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G allele was identified as predisposing to the development of otitis media with effusion and this is the first report indicates the correlation between the nitric oxide synthase G894T polymorphism and otitis media with effusion in Turkey.
eNOS (T786C) gene polymorphism was not associated with coronary atherosclerosis in Brazilian patients.
NOS3 (show NANOS3 Proteins) tagSNPs influence the effects of enalapril in essential hypertension.
The NOS3 (show NANOS3 Proteins) variant Glu298Asp was not associated with Coronary Artery Disease and the tested lipid traits but had a strong association with blood pressure.
NOSTRIN (show NOSTRIN Proteins) inhibited production of nitric oxide (NO) by suppressing the activation of endothelial nitric oxide synthase (eNOS).
Protein engineering to develop a redox insensitive endothelial nitric oxide synthase.
Our results suggest that haplotype HT1 in the eNOS gene may be capable of identifying a subset of hepatocellular carcinoma patients who are resistant to sorafenib.
Studied effect of Aliskiren on interleukin-6 (show IL6 Proteins), endothelial nitric oxide synthase and caveolin-1 (show CAV1 Proteins) in human aortic endothelial cells. Findings suggest that aliskiren reverses the effects of IL-6 (show IL6 Proteins) on eNOS and caveolin-1 (show CAV1 Proteins) thru increase in eNOS phosphorylation and nitric oxide production, decrease caveolin-1 (show CAV1 Proteins) phosphorylation, and decrease the interaction between eNOS and caveolin-1 (show CAV1 Proteins).
Studied genetic polymorphisms of human nitric oxide synthase 3(eNOS) and it's association with Coronary Heart Disease (CHD (show CHDH Proteins)); results show eNOS -786T/C, intron 4b/4a and 894G/T genotypes and haplotypes (G-C-B and T-C-B) are significantly associated with the development of CHD (show CHDH Proteins) in combination with potential risk factors.
treatment with Mito-TEMPO, a mitochondrial-specific superoxide scavenger, recovered mitochondrial fission-fusion imbalance and blunted mitochondrial superoxide production, and reduced the IDH2 (show IDH2 Proteins) knockdown-induced decrease in MnSOD (show SOD2 Proteins) expression, eNOS phosphorylation and NO production in endothelial cells
The increase of oxidative/nitrosative stress induced by NOS-3 overexpression induced DNA damage, p53 (show TP53 Proteins), CD95 (show FAS Proteins)/CD95L (show FASL Proteins) expression and cell death in hepatocellular carcinoma cells. The effectiveness of the gene therapy has been demonstrated in vitro and in vivo.
eNOS deficiency is associated with an upregulation of XOR (show XDH Proteins) facilitating the nitrate-nitrite-NO pathway and decreasing the generation of ROS (show ROS1 Proteins). This interplay between XOR (show XDH Proteins) and eNOS is proposed to play a significant role in NO homeostasis and blood pressure regulation.
On normal salt diet, renal CuZnSOD (show SOD1 Proteins) and ECSOD (show SOD3 Proteins) proteins were similar but renal MnSOD (show SOD2 Proteins) was lower in hGRK4g486V than Non-T mice and remained low on high salt diet. hGRK4gammawild-type mice were normotensive and hGRK4g142V mice were hypertensive but both were salt-resistant and in normal redox balance. Chronic tempol treatment partially prevented the salt-sensitivity of hGRK4g486V mice.
We conclude that pp60(Src (show SRC Proteins)) can directly inhibit DDAH (show DDAH2 Proteins) II and this is involved in the increased ADMA levels that enhance eNOS uncoupling during the development of acute lung injury (ALI).
these data reveal a novel NOS-independent role for BH4 in the regulation of mitochondrial redox signalling and bioenergetic metabolism
we show that TRPV4 (show TRPV4 Proteins) is activated both by damage associated molecular pattern HMGB1 (show HMGB1 Proteins) and collagen in diseased Kupffer cells that in turn activate the endothelial NOS (NOS3) to release nitric oxide (NO). The diffusible NO acts in a paracrine fashion in neighboring hepatocytes to deactivate the redox toxicity induced by CYP2E1 (show CYP2E1 Proteins)
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.
(-)-Epicatechin counteracts the negative effects that high glucose or simulated type 2 diabetes has on endothelial nitric oxide synthase function.
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.
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 (show PIN1 Proteins) 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).
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.
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 (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.
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
, nanos homolog 3
, 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