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抗Human ENOS 抗体:
抗Mouse (Murine) ENOS 抗体:
抗Rat (Rattus) ENOS 抗体:
Amphibian Polyclonal ENOS Primary Antibody for IHC (fro), IHC (p) - ABIN152659
Guo, Comhair, Zheng, Dweik, Eissa, Thomassen, Calhoun, Erzurum: Molecular mechanisms of increased nitric oxide (NO) in asthma: evidence for transcriptional and post-translational regulation of NO synthesis. in Journal of immunology (Baltimore, Md. : 1950) 2000
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Human Polyclonal ENOS Primary Antibody for IF (p), IHC (p) - ABIN725690
Li, Han, Guo, Li, Sang: Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO? inhalation exposure. in Chemosphere 2011
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Human Polyclonal ENOS Primary Antibody for ELISA, ICC - ABIN6261536
Lu, Wang, Wang, Zhang, Liu, Zhang, Geng, Shan: Beneficial effects of renal denervation on cardiac angiogenesis in rats with prolonged pressure overload. in Acta physiologica (Oxford, England) 2017
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Human Polyclonal ENOS Primary Antibody for IF (p), IHC (p) - ABIN746468
Ikemura, Yamamoto, Motomura, Yamaguchi, Zhao, Iwasaki, Iwamoto: Preventive effects of the anti-vasospasm agent via the regulation of the Rho-kinase pathway on the development of steroid-induced osteonecrosis in rabbits. in Bone 2013
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Human Monoclonal ENOS Primary Antibody for IHC, ELISA - ABIN969097
Dimmeler, Fleming, Fisslthaler, Hermann, Busse, Zeiher: Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation. in Nature 1999
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Human Polyclonal ENOS Primary Antibody for FACS, IF - ABIN655773
Yanamandra, Napper, Pramanik, Bocchini, Dhanireddy: Endothelial nitric oxide synthase genotypes in the etiology of retinopathy of prematurity in premature infants. in Ophthalmic genetics 2010
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Human Polyclonal ENOS Primary Antibody for IF (p), IHC (p) - ABIN703315
Papinska, Mordwinkin, Meeks, Jadhav, Rodgers: Angiotensin-(1-7) administration benefits cardiac, renal and progenitor cell function in db/db mice. in British journal of pharmacology 2015
Human Polyclonal ENOS Primary Antibody for IF, WB - ABIN362790
Wadman: GM advisory panel is slanted, say critics. in Nature 1999
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Human Monoclonal ENOS Primary Antibody for ICS - ABIN1176890
Shen, Zhang, Utama, Wang, Gan, Wang, Wang, Chen, Vercellotti, Coselli, Mehta, Wang: Human cytomegalovirus inhibits Akt-mediated eNOS activation through upregulating PTEN (phosphatase and tensin homolog deleted on chromosome 10). in Cardiovascular research 2006
Human Polyclonal ENOS Primary Antibody for ELISA, ICC - ABIN6256115
Ruan, Ren, Zhang, Zhu, Xu, Wang: Cardioprotective Effects of QiShenYiQi Dripping Pills on Transverse Aortic Constriction-Induced Heart Failure in Mice. in Frontiers in physiology 2018
Physical interaction between p38 (显示 CRK 抗体) and eNOS was demonstrated by immunoprecipitation, suggesting a novel, NO-independent mechanism for eNOS regulation of TLR4 (显示 TLR4 抗体). In correlation, biopsy samples in patients with systemic lupus erythematous showed reduced eNOS expression with associated elevations in TLR4 (显示 TLR4 抗体) and p38 (显示 CRK 抗体), suggesting an in vivo link.
These results indicated a negative regulatory association between miR24 and NOS3 (显示 NANOS3 抗体). Downregulation of NOS3 (显示 NANOS3 抗体) 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 (显示 CTH 抗体)) for H2S generation and the activity of endothelial NO synthase (显示 NOS 抗体) (eNOS) for NO production.Blocking CSE (显示 CSE 抗体) 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 (显示 CD36 抗体), NOS3 (显示 NANOS3 抗体) and PPARG (显示 PPARG 抗体) respond differentially to intervention of omega-3 supplements in blood lipid profiles.
