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Schizophrenia patients had reduced endothelial NOS protein expression in the frontal cortex compared to controls.
Low shear stress induces the generation of endothelial reactive oxygen species via AT1R (zeige AGTR1 Proteine)/eNOS/NO signaling pathway.
We found no sufficient evidence to support the role of any common eNOS variants in the susceptibility to neovascular age-related macular degeneration (nAMD) or polypoidal choroidalvasculopathy (PCV) in a Chinese Han population.
Omentin (zeige ITLN1 Proteine) protects against lipopysaccharides-mediated acute respiratory distress syndrome through promoting endothelial barrier via an Akt/NOS3-dependent mechanism.
Taken together, these data indicated that adiponectin promotes endothelial progenitor cell proliferation and migration via AMPK/Akt/eNOS signaling pathway and promotes tube formation through AMPK/eNOS, suggesting that adiponectin-transduced endothelial progenitor cell transplantation is a potential therapeutic target for vascular disease.
The genotypic frequency of rs11771443 was nominally associated with the risk of HSP ( p = 0.010), and the C allele significantly increased the risk of Henoch-Schonlein purpura. There was a significant difference in allelic and genotypic distribution of rs1799983 between children with Henoch-Schonlein purpura and healthy controls. Significantly fewer T-A-G haplotypes were found in children with Henoch-Schonlein purpura.
this study introduces a novel pathway by which IFN-alpha (zeige IFNA Proteine) serves as a proatherogenic mediator through repression of eNOS-dependent pathways
(-)-Epicatechin counteracts the negative effects that high glucose or simulated type 2 diabetes has on endothelial nitric oxide synthase function.
Heme increased eNOS production in HUVECs and treatment with simvastatin, hydroxyurea and ascorbic acid reduced the production.
there is no relationship between the G894T and eNOS-786C polymorphisms and the development of ascites in cirrhotic patients
Omentin (zeige ITLN1 Proteine) protects against lipopysaccharides-induced acute respiratory distress syndrome through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt (zeige AKT1 Proteine)/NOS3-dependent mechanism.
Endothelial cell Gch1 (zeige GCH1 Proteine) and BH4-dependent eNOS regulation play pivotal roles in maintaining vascular homeostasis in resistance arteries.
These results suggest that S-glutathionylation of eNOS within the microvascular endothelial cells inhibited NO production and enhanced TLR4 (zeige TLR4 Proteine) activity, which were implicated in the pathogenesis of necrotizing enterocolitis.
Genetic deletion of NOS3 in CAV1 (zeige CAV1 Proteine)-deficient mice restored intraocular pressure and conventional aqueous humor drainage to wild type level. NOS3 and CAV1 (zeige CAV1 Proteine) interaction is important to intraocular pressure regulation.
these data suggest that CD NOS3 may be involved in the diuretic response to a water load in a sex-specific manner; the mechanism of this effect remains to be determined.
CAV1 (zeige CAV1 Proteine) KO mice have elevated IOP and reduced conventional outflow facility when compared with WT mice. CAV2 (zeige CAV2 Proteine) expression was absent in CAV1 (zeige CAV1 Proteine) KO mice, but we observed increased expressions of eNOS
TNF-alph (zeige TNF Proteine)a does not regulate eNOS activity in murine endothelial cells through serine 116 phosphorylati (zeige PIN1 Proteine)on and Pin1 binding.
The eNOS expressed in smooth muscle cells in FAs (zeige FAS Proteine) attenuates alpha-adrenergic vasoconstriction.
Thioredoxin (zeige TXN Proteine)-mediated deglutathionylation of eNOS in the coronary artery in vivo protected against reperfusion injury, even in the presence of normal levels of glutathione.
S1179D substitution in eNOS increased the rate of flavin reduction, altered the conformational equilibrium of the reductase domain, and increased the rate of its conformational transitions.
These data define the mechanism responsible for the repressive effects of nitric oxide (NO) on the transcriptional activity of beta-catenin (zeige CTNNB1 Proteine) and link eNOS-derived NO to the modulation by VEGF (zeige VEGFA Proteine) of Wnt (zeige WNT2 Proteine)/beta-catenin (zeige CTNNB1 Proteine)-induced endothelial cell proliferation.
Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent ATP/P2Y1 receptor (zeige P2RY1 Proteine) signaling to endothelial nitric oxide synthase.
TNFalpha (zeige TNF Proteine) reduces eNOS activity in bovine endothelial cells through serine 116 phosphorylation and Pin1 (zeige PIN1 Proteine) binding.
