Cellular and Molecular Life Sciences

, Volume 66, Issue 20, pp 3337–3352

Alternative splicing of G protein-coupled receptors: physiology and pathophysiology

Review

DOI: 10.1007/s00018-009-0093-4

Cite this article as:
Markovic, D. & Challiss, R.A.J. Cell. Mol. Life Sci. (2009) 66: 3337. doi:10.1007/s00018-009-0093-4

Abstract

The G protein-coupled receptors (GPCRs) are a superfamily of transmembrane receptors that have a broad distribution and can collectively recognise a diverse array of ligands. Activation or inhibition of GPCR signalling can affect many (patho)physiological processes, and consequently they are a major target for existing and emerging drug therapies. A common observation has been that the pharmacological, signalling and regulatory properties of GPCRs can differ in a cell- and tissue-specific manner. Such “phenotypic” diversity might be attributable to post-translational modifications and/or association of GPCRs with accessory proteins, however, post-transcriptional mechanisms are also likely to contribute. Although approximately 50% of GPCR genes are intronless, those that possess introns can undergo alternative splicing, generating GPCR subtype isoforms that may differ in their pharmacological, signalling and regulatory properties. In this review we shall highlight recent research into GPCR splice variation and discuss the potential consequences this might have for GPCR function in health and disease.

Keywords

G protein-coupled receptor (GPCR) Alternative splicing Exon Isoform Signalling properties Pathophysiology 

Copyright information

© Birkhäuser Verlag, Basel/Switzerland 2009

Authors and Affiliations

  1. 1.Department of Cell Physiology and PharmacologyUniversity of LeicesterLeicesterUK

Personalised recommendations