β-arrestins and G protein-coupled receptor trafficking

Handb Exp Pharmacol. 2014;219:173-86. doi: 10.1007/978-3-642-41199-1_9.

Abstract

Nonvisual arrestins (β-arrestin-1 and β-arrestin-2) are adaptor proteins that function to regulate G protein-coupled receptor (GPCR) signaling and trafficking. β-arrestins are ubiquitously expressed and function to inhibit GPCR/G protein coupling, a process called desensitization, and promote GPCR trafficking and arrestin-mediated signaling. β-arrestin-mediated endocytosis of GPCRs requires the coordinated interaction of β-arrestins with clathrin, adaptor protein 2 (AP2), and phosphoinositides. These interactions are facilitated by a conformational change in β-arrestin that is thought to occur upon binding to a phosphorylated activated GPCR. In this review, we provide an overview of the key interactions involved in β-arrestin-mediated trafficking of GPCRs.

Publication types

  • Review

MeSH terms

  • Adaptor Protein Complex 2 / metabolism
  • Arrestins / chemistry
  • Arrestins / metabolism*
  • Clathrin / metabolism
  • Endocytosis / physiology
  • Humans
  • Phosphatidylinositols / metabolism
  • Phosphorylation / physiology
  • Protein Binding / physiology
  • Protein Conformation
  • Protein Transport / physiology
  • Receptors, G-Protein-Coupled / metabolism*
  • Signal Transduction / physiology*
  • beta-Arrestin 1
  • beta-Arrestin 2
  • beta-Arrestins

Substances

  • ARRB1 protein, human
  • ARRB2 protein, human
  • Adaptor Protein Complex 2
  • Arrestins
  • Clathrin
  • Phosphatidylinositols
  • Receptors, G-Protein-Coupled
  • beta-Arrestin 1
  • beta-Arrestin 2
  • beta-Arrestins