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Amphibian Polyclonal ENOS Primary Antibody für 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 für 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 für 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 Polyclonal ENOS Primary Antibody für ICC, IF - ABIN266306
Sangwung, Greco, Wang, Ischiropoulos, Sessa, Iwakiri: Proteomic identification of S-nitrosylated Golgi proteins: new insights into endothelial cell regulation by eNOS-derived NO. in PLoS ONE 2012
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Human Monoclonal ENOS Primary Antibody für 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 Monoclonal ENOS Primary Antibody für 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 für 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 für 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 für IF, WB - ABIN362790
Wadman: GM advisory panel is slanted, say critics. in Nature 1999
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NOS3 (zeige NANOS3 Antikörper) 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 Antikörper)-induced miR (zeige MLXIP Antikörper)-155 expression to prevent HUVEC cell inflammation.
The AA and GA genotypes of MTHFD1 (zeige MTHFD1 Antikörper) G1958A, TT and GT genotypes of eNOS G894T and the AA and GA genotypes of ACE (zeige ACE Antikörper) A2350G are risk factors for congenital heart defects.
27-bp VNTR polymorphism in intron 4 of eNOS gene polymorphism may be the significant risk factor for systemic lupus erythematosus in south Indian subjects.
Our findings provide evidence to support the hypothesis that eNOS -786 T>C polymorphism and the -786C-4a-894G haplotype are associated with the high risk of recurrent pregnancy loss.
6-Gin attenuated the injury of HUVECs induced by HG through the activation of PI3K (zeige PIK3CA Antikörper)-AKT (zeige AKT1 Antikörper)-eNOS signal pathway.
the two single nucleotide polymorphisms in eNOS gene, G894T and T-786C, are strongly associated with the risk of erectile dysfunction (Meta-Analysis)
Extracellular histones disarrange vasoactive mediators release through a COX1 (zeige COX1 Antikörper)-COX2 (zeige COX2 Antikörper)-eNOS interaction in human endothelial cells.
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 Antikörper) is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 (zeige PTK2B Antikörper) as a novel therapeutic target for cardioprotection
the orphan nuclear receptor (zeige NR1D1 Antikörper), estrogen related receptor alpha (ERRalpha (zeige ESRRA Antikörper)) 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 Antikörper) induced expression of eNOS.
Studied effect of eNOS uncoupling in oxidative stress during pulmonary ischaemia-reperfusion injury.
Despite robust evidence for PKG (zeige PRKG1 Antikörper) Ialpha oxidation during NOS (zeige NOS Antikörper) uncoupling in cell models, it is unlikely that PKG (zeige PRKG1 Antikörper) 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 Antikörper) isoform modulates eNOS signalling through Ca2 (zeige CA2 Antikörper)+/PKC-alpha (zeige PKCa Antikörper)-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 Antikörper) (Serelaxin) attenuates myocardial infarct size and NLRP3 (zeige NLRP3 Antikörper) 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 Antikörper)-eNOS signaling pathway.
The increase of oxidative/nitrosative stress induced by NOS-3 overexpression induced DNA damage, p53 (zeige TP53 Antikörper), CD95 (zeige FAS Antikörper)/CD95L (zeige FASL Antikörper) 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 Antikörper) and link eNOS-derived NO to the modulation by VEGF (zeige VEGFA Antikörper) of Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper)-induced endothelial cell proliferation.
Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent ATP/P2Y1 receptor (zeige P2RY1 Antikörper) signaling to endothelial nitric oxide synthase.
TNFalpha (zeige TNF Antikörper) reduces eNOS activity in bovine endothelial cells through serine 116 phosphorylation and Pin1 (zeige PIN1 Antikörper) binding.
Pomanox supplementation hinders hyperlipemia-induced coronary endothelial dysfunction by activating the Akt (zeige AKT1 Antikörper)/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 Antikörper) stimulation of eNOS. VEGF (zeige VEGFA Antikörper) 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 Antikörper))/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 Antikörper) pathway in porcine aortic endothelial cells.
Data suggest that pig sperm contain bNOS (zeige NOS1 Antikörper), iNOS (zeige NOS2 Antikörper), and eNOS; up-regulation of NOS (zeige NOS Antikörper) by leptin (zeige LEP Antikörper) 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 Antikörper) expression in endomyocardium of normal swine.
Data suggest that angiotensin II regulates nNOS (zeige NOS1 Antikörper) and eNOS expression and NOS (zeige NOS Antikörper) 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 Antikörper) activation was not affected by Slit2 (zeige SLIT2 Antikörper), but eNOS phosphorylation was diminished
Data suggest distinct localizations of eNOS at the spiral arteries/arterial sinuses and iNOS (zeige NOS2 Antikörper) 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