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Titolo:
Characterization of the carboxyl terminal-truncated endothelin B receptor coexpressed with G protein-coupled receptor kinase 2
Autore:
Shibasaki, T; Moroi, K; Nishiyama, M; Zhou, J; Sakamoto, A; Masaki, T; Ito, K; Haga, T; Kimura, S;
Indirizzi:
ChibanUniv, Dept Biochem & Mol Pharmacol, Grad Sch Med, Chiba 2608670, Japa Chiba Univ Chiba Japan 2608670 rmacol, Grad Sch Med, Chiba 2608670, Japa Natl Cardiovasc Ctr, Res Inst, Suita, Osaka 5658565, Japan Natl CardiovascCtr Suita Osaka Japan 5658565 Suita, Osaka 5658565, Japan Univ Tokyo, Dept Neurochem, Fac Med, Tokyo 1130033, Japan Univ Tokyo Tokyo Japan 1130033 Neurochem, Fac Med, Tokyo 1130033, Japan
Titolo Testata:
BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL
fascicolo: 4, volume: 47, anno: 1999,
pagine: 569 - 577
SICI:
1039-9712(199904)47:4<569:COTCTE>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
PHOSPHORYLATION SITES; CYTOPLASMIC TAIL; DESENSITIZATION; ETB; INTERNALIZATION; SPECIFICITY; CONTRACTION; EXPRESSION; RHODOPSIN; CLONING;
Keywords:
endothelin; endothelin B receptor; G protein-coupled receptor; G protein-coupled receptor kinase; phosphorylation; desensitization;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Kimura, S ChibaaUniv, Dept Biochem & Mol Pharmacol, Grad Sch Med, 1-8-1 Inohana, Chib Chiba Univ 1-8-1 Inohana Chiba Japan 2608670 -8-1 Inohana, Chib
Citazione:
T. Shibasaki et al., "Characterization of the carboxyl terminal-truncated endothelin B receptor coexpressed with G protein-coupled receptor kinase 2", BIOC MOL B, 47(4), 1999, pp. 569-577

Abstract

The role of phosphorylation of the C-terminal tail of endothelin B receptor (ETBR) in agonist-induced desensitization was investigated, using a mutant lacking C-terminal 40 amino acids (Delta 40 ETBR). In cells expressing the wild type or Delta 40 ETBR, ET-1 caused rapid desensitization of calcium responses. The wild type ETBR was phosphorylated by biotinylated ET-1, and the phosphorylation was markedly enhanced by coexpression with G protein-coupled receptor kinase 2 (GRK2). However, Delta 40 ETBR was not phosphorylated regardless of coexpression with GRK2. On the other hand, ET-1-induced IP3 formation in these cells was decreased by coexpression with GRK2 or catalytically inactive Lys220Arg GRK2 to the similar extent. The present study demonstrates the presence of phosphorylation-independent desensitization mechanism in Delta 40 ETBR and suggests that GRK2 might play a role other thanthat as a kinase.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 08:58:42