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This study set out to examine the relationship between renal colic and endothelial nitric oxide synthase gene polymorphisms, but the results show that no relation was found.
miR (show MLXIP Proteins)-195 and miR (show MLXIP Proteins)-582 regulated NO release by targeting 3'-UTR of NOS3 post-transcriptionally in endothelial cells
binding of IL-5 (show IL5 Proteins) to IL-5Ralpha receptors enhances angiogenic responses by stimulating the expression of HSP70-1 (show HSPA1A Proteins) via the eNOS signaling pathway.
that XBP1 (show XBP1 Proteins) splicing can regulate eNOS expression and cellular location, leading to EC migration and therefore contributing to wound healing and angiogenesis
Unfavorable genotype of polymorphic variant of candidate gene participating in endothelial dysfunction NOS3 (T786C ) was associated with changes in levels of their active substances in individuals exposed to mercury.
4a/b polymorphism of gene NOS3 in patients with various stages of Pneumoconiosis correlates with early development and unfavorable course of Pneumoconiosis in post-contact period.
this study provides that infants with genotype GT eNOS 894G > T have 3.4-fold higher risk of developing of IVH if they are born before 28 + 6 weeks of gestation.
Physical interaction between p38 (show CRK Proteins) and eNOS was demonstrated by immunoprecipitation, suggesting a novel, NO-independent mechanism for eNOS regulation of TLR4 (show TLR4 Proteins). In correlation, biopsy samples in patients with systemic lupus erythematous showed reduced eNOS expression with associated elevations in TLR4 (show TLR4 Proteins) and p38 (show CRK Proteins), suggesting an in vivo link.
These results indicated a negative regulatory association between miR24 and NOS3. Downregulation of NOS3 may induce vasospasm following subarachnoid hemorrhage, which may be due to the upregualtion of miR24 in VSMCs.
We found a significant relationship between eNOS gene polymorphisms and the congenital heart defects in patients with Down syndrome. Screening for the presence or absence of eNOS polymorphisms may be useful to obtain preliminary data on the risk of congenital heart defects in patients with Down syndrome.
Production of nitric oxide (NO) within eNOS-positive NGC (show CSPG5 Proteins) neurons increases after environmental perturbations, indicating a role for eNOS/NO in modulating environmentally appropriate levels of GA. Inhibition of NO production causes dysregulated behavioral arousal after exposure to environmental perturbation.
Neuronal and endothelial NO synthase double knockout mice (NOS1 (show NOS1 Proteins)/NOS3-/-) were used as a model of low nitric oxide bioavailability in priapism.
leukocyte domiciled midkine mediates increased plasma levels of VEGFA relevant for upregulation of endothelial nitric oxide synthase 1 and 3
endothelial NOS homodimer formation may have a role in the crucial role of ischemia-reperfusion injury in triggering transplant vasculopathy in transplanted aortic grafts
current studies demonstrate that PYK2 (show PTK2B Proteins) is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 (show PTK2B Proteins) as a novel therapeutic target for cardioprotection
the orphan nuclear receptor (show NR1D1 Proteins), estrogen related receptor alpha (ERRalpha (show ESRRA Proteins)) is required to coordinate the PGC-1alpha -induced eNOS expression. In conclusion, endothelial PGC-1alpha expression protects from vascular dysfunction by promoting NO* bioactivity through ERRalpha (show ESRRA Proteins) induced expression of eNOS.
Studied effect of eNOS uncoupling in oxidative stress during pulmonary ischaemia-reperfusion injury.
Despite robust evidence for PKG (show PRKG1 Proteins) Ialpha oxidation during NOS uncoupling in cell models, it is unlikely that PKG (show PRKG1 Proteins) Ialpha oxidation occurs to a significant extent in vivo during diet-induced obesity and so is unlikely to mediate the associated cardiovascular dysfunction.
LAV-BPIFB4 (show BPIFB4 Proteins) isoform modulates eNOS signalling through Ca2 (show CA2 Proteins)+/PKC-alpha (show PKCa Proteins)-dependent mechanism.
There was about five-fold decreased mRNA expression of eNOS in aortic segments from the group receiving bifidobacteria. Bifidobacterium pseudocatenulatum CECT 7765 restores the obesity-induced altered vascular function mainly by reducing nitric oxide release.
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 (show HSD11B1 Proteins) stimulation of eNOS. VEGF (show VEGFA Proteins) 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.
ATRA is able to ameliorate highfatinduced AS in rabbits, which is mediated through the activation of eNOS and downregulating CAV1 (show CAV1 Proteins) 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
, 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