Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling

被引:357
作者
Shukla, Arun K. [1 ,2 ]
Xiao, Kunhong [1 ]
Lefkowitz, Robert J. [1 ,2 ]
机构
[1] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA
基金
美国国家卫生研究院;
关键词
PROTEIN-COUPLED RECEPTOR; BETA(2)-ADRENERGIC RECEPTOR; 7-TRANSMEMBRANE RECEPTORS; PHOSPHATIDYLINOSITOL; 3-KINASE; CONFORMATIONAL-CHANGES; CRYSTAL-STRUCTURE; BETA-2-ADRENERGIC RECEPTOR; ACTIVATED RECEPTOR-2; CLATHRIN ADAPTER; VISUAL ARRESTIN;
D O I
10.1016/j.tibs.2011.06.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
beta-Arrestins, originally discovered to desensitize activated seven transmembrane receptors (7TMRs; also known as G-protein-coupled receptors, GPCRs), are now well established mediators of receptor endocytosis, ubiquitylation and G protein-independent signaling. Recent global analyses of beta-arrestin interactions and beta-arrestin-dependent phosphorylation events have uncovered several previously unanticipated roles of beta-arrestins in a range of cellular signaling events. These findings strongly suggest that the functional roles of beta-arrestins are much broader than currently understood. Biophysical studies aimed at understanding multiple active conformations of the 7TMRs and the beta-arrestins have begun to unravel the mechanistic basis for the diverse functional capabilities of beta-arrestins in cellular signaling.
引用
收藏
页码:457 / 469
页数:13
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