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Nos3 Antibody

  • 货号:
    CSB-PA16579A0Rb
  • 规格:
    ¥440
  • 促销:
    小规格抗体限时一口价
  • 其他:

产品详情

  • 产品名称:
    Rabbit anti-Rattus norvegicus (Rat) Nos3 Polyclonal antibody
  • Uniprot No.:
    Q62600
  • 基因名:
  • 别名:
    Nos3 antibody; Nitric oxide synthase antibody; endothelial antibody; EC 1.14.13.39 antibody; Constitutive NOS antibody; cNOS antibody; EC-NOS antibody; Endothelial NOS antibody; eNOS antibody; NOS type III antibody; NOSIII antibody
  • 宿主:
    Rabbit
  • 反应种属:
    Rat
  • 免疫原:
    Recombinant Rat Nitric oxide synthase, endothelial protein (519-690AA)
  • 免疫原种属:
    Rattus norvegicus (Rat)
  • 标记方式:
    Non-conjugated

    本页面中的产品,Nos3 Antibody (CSB-PA16579A0Rb),的标记方式是Non-conjugated。对于Nos3 Antibody,我们还提供其他标记。见下表:

    可提供标记
    标记方式 货号 产品名称 应用
    HRP CSB-PA16579B0Rb Nos3 Antibody, HRP conjugated ELISA
    FITC CSB-PA16579C0Rb Nos3 Antibody, FITC conjugated
    Biotin CSB-PA16579D0Rb Nos3 Antibody, Biotin conjugated ELISA
  • 克隆类型:
    Polyclonal
  • 抗体亚型:
    IgG
  • 纯化方式:
    >95%, Protein G purified
  • 浓度:
    It differs from different batches. Please contact us to confirm it.
  • 保存缓冲液:
    Preservative: 0.03% Proclin 300
    Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
  • 产品提供形式:
    Liquid
  • 应用范围:
    ELISA
  • Protocols:
  • 储存条件:
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 货期:
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

