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

Published

Journal Article

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 2AR) mutants defective in their ability to sequester, an effect enhanced by simultaneous overexpression of beta-adrenergic receptor kinase 1. Wild-type beta 2AR 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.

Full Text

Duke Authors

Cited Authors

  • Ferguson, SS; Downey, WE; Colapietro, AM; Barak, LS; Ménard, L; Caron, MG

Published Date

  • January 19, 1996

Published In

Volume / Issue

  • 271 / 5247

Start / End Page

  • 363 - 366

PubMed ID

  • 8553074

Pubmed Central ID

  • 8553074

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.271.5247.363

Language

  • eng

Conference Location

  • United States