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The chimeric RGS8 (zeige RGS8 ELISA Kits) domains containing the first or the second exon part of RGS5 showed strong inhibitory effects similar to that of wild type RGS8 (zeige RGS8 ELISA Kits), 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 (zeige FGFR3 ELISA Kits) current.
The rs16849802 of RGS5 and haplotype GAA (zeige GAA ELISA Kits) 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 (zeige PDE4D ELISA Kits), both implicated in modulation of asthma treatment.
ectopic expression of R4 subfamily members RGS2 (zeige RGS2 ELISA Kits), RGS3 (zeige RGS3 ELISA Kits), RGS4 (zeige RGS4 ELISA Kits), and RGS5 reduced activated PAR1 (zeige MARK2 ELISA Kits) wild-type signaling, whereas signaling by the PAR1 (zeige MARK2 ELISA Kits) AKKAA mutant was minimally affected.
RGS1 (zeige RGS1 ELISA Kits) is largely upregulated, whereas RGS2 (zeige RGS2 ELISA Kits) 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 (zeige NFKB1 ELISA Kits) and the MEK (zeige MDK ELISA Kits)-ERK1/2 (zeige MAPK1/3 ELISA Kits) signalling pathways
These studies show that RGS5 protects cardiomyocytes against apoptosis during myocardial ischemia-reperfusion injury through inhibiting both JNK1 (zeige MAPK8 ELISA Kits)/2 and p38 (zeige CRK ELISA Kits) signaling pathways.
findings highlight a key role of RGS5 at the interface between AngII and PPAR (zeige PPARA ELISA Kits) signaling
we demonstrate that RGS5 is a critical regulator of GPCR (zeige GPBAR1 ELISA Kits) signaling in HSCs and regulates HSC (zeige FUT1 ELISA Kits) activation and fibrogenesis in liver injury.
Collectively, these findings establish RGS5 as a novel determinant of arteriogenesis which shifts G-protein signalling from Galphaq (zeige GNAQ ELISA Kits)/11-mediated calcium-dependent contraction towards Galpha12 (zeige GNA12 ELISA Kits)/13-mediated Rho kinase (zeige ROCK2 ELISA Kits)-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