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upregulation of placentaassociated serum exosomal miR155 from patients with preeclampsia may suppress endothelial nitric oxide synthase (eNOS) expression in endothelial cells.
eNOS gene SNP rs1808593 genotype may have an important role in predicting the occurrence of pediatric systemic lupus erythematosis and central nervous system complications in pSLE.
Findings suggest that NOS3 (zeige NANOS3 Proteine) polymorphisms and physical training are important interacting variables to consider in evaluating redox status, nitric oxide availability and production, and BP control.
the eNOS rs1799983 polymorphism and T rs1799983C rs2070744 haplotype might reduce the risk of immunoglobulin A nephropathy in Chinese populations.
we reported a novel mechanism for regulation of eNOS uncoupling by low shear stress via autophagy-mediated eNOS phosphorylation, which is implicated in geometrical nature of atherogenesis.
NOS3 (zeige NANOS3 Proteine) SNPs are associated with post-exercise hypotension in ethnicity and exercise intensity dependent manner.
Acidic pHi reduced NO synthesis and eNOS serine(1177) phosphorylation. Thus, system y(+)L activity is downregulated by an acidic pHi, a phenomenon that may result in reduced NO synthesis in HUVECs.
The meta-analysis did not detect any association between eNOS 27VNTR (4b/4a) polymorphism and diabetic microvascular complications susceptibility in Chinese populations.
Pitavastatin increases eNOS expression and inhibits of LPS (zeige IRF6 Proteine)-induced miR (zeige MLXIP Proteine)-155 expression to prevent HUVEC cell inflammation.
The AA and GA genotypes of MTHFD1 (zeige MTHFD1 Proteine) G1958A, TT and GT genotypes of eNOS G894T and the AA and GA genotypes of ACE (zeige ACE Proteine) A2350G are risk factors for congenital heart defects.
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 (zeige PTK2B Proteine) is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 (zeige PTK2B Proteine) as a novel therapeutic target for cardioprotection
the orphan nuclear receptor (zeige NR1D1 Proteine), estrogen related receptor alpha (ERRalpha (zeige ESRRA Proteine)) 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 (zeige ESRRA Proteine) induced expression of eNOS.
Studied effect of eNOS uncoupling in oxidative stress during pulmonary ischaemia-reperfusion injury.
Despite robust evidence for PKG (zeige PRKG1 Proteine) Ialpha oxidation during NOS uncoupling in cell models, it is unlikely that PKG (zeige PRKG1 Proteine) 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 (zeige BPIFB4 Proteine) isoform modulates eNOS signalling through Ca2 (zeige CA2 Proteine)+/PKC-alpha (zeige PKCa Proteine)-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.
Reperfusion therapy with recombinant human relaxin-2 (zeige RLN1 Proteine) (Serelaxin) attenuates myocardial infarct size and NLRP3 (zeige NLRP3 Proteine) inflammasome following ischemia/reperfusion injury via eNOS-dependent mechanism.
These observations suggest that DATS promotes revascularization in response to hind-limb ischemia through its ability to stimulate the Akt (zeige AKT1 Proteine)-eNOS signaling pathway.
The increase of oxidative/nitrosative stress induced by NOS-3 overexpression induced DNA damage, p53 (zeige TP53 Proteine), CD95 (zeige FAS Proteine)/CD95L (zeige FASL Proteine) expression and cell death in hepatocellular carcinoma cells. The effectiveness of the gene therapy has been demonstrated in vitro and in vivo.
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 (zeige HSD11B1 Proteine) stimulation of eNOS. VEGF (zeige VEGFA Proteine) 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