Date of Award

2006

Degree Type

Thesis

Degree Name

Master of Science

Program

Pharmacology and Toxicology

Supervisor

Dr. P. Chidiac

Second Advisor

Dr. D. Bai

Third Advisor

Dr. S. Sims

Abstract

Regulator of G protein signalling (RGS) proteins are primarily known to attenuate G protein function within G protein-coupled receptor (GPCR) signalling pathways, however they can interact with additional proteins. We identified an interaction between RGS proteins (RGS4, RGS5, RGS16) and the multifunctional protein 14-3-3. Two isoforms, 14-3-3β and 14-3-3ε, interact with all three purified RGS proteins. Data from in vitro steady state GTP hydrolysis assays show that 14-3-3 inhibits the GTPase activity of RGS4 and RGSI6, but has no appreciable effect on RGS5. Furthermore in a competitive pull-down experiment, 14-3-3ε competes with Gαo for RGS4 but not for RGS5. Thus 143-3 proteins may prevent RGS from interacting with Ga and ultimately prolong signalling. Tyrosine 167 within the conserved 14-3-3 binding motif does not play a significant role in RGS inhibition by 14-3-3. In conclusion, 14-3-3 proteins appear to indirectly promote GPCR signalling via their inhibitory effects on RGS function.

Share

COinS
 
 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.