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Titolo:
Dexras1: A G protein specifically coupled to neuronal nitric oxide synthase via CAPON
Autore:
Fang, M; Jaffrey, SR; Sawa, A; Ye, KQ; Luo, XJ; Snyder, SH;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 urosci, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205USA Johns Hopkins Univ Baltimore MD USA 21205 Mol Sci, Baltimore, MD 21205USA Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 ychiat, Baltimore, MD 21205 USA
Titolo Testata:
NEURON
fascicolo: 1, volume: 28, anno: 2000,
pagine: 183 - 193
SICI:
0896-6273(200010)28:1<183:DAGPSC>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
PHOSPHOTYROSINE-BINDING DOMAIN; RELAXING FACTOR; S-NITROSOGLUTATHIONE; GUANYLATE-CYCLASE; NMDA RECEPTORS; SMOOTH-MUSCLE; MAP KINASE; L-ARGININE; B-RAF; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Snyder, SH Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205USA Johns Hopkins Univ Baltimore MD USA 21205 timore, MD 21205 USA
Citazione:
M. Fang et al., "Dexras1: A G protein specifically coupled to neuronal nitric oxide synthase via CAPON", NEURON, 28(1), 2000, pp. 183-193

Abstract

Because nitric oxide (NO) is a highly reactive signaling molecule, chemical inactivation by reaction with oxygen, superoxide, and glutathione competes with specific interactions with target proteins. NO signaling may be enhanced by adaptor proteins that couple neuronal NO synthase (nNOS) to specific target proteins. Here we identify a selective interaction of the nNOS adaptor protein CAPON with Dexras1, a brain-enriched member of the Pas family of small monomeric G proteins. We find that Dexras1 is activated by NO donors as well as by NMDA receptor-stimulated NO synthesis in cortical neurons. The importance of Dexras1 as a physiologic target of nNOS is established by the selective decrease of Dexras1 activation, but not H-Ras or four otherPas family members, in the brains of mice harboring a targeted genomic deletion of nNOS (nNOS(-/-)). We also find that nNOS, CAPON, and Dexras1 form a ternary complex that enhances the ability of nNOS to activate Dexras1. These findings identity Dexras1 as a novel physiologic NO effector and suggest that anchoring of nNOS to specific targets is a mechanism by which NO signaling is enhanced.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/07/20 alle ore 07:13:33