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Table of Contents
Vol. 17, No. 1, 2009
Issue release date: February 2009
Section title: Invited Review
Free Access
Neurosignals 2009;17:100–108

Heterotrimeric G-Proteins Interact Directly with Cytoskeletal Components to Modify Microtubule-Dependent Cellular Processes

Dave R.H.a · Saengsawang W.a · Yu J.-Z.a · Donati R.d · Rasenick M.M.a–c
Departments of aPhysiology and Biophysics and bPsychiatry, cGraduate Program in Neuroscience, University of Illinois Chicago, and dDepartment of Basic Sciences, Illinois College of Optometry, Chicago, Ill., USA
email Corresponding Author

Mark M. Rasenick

Departments of Physiology and Biophysics, Psychiatry, and

Graduate Program in Neuroscience, University of Illinois

Chicago, IL 60612-7342 (USA)

Tel. +1 312 996 6641, Fax +1 312 996 1414, E-Mail raz@uic.edu

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A large percentage of current drugs target G-protein-coupled receptors, which couple to well-known signaling pathways involving cAMP or calcium. G-proteins themselves may subserve a second messenger function. Here, we review the role of tubulin and microtubules in directly mediating effects of heterotrimeric G-proteins on neuronal outgrowth, shape and differentiation. G-protein-tubulin interactions appear to be regulated by neurotransmitter activity, and, in turn, regulate the location of Gα in membrane microdomains (such as lipid rafts) or the cytosol. Tubulin binds with nanomolar affinity to Gsα, Giα1 and Gqα (but not other Gα subunits) as well as Gβ1γ2 subunits. Gα subunits destabilize microtubules by stimulating tubulin’s GTPase, while Gβγ subunits promote microtubule stability. The same region on Gsα that binds adenylyl cyclase and Gβγ also interacts with tubulin, suggesting that cytoskeletal proteins are novel Gα effectors. Additionally, intracellular Giα-GDP, in concert with other GTPase proteins and Gβγ, regulates the position of the mitotic spindle in mitosis. Thus, G-protein activation modulates cell growth and differentiation by directly altering microtubule stability. Further studies are needed to fully establish a structural mechanism of this interaction and its role in synaptic plasticity.

© 2009 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Invited Review

Received: November 19, 2008
Accepted: November 05, 2008
Published online: February 12, 2009
Issue release date: February 2009

Number of Print Pages: 9
Number of Figures: 2
Number of Tables: 0

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

For additional information: http://www.karger.com/NSG

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