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Hypertension and longevity: role of genetic polymorphisms in renin-angiotensin-aldosterone system and endothelial nitric oxide synthase.
our study shows for the first time a sexual dimorphism in the expression, activity, and function of eNOS in M- and F-ECs. Sex-differential expression of genes has been recently related to different disease susceptibility
A strong association of G894 T eNOS polymorphism with susceptibility to EH in Morocco.
Genetic predisposition to enhanced nitric oxide signaling was associated with reduced blood pressure, improved renal and pulmonary function, and significantly reduced risks of coronary heart disease in people with rs3918226 NOS3 variant.
findings show that the 27-bp VNTR polymorphic locus, but not the c.894G>T polymorphic locus, is associated with CAD and that it may regulate NOS3 pre-mRNA splicing in a length-dependent manner.
In eNOS rs891512, rs1799983, rs2070744, and rs869109213 polymorphisms may serve as genetic biomarkers of diabetes mellitus, while rs1799983, rs2070744, and rs869109213 polymorphisms may contribute to the development of vascular complications in diabetes mellitus.[review; meta-analysis]
Polymorphism of eNOS G894T is not a risk factor for diabetic foot ulcer formation. T allele is a risk factor for diabetes, but T allele is not a risk factor for diabetic foot ulcer formation.
Infants born to environmental smokers, as judged by umbilical serum cotinine levels close to .2 ng/mL, are not associated with lower birthweight or reduced eNOS activity, or concentration in the fetal vascular bed.
analysis indicated the association between G894T gene mutation and recurrent spontaneous abortion risk (Meta-Analysis)
Cav-1 stabilizes eNOS expression and regulates its activity, whereas eNOS-derived nitric oxide promotes caveola-mediated endocytosis.
The G24943A polymorphism in the NOS3 gene is associated with coronary artery disease in Tunisian patients.
Early hyperoxia exposure led to a significant increase in NOS3 and STAT3 mRNA levels in pulmonary endothelial cells with corresponding changes in histone modification patterns such as H2aZac and H3K9ac hyperacetylation at the respective gene loci.
Salvianolic acid inhibits the effects of high glucose on vascular endothelial dysfunction by modulating the Sirt1-eNOS pathway
The relationship between eNOS polymorphisms and breast cancer hazard depended on menopause status, especially for the 894G > T polymorphism in Taiwanese women.
The endothelial nitric oxide synthase GG genotype is associated to heart failure prognosis, and this association remains present in highly admixed sample groups.
Meta-analysis indicated no association between SLE and the T786C and G894T polymorphisms. No association was found between the eNOS 4b/a, T786C, and G894T polymorphisms and RA CONCLUSIONS: This meta-analysis of published studies shows that the eNOS 4b/a polymorphism may be associated with the development of SLE, but the 4b/a, T786C, and G894T polymorphisms may be not associated with RA susceptibility.
Concomitant presence of CETP B1, NOS3 T and ANGPTL8 T alleles augments the risk of cardiovascular disease and type 2 diabetes mellitus.
HDL sphingomyelin was fundamental for intercellular adhesion molecule-1 (ICAM-1) downregulation in HMEC-1.
an association between the NOS3 rs2070744 polymorphism and periodontal disease, is reported.
The NOS3 G894T polymorphic variant also correlated with atherosclerosis, an association probably mediated by the traditional risk factors for CVD
Using a mouse disease model it was shown that the eNOS-NO pathway could be a therapeutic target for the treatment of chronic kidney disease associated with endothelial dysfunction.
In a mesenchymal colorectal cancer model, up-regulation of eNOS is maintained in the more advanced tumor genotypes.
endothelium-dependent cholinergic responses of the ophthalmic artery in the eNOS-/- mice are largely preserved and, this vascular bed has the ability to compensate for the loss of normal vasodilator responses solely via EDHFs.
Data suggest that increased nNOS (and probably eNOS) content and the consequential elevated NO production and high arterial blood flow in the penis may be the underlying mechanism of priapism in Fabry mice.
The results suggest that the interaction between Zeb1, Hdac2, and eNOS is required for early mesendodermal differentiation of naive mouse embryonic stem cells.
Decreased NOS3 expression is associated with acute lung injury.
