Classical and new roles of beta-arrestins in the regulation of G-protein-coupled receptors.

Published

Journal Article (Review)

In the classical model of G-protein-coupled receptor (GPCR) regulation, arrestins terminate receptor signalling. After receptor activation, arrestins desensitize phosphorylated GPCRs, blocking further activation and initiating receptor internalization. This function of arrestins is exemplified by studies on the role of arrestins in the development of tolerance to, but not dependence on, morphine. Arrestins also link GPCRs to several signalling pathways, including activation of the non-receptor tyrosine kinase SRC and mitogen-activated protein kinase. In these cascades, arrestins function as adaptors and scaffolds, bringing sequentially acting kinases into proximity with each other and the receptor. The signalling roles of arrestins have been expanded even further with the discovery that the formation of stable receptor-arrestin complexes initiates photoreceptor apoptosis in Drosophila, leading to retinal degeneration. Here we review our current understanding of arrestin function, discussing both its classical and newly discovered roles.

Full Text

Duke Authors

Cited Authors

  • Pierce, KL; Lefkowitz, RJ

Published Date

  • October 1, 2001

Published In

Volume / Issue

  • 2 / 10

Start / End Page

  • 727 - 733

PubMed ID

  • 11584310

Pubmed Central ID

  • 11584310

Electronic International Standard Serial Number (EISSN)

  • 1471-0048

International Standard Serial Number (ISSN)

  • 1471-003X

Digital Object Identifier (DOI)

  • 10.1038/35094577

Language

  • eng