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Omentin (show ITLN1 Proteins) 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 (show ADIPOQ Proteins) promotes endothelial progenitor cell proliferation and migration via AMPK (show PRKAA1 Proteins)/Akt (show AKT1 Proteins)/eNOS signaling pathway and promotes tube formation through AMPK (show PRKAA1 Proteins)/eNOS, suggesting that adiponectin (show ADIPOQ Proteins)-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 (show IFNA Proteins) 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
Homozygotes patients for both (T786C and G894T) polymorphisms of eNOS had significantly higher serum levels of VEGF (show VEGFA Proteins) in patients with Type 2 Diabetes . These findings indicate a close association of gene polymorphisms of eNOS with endothelial and vascular function.
NOS3 (show NANOS3 Proteins) -786 C/T rs2070744 polymorphism in Dilated Cardiomyopathy may serve as a marker for more rapid progression of Heart Failure.
This study shows that expression of SDF-1alpha, eNOS and VEGF (show VEGFA Proteins) were significantly higher in uterine leiomyoma than myometrium with a different expression pattern according to the size of uterine leiomyoma. However, expressions of visfatin (show NAMPT Proteins) and leptin (show LEP Proteins) had no significant differences between the two groups.
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 (show EGFR Proteins) pathway in porcine aortic endothelial cells.
Data suggest that pig sperm contain bNOS (show NOS1 Proteins), iNOS (show NOS2 Proteins), and eNOS; up-regulation of NOS by leptin (show LEP Proteins) 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 (show NOS1 Proteins) 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.
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 (show CTNNB1 Proteins) and link eNOS-derived NO to the modulation by VEGF (show VEGFA Proteins) of Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins)-induced endothelial cell proliferation.
Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent ATP/P2Y1 receptor (show P2RY1 Proteins) signaling to endothelial nitric oxide synthase.
TNFalpha (show TNF Proteins)reduces eNOS activity in bovine endothelial cells through serine 116 phosphorylation and Pin1 binding.
Pomanox supplementation hinders hyperlipemia-induced coronary endothelial dysfunction by activating the Akt (show AKT1 Proteins)/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 (show CAV1 Proteins))/endothelial nitric oxide synthase (eNOS) expressions in high glucose cultured bovine aortic endothelial cells (BAECs).
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 (show KDR Proteins) activation was not affected by Slit2 (show SLIT2 Proteins), but eNOS phosphorylation was diminished
Data suggest distinct localizations of eNOS at the spiral arteries/arterial sinuses and iNOS (show NOS2 Proteins) 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.
Omentin (show ITLN1 Proteins) protects against lipopysaccharides-induced acute respiratory distress syndrome through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt (show AKT1 Proteins)/NOS3-dependent mechanism.
Endothelial cell Gch1 (show GCH1 Proteins) 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 (show TLR4 Proteins) activity, which were implicated in the pathogenesis of necrotizing enterocolitis.
Genetic deletion of NOS3 in CAV1 (show CAV1 Proteins)-deficient mice restored intraocular pressure and conventional aqueous humor drainage to wild type level. NOS3 and CAV1 (show CAV1 Proteins) 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 (show CAV1 Proteins) KO mice have elevated IOP and reduced conventional outflow facility when compared with WT mice. CAV2 (show CAV2 Proteins) expression was absent in CAV1 (show CAV1 Proteins) KO mice, but we observed increased expressions of eNOS
TNF-alpha (show TNF Proteins) does not regulate eNOS activity in murine endothelial cells through serine 116 phosphorylation and Pin1 (show PIN1 Proteins) binding.
The eNOS expressed in smooth muscle cells in FAs (show FAS Proteins) attenuates alpha-adrenergic vasoconstriction.
Thioredoxin (show TXN Proteins)-mediated deglutathionylation of eNOS in the coronary artery in vivo protected against reperfusion injury, even in the presence of normal levels of glutathione.
The present evidence indicated that the customary HBOT protocol may increase constitutive NOS 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.
nitric oxide synthase 3 (endothelial cell)
, nitric oxide synthase, endothelial-like
, NOS type III
, constitutive NOS
, endothelial NOS
, nitric oxide synthase, endothelial
, endothelial nitric oxide synthase
, endothelial nitric oxide synthase NOS3
, endothelial nitric oxide synthase 3