Beta-arrestins and heterotrimeric G-proteins: collaborators and competitors in signal transduction

Br J Pharmacol. 2008 Mar;153 Suppl 1(Suppl 1):S298-309. doi: 10.1038/sj.bjp.0707508. Epub 2007 Nov 26.

Abstract

G-protein-coupled receptors (GPCRs), also known as seven transmembrane receptors (7-TMRs), are the largest protein receptor superfamily in the body. These receptors and their ligands direct a diverse array of physiological responses, and hence have broad relevance to numerous diseases. As a result, they have generated considerable interest in the pharmaceutical industry as drug targets. Recently, GPCRs have been demonstrated to elicit signals through interaction with the scaffolding proteins, beta-arrestins-1 and 2, independent of heterotrimeric G-protein coupling. This review discusses several known G-protein-independent, beta-arrestin-dependent pathways and their potential physiological and pharmacological significance. The emergence of G-protein-independent signalling changes the way in which GPCR signalling is evaluated, from a cell biological to a pharmaceutical perspective and raises the possibility for the development of pathway specific therapeutics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Actin Depolymerizing Factors / physiology
  • Animals
  • Arrestins / chemistry
  • Arrestins / physiology*
  • Enzyme Activation / physiology
  • GTP-Binding Proteins / chemistry
  • GTP-Binding Proteins / physiology*
  • Humans
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / physiology
  • Phosphatidylinositol 3-Kinases / physiology
  • Signal Transduction / physiology*
  • beta-Arrestins

Substances

  • Actin Depolymerizing Factors
  • Arrestins
  • NF-kappa B
  • beta-Arrestins
  • Phosphatidylinositol 3-Kinases
  • Mitogen-Activated Protein Kinases
  • GTP-Binding Proteins