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PP2A dephosphorylates MYPT1(pThr696) and thereby stimulates MP activity inducing dephosphorylation of eNOS(pThr497) and the 20 kDa myosin II light chains.
NOS3 895(G>T) is significantly associated with recurrence- free survival in patients who received intravesical chemotherapy with pirarubicin after complete transurethral resection.
Human gastric cancer tissues with low BUBR1 expression showed no eNOS expression. A decrease in BUBR1 reduced eNOS bioavailability through a pathway other than eNOS phosphorylation.
These results suggest that overexpressing or activating eNOS in EOCs increases their survival and enhances their capacity to regulate SMC migration through paracrine effects.
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-195 and miR-582 regulated NO release by targeting 3'-UTR of NOS3 post-transcriptionally in endothelial cells
binding of IL-5 to IL-5Ralpha receptors enhances angiogenic responses by stimulating the expression of HSP70-1 via the eNOS signaling pathway.
that XBP1 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 and eNOS was demonstrated by immunoprecipitation, suggesting a novel, NO-independent mechanism for eNOS regulation of TLR4. In correlation, biopsy samples in patients with systemic lupus erythematous showed reduced eNOS expression with associated elevations in TLR4 and p38, 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.
Our findings suggest that common genetic polymorphisms in the eNOS gene contribute to risk of erectile dysfunction, presumably by effects on eNOS activity and NO availability.
ZYZ-803 stimulated the expression of cystathionine gamma-lyase (CSE) for H2S generation and the activity of endothelial NO synthase (eNOS) for NO production.Blocking CSE and/or eNOS suppressed ZYZ-803-induced H2S and NO production and cardioprotection.
Meta-analysis found that eNOS CC genotype was not related to higher susceptibility of migraine compared with TT+ TC genotypes; subgroup analysis showed CC variant increase the risk for migraine compared with TT+ TC genotypes in Caucasian populations, which could not be observed in non-Caucasian populations. There was no significant difference for other genotypes and alleles between migraine patients and healthy controls.
This study suggests that T2D patients with different genotypes at CD36, NOS3 and PPARG respond differentially to intervention of omega-3 supplements in blood lipid profiles.
Investigated the effect of statins on the expression of sirtuin 1 (SIRT1) and endothelial nitric oxide synthase 3 (eNOS) proteins in young premature myocardial infarction (PMI) patients. Found patients with PMI who were taking statins had a markedly higher level of SIRT1 compared with the controls. The level of eNOS protein was considerably lower in PMI patients compared with the control group.
The eNOS-Glu298Asp variant (in mothers and newborns) in association with dyslipidemia (increased cholesterol, LDL and TG levels, and decreased HDL levels) could affect bioavailability of NO and could represent an increased risk for preeclampsia.
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
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.
Analysis of the 2.1 kb 5' flanking region reveals that the swine eNOS promoter is, like its counterparts in human and other species, a TATA-less promoter; the proximal region from -227 to -82 is necessary for eNOS basal promoter activity.
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