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Results show that RGS5 was highly expressed in the cytoplasm of epithelial ovarian cancer (EOC) cells and in microvascular structures. The expression of RGS5 in EOC was negatively associated with peritoneal metastasis. Hypoxia increased RGS5 expression in ovarian carcinomaderived endothelial cells (ODMECs). Further data indicated that RGS5 is crucial for the occurrence and development of ovarian cancer.
The chimeric RGS8 domains containing the first or the second exon part of RGS5 showed strong inhibitory effects similar to that of wild type RGS8, 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 current.
The rs16849802 of RGS5 and haplotype GAA 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, both implicated in modulation of asthma treatment.
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.
RGS1 is largely upregulated, whereas RGS2 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.
demonstrate RGS5 in the blood vessels of other cancer models endowed with a proangiogenic environment, such as human melanoma and renal carcinoma xenografts
Low expression of RGS5 was strongly associated with cancer vasculature invasion and lymph node metastasis in non-small cell lung cancer.
examined polymorphisms in three genes (ATP1B1, RGS5 and SELE) in relation to hypertension and blood pressure in a cohort of African-Americans
regulator of G-protein signaling 5 can act as a physiological regulator of calcium sensing by calcium sensing receptor in the parathyroid gland
Repetitive beta(2)-agonist use may not only lead to reduced bronchoprotection but also to sensitization of excitation-contraction signaling pathways as a result of reduced RGS5 expression
RGS5 expression level in gastric carcinoma is associated with the differentiation and microvascular density of the tumor, and may be used as an important parameter for determining the prognosis of gastric carcinoma patients.
used transgenic mice show that the cardiac constitutive expression of human Rgs5 protects against cardiac hypertrophy and fibrosis by blocking MEK-ERK1/2 signaling, whereas Rgs5-/- mice displayed the opposite phenotype.
Multiple SNPs in combination in RGS5 may confer risk for hypertension. Our results also lend support for the effect of RGS5 SNPs on lipid metabolism
There is a contribution of RGS5 to schizophrenia susceptibility.
RGS5 was more highly transcribed in ruminal papillae of more efficient low residual feed intake vs. less efficient animals.
RGS5 is required for hypertension-evoked RhoA activity in vascular smooth muscle.
RGS5 is a novel modulator of pathological progression after myocardial infarction that functions NF-kappaB and MAPK signalling.
RGS5 inhibits sonic hedgehog function during cortical neurons development.
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 JNK1/2 and p38 signaling pathways.
findings highlight a key role of RGS5 at the interface between AngII and PPAR signaling
we demonstrate that RGS5 is a critical regulator of GPCR signaling in HSCs and regulates HSC activation and fibrogenesis in liver injury.
Collectively, these findings establish RGS5 as a novel determinant of arteriogenesis which shifts G-protein signalling from Galphaq/11-mediated calcium-dependent contraction towards Galpha12/13-mediated Rho kinase-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.
Rgs5 is an important regulator of arrhythmogenesis in the mouse atrium and that the enhanced susceptibility to atrial tachyarrhythmias in Rgs5(-/-) mice may contribute to abnormalities of atrial repolarization.
Rgs5(-/-) induced prolonged repolarization and ventricular tachyarrhythmia, which were closely related to the remodeling of voltage-dependent K(+) currents.
Data show that PPARgamma regulates myogenic tone through downregulation of regulator of G protein signaling 5 (RGS5), which overactivating the protein kinase C (PKC) pathway and inhibition of the large conductance calcium-activated potassium channel (BKCa).
Results indicate the role of RGS5 in obesity-associated metabolic dysfunction and insulin sensitivity.
Vessel bed-specific changes in regulation of Rgs5 expression occurred during blood vessel maturation.
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