产品评价

靶点详情

  • 功能:
    Produces nitric oxide (NO) which is implicated in vascular smooth muscle relaxation through a cGMP-mediated signal transduction pathway. NO mediates vascular endothelial growth factor (VEGF)-induced angiogenesis in coronary vessels and promotes blood clotting through the activation of platelets.
  • 基因功能参考文献:
    1. Low NOS3 expression is associated with diabetic endothelial dysfunction. PMID: 29471582
    2. AM and L-NAME eliminated the CAPE-oNO2-mediated cardioprotection by restraining SIRT1 and eNOS expression, respectively. It suggested that CAPE-oNO2 ameliorated MIRI by suppressing the oxidative stress, inflammatory response, fibrosis and necrocytosis via the SIRT1/eNOS/NF-kappaB pathway PMID: 29220696
    3. The present results indicate that Advanced glycation endproducts impairs endothelial-dependent vasodilation, and this effect is mediated via arginase overexpression and NADPH oxidase stimulation. PMID: 29627571
    4. Activation of ACE2 had a protective role in the development of pulmonary arterial hypertension in rat model via improving the function of pulmonary arterial endothelium. This effect was potentially mediated by promoted NO release as a consequence of increased phosphorylation of eNOS at Ser1177 and dephosphorylation of eNOS at Thr495. PMID: 29146157
    5. 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 PMID: 28444132
    6. microparticles from AMI patients decreased eNOS phosphorylation at Ser1177, increased eNOS phosphorylation at T495 and caveolin-1 expression, decreased eNOS association with Hsp90, decreased NO production but increased (O2) generation, damaged endothelial-dependent vasodilatation. PMID: 28002238
    7. The data of the present data provide evidence that hyperhomocysteinaemia is a vascular risk factor for erectile dysfunction by impairing cavernosa endothelial nitric oxide synthase activity. PMID: 27221552
    8. Mitochondrial dysfunction in the aging heart is accompanied by constitutive eNOS uncoupling on the background of oxidative and nitrosative stress. PMID: 29537218
    9. Expression of eNOS protein was significantly increased in Sedimentary female when compared to Sed male rats PMID: 27562066
    10. HIgh fat diet increases testicular eNOS expression and this was reduced by antioxidants. PMID: 29023053
    11. Pulmonary vascular reactivity is altered in a model of murine bronchopulmonary dysplasia, the cellular mechanisms involve a decreased eNOS phosphorylation at its activating site. PMID: 28235094
    12. these results show that coronary endothelial cells rather than cardiomyocytes play a key role in the eNOS-dependent cardioprotection of exercise. PMID: 27866931
    13. a novel mechanism and model in which CAV1 phosphorylation facilitates CAV1 scaffolding and GRK2-CAV1 interaction, thus clustering eNOS within a complex that inhibits eNOS activity, is reported. PMID: 28162981
    14. Intravenous delivery of rBMSCs expressing eNOS/F92A-Cav1 to PAH rats inhibits pulmonary vascular smooth muscle cell proliferation, and improves pulmonary haemodynamics, vascular remodelling and short-term survival. PMID: 27771236
    15. Activation of endothelial NO synthase by a xanthine derivative, KMUP-1, ameliorates hypoxia-induced apoptosis in endothelial progenitor cells. PMID: 27109251
    16. Epoetin beta pegol ameliorates flow-mediated dilation and improves endothelial nitric oxide synthase coupling state in nonobese diabetic rats. PMID: 28054454
    17. that tempol causes hypernatremia after acute sodium overload by inhibiting the thirst mechanism and facilitating diuresis, despite increasing renal eNOS expression and natriuresis PMID: 27849390
    18. results suggest that the AT1 receptor is involved in development of hypertension and cardiac fibrosis. Selective activating ACE2/eNOS and inhibiting CD44/HA interaction might be considered as the therapeutic targets for attenuating Ang II induced deleterious cardiovascular effects PMID: 27085217
    19. 3, 5, 7, 3', 4'-pentamethoxyflavone treatment of middle aged rats appeared to increase production of NO and H2S from the blood vessels by upregulating the expression of eNOS and cystathione-gamma-lyase.. PMID: 27468988
    20. Antioxidant N-acetylcysteine attenuated myocardial dysfunction and myocardial I/R injury by improving Cav-3/eNOS signaling. PMID: 27733157
    21. down-regulation of CD47 exerts a protective effect against myocardial I/R injury, which may be attributable to attenuation of oxidative stress via activation of the eNOS/nitric oxide signaling pathway. PMID: 27960187
    22. eNOS expression at mRNA and protein levels and the number of circulating EPCs were reduced significantly in rats with monocrotaline-induced pulmonary arterial hypertension. These were reduced less in rats treated with rosuvastatin, suggesting that it ameliorates remodeling by increasing the circulating EPCs and upregulating eNOS. PMID: 27655493
    23. hese results suggest that the protein adjustments observed in lipid raft/caveolin-1 microdomains could be visualized as a process required to protect the cells against NO overproduction and aberrant calpain activation. Alterations in eNOS, calpain-1 and HSP90 levels have been observed in aorta of Zucker Diabetic Rats (ZDR). PMID: 27956030
