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Volume 11, Pages 709-714
Mini-Review Article

The Paradigm of G Protein Receptor Transactivation: A Mechanistic Definition and Novel Example

1Discipline of Pharmacy, School of Medical Sciences, RMIT University, Melbourne, Victoria, Australia
2Diabetes Complications Group, Health Innovations Research Institute, RMIT University, Melbourne, Victoria, Australia
3Diabetes and Cell Biology Laboratory, BakerIDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
4Monash University, Departments of Medicine and Immunology, Central and Eastern Clinical School, Alfred Health, Melbourne, Victoria, Australia
5Neuropharmacology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, China

Received 29 October 2010; Revised 18 February 2011; Accepted 1 March 2011

Academic Editor: Govindan Dayanithi

Copyright © 2011 Peter J. Little et al.


Seven transmembrane G protein—coupled receptors are among the most common in biology and they transduce cellular signals from a plethora of hormones. As well as their own well-characterized signaling pathways, they can also transactivate tyrosine kinase growth factor receptors to greatly expand their own cellular repertoire of responses. Recent data in vascular smooth muscle cells have expanded the breadth of transactivation to include serine/threonine kinase receptors, specifically the receptor for transforming growth factor beta (TGF-β). Stimulation with endothelin and thrombin leads to the rapid formation of C-terminal phosphorylated Smad2, which is the immediate product of activation of the TGF-β receptor. Additionally, it appears that no definition of transactivation based on mechanism is available, so we have provided a definition involving temporal aspects and the absence of de novo protein synthesis. The phenomenon of transactivation is an important biochemical mechanism and potential drug target in multiple diseases.