Is the model of signal amplification by GPCRs/GEFs activating multiple GTPases relevant to a broad spectrum of heterotrimeric and RAS superfamily GTPases?

• Type of Material: Article
• Authors: Richard Kahn, Emory University
• Language: English
• Date: 2014-06
• Publisher: Taylor & Francis
• Publication Version: Final Published Version
• Copyright Statement: © 2014 Richard A Kahn. Published with license by Taylor & Francis Group, LLC
• License: Creative Commons Attribution-Noncommercial 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.4161/21592780.2014.943602
• Title of Journal or Parent Work: Cellular Logistics
• ISSN: 2159-2780
• Volume: 4
• Issue: 2
• Start Page: e943602
• End Page: e943602
• Grant/Funding Information: This work was supported in part by a grant from the National Institutes of Health R01-GM-090158.
• Keywords: G-protein coupled receptor (GPCR); GTPase activating protein (GAP); Guanine nucleotide exchange factor (GEF); Receptor tyrosine kinase (RTK); ADP-ribosylation factor (ARF)
• Research Categories: Chemistry, Biochemistry; Biology, Cell

Abstract

Concepts or models of biological processes shape how we think about them, discuss them, and design experiments to test aspects of them. Because of the importance of our models of cell signaling by regulatory GTPases and the desire to extend those models to related signaling modules, I have throughout my career been fascinated by the similarities and differences between the modeling of heterotrimeric G protein and monomeric RAS superfamily GTPases. Recent discussions with colleagues led me to conclude that there is a growing divergence in how researchers model the activation and signaling processes of monomeric and trimeric GTPases and also a surprising lack of consensus within each camp. This series of articles arose in response to these discussions and is intended to spark new ones.