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Human RGS4 Protein expressed in Wheat germ - ABIN1317968
Rivero, Gabilondo, García-Sevilla, La Harpe, Morentín, Javier Meana: Characterization of regulators of G-protein signaling RGS4 and RGS10 proteins in the postmortem human brain. in Neurochemistry international 2010
Study investigated whether RGS4 could participate in signalling pathways to regulate neurotropic events. These observations suggest that RGS4 is implicated in opioid dependent neuronal differentiation and neurite outgrowth via a "non-canonical" signaling pathway regulating STAT5B-directed responses.
Data support the notion that the Galpha, but not Gbetagamma, arm of the Gi/o signalling is involved in TRPC4 activation and unveil new roles for RGS and RGS4 in fine-tuning TRPC4 activities.
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 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, RGS3, RGS4, and RGS5 reduced activated PAR1 wild-type signaling, whereas signaling by the PAR1 AKKAA mutant was minimally affected.
Data indicate that Rab5, Rab7 and Rab11 are involved in RGS4 traffics through plasma membrane recycling or endosome.
The results suggest unaltered membrane RGS4 and cytosolic RGS10 proteins levels in schizophrenia and major depression.
dramatic up-regulation of RGS4 expression in the nucleus accumbens of subjects treated with monoamine-directed antidepressants
Lack of association between the regulator of G-protein signaling 4 (RGS4) rs951436 polymorphism and schizophrenia.
Cys-2 and Cys-12 play markedly different roles in the regulation of RGS4 membrane localization, intracellular trafficking, and G(q) inhibitory function via mechanisms that are unrelated to RGS4 protein stabilization.
RGS4 gene variations specifically disrupt prefrontal control of saccadic eye movements.
These studies indicate that increased RGS4 expression promotes a phenotypic switch of airway smooth muscle, evoking irreversible airway obstruction in subjects with severe asthma.
The researchers found evidence that there were significant differences between the D1S1656 locus in the Maghreb population and other populations.
RGS4 and RGS10 proteins are detected in postmortem prefrontal cortex.
Opioid-induced down-regulation of RGS4: role of ubiquitination and implications for receptor cross-talk.
expression of GATA-6 but not GATA-1 significantly increased the constitutive and IL-1beta-induced mRNA expression of the endogenous RGS4 in colonic smooth muscle cells
Activation of MEKK1-MKK4-JNK-AP1 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 are essential for the instability of RGS4 mRNA.
The 5'-untranslated region (UTR) extended 120 bp nucleotides upstream of the Rgs4 start codon; a putative promoter sequence (1389 bp) showed a consensus TATA box and cis-acting binding sites for several potential transcriptional factors.
The canonical IKK2/IkappaBalpha pathway of NF-kappaB activation mediates the up-regulation of RGS4 expression in response to IL-1beta.
Upregulation of RGS4 expression by IL-1beta in colonic smooth muscle is enhanced by ERK1/2 and p38 MAPK and inhibited by the PI3K/Akt/GSK3beta pathway.
The nucleus-accumbens-specific knockdown of RGS4 significantly increased the behaviors associated with morphine and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc.
These results provide support for the hypothesis that increasing RGS4 expression and/or function could be a viable therapeutic strategy for asthma.
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-Gbeta5, but not RGS4, is the primary RGS 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 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 on M3R 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, 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.
Data show that absence of the regulatory protein RGS4 rescues several fragile-X related phenotypes, including increased body weight, abnormal synaptic protein expression and inhibition of social behaviors, in FMR1 knockout mice.
The RGS protein family may play an important role in the functioning of neural systems that are affected by chronic alcohol abuse; cirrhotic alcoholics have lower expression levels of RGS4 mRNA than controls and non-cirrhotic alcoholics.
These findings provide fundamentally novel information concerning the role of RGS4 in the cellular mechanisms underlying the diverse actions of opiate drugs in the nervous system
RGS4 is a potent negative regulator of M3R function in pancreatic beta-cells, and may represent a potential target to promote insulin release for therapeutic purposes.
In embryonic development transcription of RGS4 occurs in a highly dynamic manner in a small set of peripheral and central neuronal precursors. This expression pattern overlaps extensively with that of the neuronal identity determinant Phox2b
Rgs4 regulates vascular endothelial growth factor signaling.
RGS4 transgenic mice were resistant to streptozotocin induced cardiac fetal gene induction.
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