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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Regulator of G-protein signaling 2, 24kDa

RGS2, regulator of G-protein signaling 2
Regulator of G protein signaling (RGS) family members are regulatory molecules that act as GTPase activating proteins (GAPs) for G alpha subunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Gi alpha, Go alpha and Gq alpha subtypes. They drive G proteins into their inactive GDP-bound forms. Regulator of G protein signaling 2 belongs to this family. The protein acts as a mediator of myeloid differentiation and may play a role in leukemogenesis. [provided by RefSeq, Aug 2009] (from NCBI)
Papers using RGS2 antibodies
RGS2 is upregulated by and attenuates the hypertrophic effect of alpha1-adrenergic activation in cultured ventricular myocytes
Chidiac Peter et al., In The Journal of Cell Biology, 2005
... The purified RGS2 peptide was made by custom peptide synthesis, and the RGS2-ala mutants were made by custom gene synthesis (Genscript Corporation) ...
Papers on RGS2
Regulator of G protein signaling 2 deficiency causes endothelial dysfunction and impaired endothelium-derived hyperpolarizing factor-mediated relaxation by dysregulating Gi/o signaling.
Blumer et al., Saint Louis, United States. In J Biol Chem, 2012
systemic or endothelium-specific RGS2 deficiency causes endothelial dysfunction resulting in impaired EDHF-dependent vasodilatation.
RGS2 is a negative regulator of STAT3-mediated Nox1 expression.
Baek et al., Taegu, South Korea. In Cell Signal, 2012
RGS2 negatively regulates TLR2-mediated Nox1 expression via PKC-eta and PLD2 pathway.
RGS2-mediated intracellular Ca2+ level plays a key role in the intracellular replication of Brucella abortus within phagocytes.
Kim et al., Japan. In J Infect Dis, 2012
These results indicate that Brucella abortus infection induces host RGS2 expression and that up-regulation of [Ca(2+)](i) levels is an essential factor for the intracellular survival of the bacteria within phagocytes.
Identification of a cAMP-response element in the regulator of G-protein signaling-2 (RGS2) promoter as a key cis-regulatory element for RGS2 transcriptional regulation by angiotensin II in cultured vascular smooth muscles.
Guo et al., Lexington, United States. In J Biol Chem, 2012
Identification of a cAMP-response element in the regulator of G-protein signaling-2 (RGS2) promoter as a key cis-regulatory element for RGS2
β2-Adrenoceptor agonist-induced RGS2 expression is a genomic mechanism of bronchoprotection that is enhanced by glucocorticoids.
Newton et al., Calgary, Canada. In Proc Natl Acad Sci U S A, 2012
Data show that Rgs2-deficient mice revealed enhanced bronchoconstriction to spasmogens and an absence of beta(2)-adrenoceptor agonist (LABA)-induced bronchoprotection.
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