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The chimeric RGS8 (show RGS8 Proteins) domains containing the first or the second exon part of RGS5 showed strong inhibitory effects similar to that of wild type RGS8 (show RGS8 Proteins), but the chimeric domain with the third exon part of RGS5 lost its activity
Rgs5 prevents vagal-related bradycardia and atrial tachycardia by negatively regulating the IKA Ach (show FGFR3 Proteins) current.
The rs16849802 of RGS5 and haplotype GAA (show GAA Proteins) independently increased the risk of essential hypertension in Mongolian patients, and may be used as a risk factor for the prediction of high blood pressure.
Downregulation of RGS5 is an important prerequisite for smooth muscle cell proliferation in vascular injury model.
The pericyte marker RGS5 may be of future clinical utility for the evaluation of pericytic differentiation in soft tissue tumors.
RGS5 enhanced the cytotoxic effect of radiation in the human lung cancer cells. Our results indicated that RGS5 may be a potential target for cancer therapy.
Our work identifies a new genetic variant in RGS5 demonstrating additive effect with PDE4D (show PDE4D Proteins), both implicated in modulation of asthma treatment.
ectopic expression of R4 subfamily members RGS2 (show RGS2 Proteins), RGS3 (show RGS3 Proteins), RGS4 (show RGS4 Proteins), and RGS5 reduced activated PAR1 (show MARK2 Proteins) wild-type signaling, whereas signaling by the PAR1 (show MARK2 Proteins) AKKAA mutant was minimally affected.
RGS1 (show RGS1 Proteins) is largely upregulated, whereas RGS2 (show RGS2 Proteins) is downregulated in the majority of solid tumors, whereas RGS5 transcripts are greatly increased in eight subtypes of lymphoma with no reports of downregulation in hematological malignancies
Over-expression of regulator of G protein signaling 5 promotes tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma cells.
RGS5 was more highly transcribed in ruminal papillae of more efficient low residual feed intake vs. less efficient animals.
RGS5 deletion accelerated development of atherosclerosis and decreased the stability of atherosclerotic plaques partly through activating NF-kappaB and the MEK-ERK1/2 signalling pathways
These studies show that RGS5 protects cardiomyocytes against apoptosis during myocardial ischemia-reperfusion injury through inhibiting both JNK1 (show MAPK8 Proteins)/2 and p38 (show CRK Proteins) signaling pathways.
findings highlight a key role of RGS5 at the interface between AngII and PPAR (show PPARA Proteins) signaling
we demonstrate that RGS5 is a critical regulator of GPCR (show GPBAR1 Proteins) signaling in HSCs and regulates HSC (show FUT1 Proteins) activation and fibrogenesis in liver injury.
Collectively, these findings establish RGS5 as a novel determinant of arteriogenesis which shifts G-protein signalling from Galphaq (show GNAQ Proteins)/11-mediated calcium-dependent contraction towards Galpha12/13-mediated Rho kinase (show ROCK2 Proteins)-dependent smooth muscle cell activation.
Loss of RGS5 promotes airway hyperresponsiveness in the absence of allergic inflammation.
study concludes that RGS5 is an endogenous regulator of Hh-mediated signaling
Regulator of G-protein signaling 5 controls blood pressure homeostasis and vessel wall remodeling.
This gene encodes a member of the regulators of G protein signaling (RGS) family. The RGS proteins are signal transduction molecules which are involved in the regulation of heterotrimeric G proteins by acting as GTPase activators. This gene is a hypoxia-inducible factor-1 dependent, hypoxia-induced gene which is involved in the induction of endothelial apoptosis. This gene is also one of three genes on chromosome 1q contributing to elevated blood pressure. Alternatively spliced transcript variants have been identified.
regulator of G-protein signaling 5
, regulator of G-protein signalling 5
, regulator of G protein signaling 5