Investigated the effect of statins on the expression of sirtuin 1 (SIRT1 (显示 SIRT1 抗体)) and endothelial nitric oxide synthase 3 (eNOS) proteins in young premature myocardial infarction (PMI (显示 MPI 抗体)) patients. Found patients with PMI (显示 MPI 抗体) who were taking statins had a markedly higher level of SIRT1 (显示 SIRT1 抗体) compared with the controls. The level of eNOS protein was considerably lower in PMI (显示 MPI 抗体) 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 (显示 HSD11B1 抗体) levels) could affect bioavailability of NO and could represent an increased risk for preeclampsia.
Increased level of nitric oxide in men with arterial hypeertension did not depend on polymorphic genotypes GG and GT of eNOS gene.
Production of nitric oxide (NO) within eNOS-positive NGC (显示 CSPG5 抗体) 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 (显示 NOS 抗体) double knockout mice (NOS1 (显示 NOS1 抗体)/NOS3-/-) were used as a model of low nitric oxide bioavailability in priapism.
leukocyte domiciled midkine (显示 MDK 抗体) mediates increased plasma levels of VEGFA (显示 VEGFA 抗体) relevant for upregulation of endothelial nitric oxide synthase 1 (显示 NOS 抗体) 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 (显示 PTK2B 抗体) is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 (显示 PTK2B 抗体) as a novel therapeutic target for cardioprotection
the orphan nuclear receptor (显示 NR1D1 抗体), estrogen related receptor alpha (ERRalpha (显示 ESRRA 抗体)) 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 (显示 ESRRA 抗体) induced expression of eNOS.
Studied effect of eNOS uncoupling in oxidative stress during pulmonary ischaemia-reperfusion injury.
Despite robust evidence for PKG (显示 PRKG1 抗体) Ialpha oxidation during NOS (显示 NOS 抗体) uncoupling in cell models, it is unlikely that PKG (显示 PRKG1 抗体) 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 (显示 BPIFB4 抗体) isoform modulates eNOS signalling through Ca2 (显示 CA2 抗体)+/PKC-alpha (显示 PKCa 抗体)-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 (显示 CTNNB1 抗体) and link eNOS-derived NO to the modulation by VEGF (显示 VEGFA 抗体) of Wnt (显示 WNT2 抗体)/beta-catenin (显示 CTNNB1 抗体)-induced endothelial cell proliferation.
Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent ATP/P2Y1 receptor (显示 P2RY1 抗体) signaling to endothelial nitric oxide synthase.
TNFalpha (显示 TNF 抗体) reduces eNOS activity in bovine endothelial cells through serine 116 phosphorylation and Pin1 (显示 PIN1 抗体) binding.
Pomanox supplementation hinders hyperlipemia-induced coronary endothelial dysfunction by activating the Akt (显示 AKT1 抗体)/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 (显示 HSD11B1 抗体) stimulation of eNOS. VEGF (显示 VEGFA 抗体) 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 (显示 CAV1 抗体))/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 (显示 EGFR 抗体) pathway in porcine aortic endothelial cells.
Data suggest that pig sperm contain bNOS (显示 NOS1 抗体), iNOS (显示 NOS2 抗体), and eNOS; up-regulation of NOS (显示 NOS 抗体) by leptin (显示 LEP 抗体) 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 (显示 NOS1 抗体) expression in endomyocardium of normal swine.
Data suggest that angiotensin II regulates nNOS (显示 NOS1 抗体) and eNOS expression and NOS (显示 NOS 抗体) 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 (显示 CAV1 抗体) 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 (显示 KDR 抗体) activation was not affected by Slit2 (显示 SLIT2 抗体), but eNOS phosphorylation was diminished
Data suggest distinct localizations of eNOS at the spiral arteries/arterial sinuses and iNOS (显示 NOS2 抗体) 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