Pomanox supplementation hinders hyperlipemia-induced coronary endothelial dysfunction by activating the Akt (zeige AKT1 Proteine)/endothelial nitric oxide-synthase pathway and favorably counteracting vascular inflammation and oxidative damage.
Signals that activate and phosphorylate eNOS are transmitted through distinct membrane domains in endothelial cells. Cholesterol domains, but not individual caveolae, mediate HDL stimulation of eNOS. VEGF and shear stress may act through caveolae.
eNOS serine 1179 phosphorylation, in addition to enhancing NO production, also profoundly affects superoxide generation
In addition to the heme center of eNOS oxygenase domain, we confirmed another O2.- generation site in the eNOS reductase domain and characterized its regulatory properties.
A dimer-destabilized mutant of bovine eNOS where cysteine 101 was replaced by alanine, cloned and introduced into an eNOS-deficient mouse strain and that results provide the first in vivo evidence that eNOS-dependent oxidative stress is unlikely to be an initial cause of impaired endothelium-dependent vasodilation and/or a pathologic factor promoting intimal hyperplasia.
Data show that resveratrol (Res) reversed caveolin-1 (Cav-1 (zeige CAV1 Proteine))/endothelial nitric oxide synthase (eNOS) expressions in high glucose cultured bovine aortic endothelial cells (BAECs).
NOS3 was lowest in kidneys removed from live pigs, greater in kidneys from pigs with brain death, and greatest in kidneys from pigs with cardiac arrest.
Rapid atrial pacing increases ADMA and down-regulates eNOS expression in an ADMA-independent manner.
Icariin and icariside II may increase the eNOS expression through activating EGF-EGFR (zeige EGFR Proteine) pathway in porcine aortic endothelial cells.
Data suggest that pig sperm contain bNOS (zeige NOS1 Proteine), iNOS (zeige NOS2 Proteine), and eNOS; up-regulation of NOS by leptin (zeige LEP Proteine) during acrosome reaction and inhibition of acrosome reaction by inhibitors of nitric oxide synthases suggests these enzymes are involved in acrosome reaction.
Periodic acceleration (pGz) acutely increases endothelial and neuronal nitric oxide synthase (zeige NOS1 Proteine) expression in endomyocardium of normal swine.
Data suggest that angiotensin II regulates nNOS and eNOS expression and NOS activity in afferent arterioles of the developing kidney via angiotensin 1 and 2 receptors.
Endothelial nitric oxide synthase mRNA expression was elevated in gestational day 50 intrauterine growth retardation placenta and areola compared to gd50 control.
Oligonol prevented the impairment of eNOS activity induced by high glucose through reversing altered eNOS phosphorylation status.
Exercise training significantly increased total eNOS and phosphorylated levels of eNOS (pSer(1179)) in collateral-dependent arteries of experimental minipigs.
Data show that wall shear stress increases with a decrease in artery diameter; eNOS protein contents decrease with an increase in diameter.
The present evidence indicated that the customary HBOT protocol may increase constitutive NOS expression.
Kidneys from circulation-restricted fetuses showed endothelial nitric oxide synthase phosphorylation inhibition.
Antidiabetic drug pioglitazone protects the heart via activation of endothelial nitric oxide synthase (eNOS/Nos3) pathway in a rabbit model of myocardial infarction.
VEGFR2 (zeige KDR Proteine) activation was not affected by Slit2 (zeige SLIT2 Proteine), but eNOS phosphorylation was diminished
Data suggest distinct localizations of eNOS at the spiral arteries/arterial sinuses and iNOS (zeige NOS2 Proteine) along the radial arteries in the developing placenta.
Pulmonary ischaemia-reperfusion up-regulates inducible nitric oxide synthesis and/activity, which coincides with reduced endothelial nitric oxide synthase activity.
eNOS dysregulation may be a central mechanism of impaired cardioprotection during hyperglycemia.
Quercetin inhibited myocardial ischemia-reperfusion-induced NOS3 mRNA and protein expression.
Nitric oxide is a reactive free radical which acts as a biologic mediator in several processes, including neurotransmission and antimicrobial and antitumoral activities. Nitric oxide is synthesized from L-arginine by nitric oxide synthases. Variations in this gene are associated with susceptibility to coronary spasm. Multiple transcript variants encoding different isoforms have been found for this gene.
, NOS type III
, constitutive NOS
, endothelial NOS
, nitric oxide synthase, endothelial
, endothelial nitric oxide synthase
, nitric oxide synthase 3 (endothelial cell)
, nitric oxide synthase, endothelial-like
, endothelial nitric oxide synthase 3
, endothelial nitric oxide synthase NOS3