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Mol Cell Endocrinol. 2011 Jan 15;331(2):222-31. doi: 10.1016/j.mce.2010.04.008. Epub 2010 Apr 14.

EGF receptor activation by GPCRs: an universal pathway reveals different versions.

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1
Center of Molecular Biomedicine (CMB), Institute of Biochemistry and Biophysics, Friedrich-Schiller-University Jena, Hans-Knöll-Str. 2, D-07745 Jena, Germany. Claus.Liebmann@uni-jena.de

Abstract

About one decade ago has been demonstrated that G protein-coupled receptors (GPCRs) are able to utilize the epidermal growth factor (EGF) receptor (EGFR) as signalling intermediate. Thereby GPCRs are enabled to regulate cell growth, differentiation, and migration. A molecular mechanism for this process has been proposed that involves the activation of a distinct set of metalloproteases and the subsequent generation and release of particular members of the EGF peptide family which in turn activate the EGFR in an autocrine/paracrine manner. This model that allows GPCRs direct access to the signalling network of the EGFR family has emerged as a valid concept in a variety of cell types including cancer cells. The present review briefly summarizes the current knowledge but will be focussed on the ligand-dependency of EGFR transactivation. Several alternative mechanisms and novel aspects will be introduced. Using the example of head and neck squamous carcinoma, the potency of EGFR transactivation as a therapeutical target will be discussed.

PMID:
20398727
DOI:
10.1016/j.mce.2010.04.008
[Indexed for MEDLINE]
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