| First Author | Liebmann C | Year | 2011 |
| Journal | Mol Cell Endocrinol | Volume | 331 |
| Issue | 2 | Pages | 222-31 |
| PubMed ID | 20398727 | Mgi Jnum | J:168386 |
| Mgi Id | MGI:4888111 | Doi | 10.1016/j.mce.2010.04.008 |
| Citation | Liebmann C (2011) EGF receptor activation by GPCRs: an universal pathway reveals different versions. Mol Cell Endocrinol 331(2):222-31 |
| abstractText | 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. |
