When a G protein-coupled receptor does not couple to a G protein. Review uri icon

Overview

abstract

  • Classically, G protein-coupled receptors (GPCRs) relay signals by directly activating heterotrimeric guanine nucleotide-binding proteins (G proteins). Increasing evidence indicates that GPCRs may also signal through G protein-independent pathways. JAK/STATs, Src-family tyrosine kinases, GRKs/beta-arrestins, and PDZ domain-containing proteins have been suggested to directly relay signals from GPCRs independent of G proteins. In addition, our laboratory recently reported that the beta(2) adrenergic receptor (beta(2)AR) could switch from G protein-coupled to G protein-independent ERK (extracellular signal-regulated kinase) activation in an agonist dosage-dependent manner. This finding provides a novel mechanism for G protein-independent GPCR signaling. This review focuses on recent progress in understanding the mechanisms by which G protein-independent GPCR signaling occurs.

publication date

  • October 4, 2007

Research

keywords

  • GTP-Binding Proteins
  • Receptors, G-Protein-Coupled

Identity

Scopus Document Identifier

  • 36148944785

Digital Object Identifier (DOI)

  • 10.1039/b706343a

PubMed ID

  • 18000562

Additional Document Info

volume

  • 3

issue

  • 12