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β‐arrestins and heterotrimeric G‐proteins: collaborators and competitors in signal transduction
Author(s) -
DeFea K
Publication year - 2008
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0707508
Subject(s) - heterotrimeric g protein , g protein coupled receptor , g protein , signal transduction , receptor , biology , microbiology and biotechnology , arrestin , rhodopsin like receptors , neuroscience , computational biology , biochemistry , metabotropic receptor , glutamate receptor
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, β‐arrestins‐1 and 2, independent of heterotrimeric G‐protein coupling. This review discusses several known G‐protein‐independent, β‐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. British Journal of Pharmacology (2008) 153 , S298–S309; doi: 10.1038/sj.bjp.0707508 ; published online 26 November 2007