BETA-ADRENERGIC-RECEPTOR KINASE-2 AND BETA-ARRESTIN-2 AS MEDIATORS OF ODORANT-INDUCED DESENSITIZATION

被引：174

作者：

DAWSON, TM

ARRIZA, JL

JAWORSKY, DE

BORISY, FF

ATTRAMADAL, H

LEFKOWITZ, RJ

RONNETT, GV

机构：

[1] JOHNS HOPKINS MED INST,DEPT NEUROSCI,725 N WOLFE ST,BALTIMORE,MD 21205

[2] JOHNS HOPKINS MED INST,DEPT NEUROL,BALTIMORE,MD 21205

[3] DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT MED & BIOCHEM,DURHAM,NC 27710

来源：

SCIENCE | 1993年 / 259卷 / 5096期

关键词：

D O I：

10.1126/science.8381559

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Beta-adrenergic receptor kinase (betaARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms betaARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against betaARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that betaARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.

引用

页码：825 / 829

页数：5

共 33 条

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