Format

Send to

Choose Destination
Trends Pharmacol Sci. 2011 Aug;32(8):443-50. doi: 10.1016/j.tips.2011.04.002. Epub 2011 May 24.

Receptor tyrosine kinase-G-protein-coupled receptor signalling platforms: out of the shadow?

Author information

1
Cell Biology Group, Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow, G4 0RE, UK. n.j.pyne@strath.ac.uk

Abstract

Receptor tyrosine kinases (RTKs) and G-protein-coupled receptors (GPCRs) can form platforms in which protein signalling components specific for each receptor are shared (owing to close proximity) to produce an integrated response upon engagement of ligands. RTK-GPCR signalling platforms respond to growth factors and GPCR agonists to increase gain over and above that which is normally produced by separate receptors. They can also function to change the spatial context of signalling in response to growth factor activation. The function of RTK-GPCR signalling platforms can be modulated with conformational-specific inhibitors that stabilise defined GPCR states to abrogate both GPCR agonist- and growth factor-stimulated cell responses. In this paper, we provide an opinion of the biology and unusual pharmacology of RTK-GPCR signalling platforms and make comparisons with a more traditional model of crosstalk between RTKs and GPCRs.

PMID:
21612832
DOI:
10.1016/j.tips.2011.04.002
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center