Transplantation of a denuded aorta into carotid artery leads to plaque formation. Caveolin-1 knockout leads to increased plaque formation. Additional knockout of eNOS in Cav1-/- aortae reduces plaque formation.
excessive sFlt1 and lack of eNOS synergistically induce hepatic dysfunction and thrombocytopenia, suggesting a novel role for VEGF and nitric oxide signaling in hepatocyte-endothelial cross-talk in health and in liver injury states.
Production of nitric oxide (NO) within eNOS-positive NGC 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/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 is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 as a novel therapeutic target for cardioprotection
the orphan nuclear receptor, estrogen related receptor alpha (ERRalpha) 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 induced expression of eNOS.
Studied effect of eNOS uncoupling in oxidative stress during pulmonary ischaemia-reperfusion injury.
Despite robust evidence for PKG Ialpha oxidation during NOS uncoupling in cell models, it is unlikely that PKG 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 isoform modulates eNOS signalling through Ca2+/PKC-alpha-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 (Serelaxin) attenuates myocardial infarct size and NLRP3 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-eNOS signaling pathway.
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 and link eNOS-derived NO to the modulation by VEGF of Wnt/beta-catenin-induced endothelial cell proliferation.
Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent ATP/P2Y1 receptor signaling to endothelial nitric oxide synthase.
TNFalpha 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/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)/endothelial nitric oxide synthase (eNOS) expressions in high glucose cultured bovine aortic endothelial cells (BAECs).
Fluorescence decays of fluorescently labeled CaM bound to eNOS reveal four distinct conformational states and single-molecule fluorescence trajectories show multiple fluorescence states with transitions between states
Endothelial nitric oxide synthase is regulated by ERK phosphorylation at Ser602.
key regulatory role of CaM involves the stabilization of structural intermediates and precise positioning of the pivot for the FMN domain tethered shuttling motion to accommodate efficient and rapid electron transfer in the homodimer of eNOS.
endogenous activity is critical for the luteinizing hormone-induced ovulatory cascade in granulosa cells
radiation-induced eNOS activation in bovine aortic endothelial cells is regulated by ATM and HSP90
Heparan sulfate is involved in both centralized and decentralized glycocalyx-mediated mechanotransduction, with GPC1 acting as a centralized agent and SDC1 functioning in decentralized mechanotransmission. GPC1 mediates NOS3 activation.
these data provide the first detailed analysis of Cav-1 binding to one of its most significant client proteins, eNOS.
The expression, localization, and distribution of 3 nitric oxide synthase enzymes through the estrous cycle in bovien fallopian tubes are reported.
The downregulation of eNOS by ox-low-density lipoprotein, as driven by LOX-1-mediated endoplasmic stress, is associated with the PI3K-Akt-eNOS signaling pathway.
TRPV1 activation in endothelial cells may elicit a Ca(2+) -dependent effect on PP2B-PKC signalling, which leads to dephosphorylation of eNOS
eNOS protein and nitric oxide content in endothelial cells of conduit arteries is increased compared with the microcirculation endothelial cells.
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 pathway in porcine aortic endothelial cells.
Data suggest that pig sperm contain bNOS, iNOS, and eNOS; up-regulation of NOS by leptin 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 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 inhibitory domain of eNOs stimulates vasodilation of the pulmonary artery.
endothelium-derived NO stimulates guanylyl cyclase in vascular smooth muscle cells and, thereby, permits CO to cause dilation by activating K(Ca) channels
the p38 MAPK is an upstream component of Akt-mediated eNOS activation
Ritonavir significantly impairs vasomotor function and reduces eNOS expression in porcine coronary artery endothelial cells.
AMPK activity is essential for estradiol-induced eNOS activation in vascular endothelial cells via the promotion of eNOS interaction with HSP90
Hsp90 is a modulator of eNOS activity and vascular reactivity in the newborn piglet pulmonary circulation
Glomerular eNOS gene expression was studied during postnatal maturation and AT1 receptor inhibition.
in the aortic arch, nitric oxide synthase 3 endothelial (eNOS) was downregulated, compared with the thoracic aorta
eNOS phosphorylation at Ser-116, therefore, appears to contribute to negative modulation of eNOS activity and hence to regulation of vascular tone.
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 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 activation was not affected by Slit2, but eNOS phosphorylation was diminished
Data suggest distinct localizations of eNOS at the spiral arteries/arterial sinuses and iNOS 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.
Diabetes enhances the vasodilator response of the rabbit carotid artery to testosterone by a mechanism that includes an increased modulatory activity of the endothelial nitric oxide.
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