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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. Additionally we are shipping RGS4 Antibodies (67) and RGS4 Proteins (14) and many more products for this protein.
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The results of this study demonstrated the association between the variation in the regulator of G-protein signaling 4 (RGS4) gene, a putative candidate gene for psychosis previously associated with schizophrenia endophenotypes, and psychotic-like experiences (PLEs).
All of these results confirmed the critical role of RGS4 in NSCLC progression.
After alphao dissociates from MOR, RGS4 remains bound to the C-terminal region of MOR
RGS4 deletion results in a predisposition to atrial fibrillation from enhanced activity in the G-protein pathway, resulting in abnormal calcium release and corresponding electrical events.
RGS2 and RGS4 are new interacting partners that play key roles in G protein coupling to negatively regulate kappa-OmicronR signaling.
RGS4 and COMT (show COMT ELISA Kits) risk variants are associated with brain structural alterations in patient with schizophrenia.
genetic association study in Chinese Han population: Data suggest an SNP in RGS4 (rs10759) is associated with increased predisposition to schizophrenia via down-regulation of miroRNA (MIRN124) binding to 3-prime-untranslated region of RGS4 mRNA.
ectopic expression of R4 subfamily members RGS2 (show RGS2 ELISA Kits), RGS3 (show RGS3 ELISA Kits), RGS4, and RGS5 (show RGS5 ELISA Kits) reduced activated PAR1 (show MARK2 ELISA Kits) wild-type signaling, whereas signaling by the PAR1 (show MARK2 ELISA Kits) AKKAA mutant was minimally affected.
Data indicate that Rab5 (show RAB5A ELISA Kits), Rab7 (show RAB7B ELISA Kits) and Rab11 (show RAB11A ELISA Kits) are involved in RGS4 traffics through plasma membrane recycling or endosome.
The results suggest unaltered membrane RGS4 and cytosolic RGS10 (show RGS10 ELISA Kits) proteins levels in schizophrenia and major depression.
Activation of MEKK1 (show MAP3K1 ELISA Kits)-MKK4 (show MAP2K4 ELISA Kits)-JNK (show MAPK8 ELISA Kits)-AP1 (show JUN ELISA Kits) signaling pathway plays a tonic inhibitory role in regulating Rgs4 transcription in rabbit colonic smooth muscle cells.
These findings suggest that 3'-most AU-rich elements sites within RGS4 3'-UTR (show UTS2R ELISA Kits) are essential for the instability of RGS4 mRNA.
The 5'-untranslated region (UTR (show UTS2R ELISA Kits)) extended 120 bp nucleotides upstream of the Rgs4 start codon; a putative promoter sequence (1389 bp) showed a consensus TATA box and cis (show CISH ELISA Kits)-acting binding sites for several potential transcriptional factors.
The canonical IKK2 (show IKBKB ELISA Kits)/IkappaBalpha (show NFKBIA ELISA Kits) pathway of NF-kappaB (show NFKB1 ELISA Kits) activation mediates the up-regulation of RGS4 expression in response to IL-1beta (show IL1B ELISA Kits).
Upregulation of RGS4 expression by IL-1beta (show IL1B ELISA Kits) in colonic smooth muscle is enhanced by ERK1/2 (show MAPK1/3 ELISA Kits) and p38 MAPK (show MAPK14 ELISA Kits) and inhibited by the PI3K/Akt (show AKT1 ELISA Kits)/GSK3beta pathway.
RGS4 in the paraventricular nucleus regulates blood corticosteroid-related GABAB receptor signaling during the acute stress response.
Thus, RGS4 expression, specific to renal vascular smooth muscle cells, inhibits angiotensin II-mediated cytokine signaling and macrophage recruitment during reperfusion, distinct from vasomotor regulation.
Spinal RGS4 inhibited the endogenous or exogenous OR-mediated antinociceptive effect in the formalin pain test.
RGS6 (show RGS6 ELISA Kits)-Gbeta5 (show GNB5 ELISA Kits), but not RGS4, is the primary RGS (show PITX2 ELISA Kits) modulator of parasympathetic HR regulation and SAN M2R-IKACh signaling in mice.
dramatic up-regulation of RGS4 expression in the nucleus accumbens of mice treated with monoamine-directed antidepressants
RGS4 expression in mouse embryo is regulated by Lmx1a (show LMX1A ELISA Kits) transcription factor.
A novel nitric oxide-RGS4 signal pathway mechanism that couples cardiac vessel growth with myocyte growth and heart size.
Findings support the concept that the inhibitory effects of SPL (show SGPL1 ELISA Kits) on M3R (show CHRM3 ELISA Kits) activity are mediated by RGS4.
Rgs4 is expressed in endocrine progenitors of both zebrafish and mouse, and its expression in the mouse pancreatic epithelium is strictly dependent upon Ngn3 (show NEUROG3 ELISA Kits), and loss of function of Rgs4 results in islet fragmentation in both organisms.
RGS4 antagonizes the development of renal dysfunction in response to ischemia reperfusion injury.
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 4 belongs to this family. All RGS proteins share a conserved 120-amino acid sequence termed the RGS domain. Regulator of G protein signaling 4 protein is 37% identical to RGS1 and 97% identical to rat Rgs4. This protein negatively regulate signaling upstream or at the level of the heterotrimeric G protein and is localized in the cytoplasm. Alternatively spliced transcript variants have been found for this gene.
schizophrenia disorder 9
, regulator of G-protein signalling 4