Molecular mechanisms of G protein-coupled receptor signaling: role of G protein-coupled receptor kinases and arrestins in receptor desensitization and resensitization.

Published

Journal Article (Review)

Dynamic regulation of G protein-coupled receptor signaling demands a coordinated balance between mechanisms leading to the generation, turning off and re-establishment of agonist-mediated signals. G protein-coupled receptor kinases (GRKs) and arrestin proteins not only mediate agonist-dependent G protein-coupled receptor desensitization, but also initiate the internalization (sequestration) of activated receptors, a process leading to receptor resensitization. Studies on the specificity of beta-arrestin functions reveal a multiplicity of G protein-coupled receptor endocytic pathways and suggest that beta-arrestins might serve as adaptors specifically targeting receptors for dynamin-dependent clathrin-mediated endocytosis. Moreover, inactivation of the GRK2 gene in mice has lead to the discovery of an unexpected role of GRK2 in cardiac development, further emphasizing the pleiotropic function of GRKs and arrestins.

Full Text

Duke Authors

Cited Authors

  • Zhang, J; Ferguson, SS; Barak, LS; Aber, MJ; Giros, B; Lefkowitz, RJ; Caron, MG

Published Date

  • 1997

Published In

Volume / Issue

  • 5 / 3-4

Start / End Page

  • 193 - 199

PubMed ID

  • 9606723

Pubmed Central ID

  • 9606723

International Standard Serial Number (ISSN)

  • 1060-6823

Language

  • eng

Conference Location

  • England