Journal
CELLULAR SIGNALLING
Volume 16, Issue 6, Pages 711-721Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2003.11.006
Keywords
regulator of G-protein signaling; RGS; adenylyl cyclase; 5-HT1A receptor; 5-HT2A receptor; dopamine receptor
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Regulator of G protein signaling, (RGS) proteins function as GTPase accelerating proteins (GAP) for Galpha subunits, attenuating G-protein-coupled receptor signal transduction. The present study tested the ability of members of different subfamilies of RGS proteins to modulate both G-protein-dependent and -independent signaling in mammalian cells. RGS4, RGS 10, and RGSZ1 significantly attenuated Galpha(i)-mediated signaling by 5-HT1A, but not by dopamine D2, receptor-expressing cells. Additionally, RGS4 and RGS 10 significantly inhibited forskolin-stimulated cAMP production in both cell lines. In contrast, RGS2, RGS7, and RGSZ1 had no effect on forskolin-stimulated cAMP production in these cells. RGS2 and RGS7 significantly decreased Galpha(q)-mediated signaling by 5-HT2A receptors, confirming that the RGS4 and RGS10 effects on forskolin-stimulated cAMP production were specific, and not simply due to overexpression. Interestingly, similar expression levels of RGS4 protein resulted in greater inhibition of G-protein-independent cAMP production compared to G-protein-dependent GAP activity. Our results suggest specificity and selectivity of RGS proteins on G-protein-de pen dent and -independent signaling in mammalian cells. (C) 2003 Elsevier Inc. All rights reserved.
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