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

Published

Journal Article

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, i.e. 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-1-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.

Full Text

Duke Authors

Cited Authors

  • Lin, FT; Daaka, Y; Lefkowitz, RJ

Published Date

  • November 27, 1998

Published In

Volume / Issue

  • 273 / 48

Start / End Page

  • 31640 - 31643

PubMed ID

  • 9822622

International Standard Serial Number (ISSN)

  • 0021-9258

Digital Object Identifier (DOI)

  • 10.1074/jbc.273.48.31640

Language

  • eng

Conference Location

  • United States