β-arrestins regulate mitogenic signaling and clathrin-mediated endocytosis of the insulin-like growth factor I receptor

被引:159
作者
Lin, FT
Daaka, Y
Lefkowitz, RJ
机构
[1] Duke Univ, Med Ctr, Dept Med, Howard Hughes Med Inst, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA
关键词
D O I
10.1074/jbc.273.48.31640
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 mediate agonist-dependent desensitization of G protein-coupled receptors and target the receptors to clathrin-coated pits for internalization. Here we report an expanded role of beta-arrestins in promoting clathrin-mediated endocytosis of a tyrosine kinase growth factor receptor, ie. the insulin-like growth factor I (IGF-1) receptor. beta-Arrestins bind to the ligand-occupied IGF-1 receptors, promote their endocytosis, and enhance IGF-l-dependent mitogen-activated protein kinase phosphorylation and DNA synthesis. Our results suggest a role for beta-arrestins in regulating mitogenic signaling and clathrin-mediated endocytosis of receptors not classically coupled to G proteins.
引用
收藏
页码:31640 / 31643
页数:4
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