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EMBO J. 2007 Jan 10;26(1):53-64. Epub 2006 Dec 14.

Dosage-dependent switch from G protein-coupled to G protein-independent signaling by a GPCR.

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1
Department of Physiology, Weill Medical College, Cornell University, New York, NY 10021, USA.

Abstract

G-protein-coupled receptors (GPCRs) mostly signal through heterotrimeric G proteins. Increasing evidence suggests that GPCRs could function in a G-protein-independent manner. Here, we show that at low concentrations of an agonist, beta(2)-adrenergic receptors (beta(2)-ARs) signal through Galpha(s) to activate the mitogen-activated protein kinase pathway in mouse embryonic fibroblast cells. At high agonist concentrations, signals are also transduced through beta(2)-ARs via an additional pathway that is G-protein-independent but tyrosine kinase Src-dependent. This new dosage-dependent switch of signaling modes of GPCRs has significant implications for GPCR intrinsic properties and desensitization.

PMID:
17170700
PMCID:
PMC1782364
DOI:
10.1038/sj.emboj.7601502
[Indexed for MEDLINE]
Free PMC Article
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