCTION; PRESSURE-OVERLOAD; MECHANICAL-STRESS; HYPERTROPHY; HEART;
Keywords:
hypertrophy; genes; growth substances; atrial natriuretic factor; proteins;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Muslin, AJ Washingtonidniv, Sch Med, Cardiovasc Res Ctr, Dept Med, Box 8086,660 S Eucl Washington Univ Box 8086,660 S Euclid Ave St Louis MO USA 63110
Citazione:
P. Tamirisa et al., "RGS4 inhibits G-protein signaling in cardiomyocytes", CIRCULATION, 99(3), 1999, pp. 441-447

Abstract

Background-RGS family members are GTPase-activating proteins for heterotrimeric G(q) and G(i) proteins. RGS genes are expressed in heart tissue and in cultured cardiomyocytes. There is evidence that altered RGS gene expression may contribute to the pathogenesis of cardiac hypertrophy and failure. Methods and Results-We investigated the ability of RGS proteins to block G-protein signaling in vivo by using a cultured cardiomyocyte transfection system. Endothelin-1, angiotensin II, and phenylephrine signal through G(q) or G(i) family members and promote the hypertrophy of cardiomyocytes. We found that phenylephrine-mediated and endothelin-1-mediated induction of the atrial natriuretic factor and myosin light chain-2 genes was inhibited in cells that were transfected with RGS4. Phenylephrine-mediated gene inductionwas not inhibited in cells that were transfected with N128A-RGS4, a point mutant form that lacks GTPase-activating protein activity. Phenylephrine-mediated myofilament organization and cell growth were also blocked in cells by RGS4. Conclusions-These results demonstrate that RGS protein can inhibit G-protein-mediated signaling in vivo and suggest that increased expression of RGS protein may be a counterregulatory mechanism to inhibit G protein signaling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 07:57:47