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Titolo:
GRK3 mediates desensitization of CRF1 receptors: a potential mechanism regulating stress adaptation
Autore:
Dautzenberg, FM; Braun, S; Hauger, RL;
Indirizzi:
Vet Affairs Med Ctr, La Jolla, CA 92093 USA Vet Affairs Med Ctr La Jolla CA USA 92093 Med Ctr, La Jolla, CA 92093 USA Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA Univ Calif SanDiego La Jolla CA USA 92093 ychiat, La Jolla, CA 92093 USA F Hoffmann La Roche & Co Ltd, Div Pharma, CH-4070 Basel, Switzerland F Hoffmann La Roche & Co Ltd Basel Switzerland CH-4070 asel, Switzerland Max Planck Inst Expt Med, Dept Mol Neuroendocrinol, D-37075 Gottingen, Germany Max Planck Inst Expt Med Gottingen Germany D-37075 75 Gottingen, Germany
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
fascicolo: 4, volume: 280, anno: 2001,
pagine: R935 - R946
SICI:
0363-6119(200104)280:4<R935:GMDOCR>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORTICOTROPIN-RELEASING FACTOR; AGONIST-INDUCED DESENSITIZATION; PROTEIN-COUPLED RECEPTORS; DOMINANT-NEGATIVE MUTANT; HISTAMINE H-2 RECEPTORS; HOMOLOGOUS DESENSITIZATION; BETA(2)-ADRENERGIC RECEPTOR; ANTISENSE OLIGONUCLEOTIDES; TYPE-2 RECEPTOR; RAT-BRAIN;
Keywords:
antisense; G protein-coupled receptor kinase; corticotropin-releasing factor type 1 receptor regulation; homologous and heterologous desensitization of the CRF1 receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Hauger, RL Vet Affairs Med Ctr, 9500 Gilman Dr, La Jolla, CA 92093 USA VetAffairs Med Ctr 9500 Gilman Dr La Jolla CA USA 92093 93 USA
Citazione:
F.M. Dautzenberg et al., "GRK3 mediates desensitization of CRF1 receptors: a potential mechanism regulating stress adaptation", AM J P-REG, 280(4), 2001, pp. R935-R946

Abstract

Potential G protein-coupled receptor kinase (GRK) and protein kinase A (PKA) mediation of homologous desensitization of corticotropin-releasing factor type 1 (CRF1) receptors was investigated in human retinoblastoma Y-79 cells. Inhibition of PKA activity by PKI5-22 or H-89 failed to attenuate homologous desensitization of CRF1 receptors, and direct activation of PKA by forskolin or dibutyryl cAMP failed to desensitize CRF-induced cAMP accumulation. However, treatment of permeabilized Y-79 cells with heparin, a nonselective GRK inhibitor, reduced homologous desensitization of CRF1 receptors bysimilar to 35%. Furthermore, Y-79 cell uptake of a GRK3 antisense oligonucleotide (ODN), but not of a random or mismatched ODN, reduced GRK3 mRNA expression by similar to 50% without altering GRK2 mRNA expression and inhibited homologous desensitization of CRF1 receptors by similar to 55%. Finally,Y-79 cells transfected with a GRK3 antisense cDNA construct exhibited an similar to 50% reduction in GRK3 protein expression and an similar to 65% reduction in homologous desensitization of CRF1 receptors. We conclude that GRK3 contributes importantly to the homologous desensitization of CRF1 receptors in Y-79 cells, a brain-derived cell line.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 19:22:10