Role of beta-arrestin in mediating agonist-promoted G protein-coupled receptor internalization

被引：832

作者：

Ferguson, SSG

Downey, WE

Colapietro, AM

Barak, LS

Menard, L

Caron, MG

机构：

[1] DUKE UNIV,MED CTR,HOWARD HUGHES MED INST LABS,DURHAM,NC 27710

[2] DUKE UNIV,MED CTR,DEPT CELL BIOL,DURHAM,NC 27710

[3] DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710

来源：

SCIENCE | 1996年 / 271卷 / 5247期

关键词：

D O I：

10.1126/science.271.5247.363

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-Arrestins are proteins that bind phosphorylated heterotrimeric GTP-binding protein (G protein)-coupled receptors (GPCRs) and contribute to the desensitization of GPCRs by uncoupling the signal transduction process. Resensitization of GPCR responsiveness involves agonist-mediated receptor sequestration. Overexpression of beta-arrestins in human embryonic kidney cells rescued the sequestration of beta(2)-adrenergic receptor (beta(2)AR) mutants defective in their ability to sequester, an effect enhanced by simultaneous overexpression of beta-adrenergic receptor kinase 1, Wild-type beta(2)AR sequestration was inhibited by the overexpression of two beta-arrestin mutants. These findings suggest that beta-arrestins play an integral role in GPCR internalization and thus serve a dual role in the regulation of GPCR function.

引用

页码：363 / 366

页数：4

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