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Abstract
The signaling cascades evoked by G protein-coupled receptors are a predominant mechanism of cellular communication. The regulators of G protein signaling (RGS) comprise a family of proteins that attenuate G protein-mediated signal transduction. Here we report the characterization of RGS13, the smallest member of the RGS family, which has been cloned from human lung. RGS13 has been found most abundantly in human tonsil, followed by thymus, lung, lymph node, and spleen. RGS13 is a GTPase-activating protein for Galpha(i) and Galpha(o) but not Galpha(s). RGS13 binds Galpha(q) in the presence of aluminum magnesium fluoride, suggesting that it bears GTPase-activating protein activity toward Galpha(q). RGS13 blocks MAPK activity induced by Galpha(i)- or Galpha(q)-coupled receptors. RGS13 also attenuates GTPase-deficient Galpha(q) (Galpha(q)QL) mediated cAMP response element activation but not transcription evoked by constitutively active Galpha(12) or Galpha(13). Surprisingly, RGS13 inhibits cAMP generation elicited by stimulation of the beta(2)-adrenergic receptor. These data suggest that RGS13 may regulate Galpha(i)-, Galpha(q)-, and Galpha(s)-coupled signaling cascades.
Highlights
regulators of G protein signaling (RGS) proteins share a common domain, the RGS box
We found RGS13 most abundantly in the tonsil followed by thymus, lymph node, lung, and spleen (Fig. 1A)
RGS13 May Act as an Effector Antagonist for G␣q—Because some RGS proteins block the interaction between G␣q and its effector, PLC, we examined the ability of RGS13 to regulate transcription stimulated by GTPase-deficient G proteins
Summary
RGS13 inhibits cAMP generation elicited by stimulation of the 2-adrenergic receptor These data suggest that RGS13 may regulate G␣i-, G␣q-, and G␣s-coupled signaling cascades. Most RGS proteins do not exhibit GAP activity toward G␣s; a short form of RGS3 (RGS3T) blocks calcitonin gene-related peptide-induced cAMP generation [16]. As with other RGS proteins, recombinant RGS13 exhibits GAP activity toward G␣i family members and not G␣s. Transfected RGS13 blunts MAPK activation evoked by either G␣q- or G␣i-coupled receptors It blocks G␣qQL-induced CRE-dependent transcription, consistent with a potential role for RGS13 as an effector antagonist of G␣q. RGS13 inhibits receptor-stimulated cAMP generation, suggesting that it regulates G␣s signaling despite its lack of G␣s GAP activity. RGS13 may regulate G protein-mediated processes in the lung and immune system
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