    24. role in lung-protective effects of bubble continuous positive airway pressure after extubation PMID: 26800273
    25. Combined therapy with Carthamus tinctorius L. extract and captopril in L-NAME-induced hypertensive rats normalized eNOS levels. PMID: 26938552
    26. The enhanced expression of eNOS in L-arginine treated LVH rats resulted in the amelioration of oxidative and haemodynamic parameters. PMID: 27010893
    27. This study demonstrated that enos increases in male rat with aneurysmal subarachnoid hemorrhage. PMID: 26923576
    28. Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. PMID: 26644274
    29. Combined stress decreased eNOS expression in the endothelium of microvessels and almost complete disappearance of eNOS expression in endothelial cells of the majority of capillaries. PMID: 26608376
    30. Data suggest that mild hyperglycemia in type 2 diabetes (as seen in GK rats) preserves eNOS expression in vascular endothelium and thus enhances endothelium-dependent relaxation after acute myocardial infarction preventing myocardial reperfusion injury. PMID: 26219999
    31. ZFP580 promotes not only the differentiation of EPCs into ECs by increasing the expression of eNOS and the availability of nitric oxide, but also the vessel formation in vitro and in vivo PMID: 26268592
    32. These results suggest that administration of ghrelin ameliorates impaired angiogenesis in diabetic MI rats. And these beneficial effects derive from regulating GHSR1a-mediated AMPK/eNOS signal pathway PMID: 26364514
    33. This result confirmed that Arctigenin might exert dural effects in preventing SAH-induced vasospasm through upregulating eNOS expression via the PI3K/Akt signaling pathway and attenuate endothelins after subarachnoid hemorrhage PMID: 26539501
    34. Jujuboside B increased extracellular Ca2+ influx through endothelial transient receptor potential cation (TRPC) channels, phosphorylated eNOS and promoted NO generation in vascular endothelial cells. PMID: 26901291
    35. PAR2 stimulation of NO production via an additional pathway that targets phosphorylation of Ser1177-eNOS suggests a regulatory mechanism for sustaining agonist-mediated vasodilation in metabolic syndrome. PMID: 26760532
    36. Perivascular adipose tissue in Dahl SS rats buffers vasoconstriction by activating endothelial NOS via mechanisms that may include the involvement of leptin. PMID: 26608658
    37. There was a significant reduction in eNOS expression in Metabolic Syndrome thoracic ducts suggesting that diminished NO production is partially responsible for impaired flow response. PMID: 26637560
    38. Results suggest that eNOS-mediated endoplasmic reticulum stress may participate in status epilepticus-induced vasogenic edema formation PMID: 26115585
    39. These findings provide direct evidence that in vivo I/R induces eNOS dysfunction secondary to BH4 depletion, and that pre-ischemic liposomal BH4 administration preserves eNOS function conferring cardioprotection with reduced oxidative stress PMID: 26116866
    40. Results suggest that status epilepticus-induced ETB receptor/eNOS-mediated MMP-9 activation may lead to impairments of endothelial cell function via tight junctions protein degradation PMID: 26232046
    41. Suggest that telmisartan reduced susceptibility to atrial arrhythmia to a greater extent than valsartan, ameliorated atrial remodeling, and reversed imbalances in the RAS-ERK and PI3K-Akt-eNOS pathways. PMID: 26158699
    42. miR-22 down-regulated Cav3, leading to restored eNOS activity/NO production, which inhibited cardiac myocyte apoptosis and promoted cardiac function after myocardial ischemia and reperfusion. PMID: 26191152
    43. Data suggest that activity of Nos3 in aorta endothelium can be regulated by dietary factors; here, activity of aorta Nos3 is up-regulated by high-fructose diet and further up-regulated by an antioxidant dietary supplement, epicatechin. PMID: 25943039
    44. Vasculoprotective effect of insulin after arterial injury is mediated by an eNOS-dependent mechanism. PMID: 25974101
    45. Study showed that the mRNA expression of eNOS did not increase on day 3 after the experimental spinal cord injury, with a consistent result as compared with the sham-operated and healthy control groups PMID: 25644387
    46. Data suggest that, in polycystic ovary syndrome, heart exhibits down-regulation of both eNOS (nitric oxide synthase 3) and Na+/K+-ATPase (Na+/K+ transporting ATPase alpha 1) activities, but up-regulation of iNOS (nitric oxide synthase 2) activity. PMID: 25988879
    47. Data show that resveratrol (Res) reversed caveolin-1 (Cav-1)/endothelial nitric oxide synthase (eNOS) expressions in high-fat/sucrose diet (HFS) rats. PMID: 25419974
    48. Data from in vitro studies suggest that genistein and magnesium (sometimes used as dietary supplements) enhance vasodilation of vascular smooth muscle via mechanisms involving eNOS and BK(Ca) [KCa1.1 calcium-activated potassium channel]. PMID: 25494655
    49. In response to CI-1044, activation of eNOS produces excessive levels of Nitric Oxide and vascular injury, and modulation of upstream activators of eNOS leads to regulation of eNOS activity. PMID: 24705881
    50. Suggest a potential role for ILK, the cytoskeleton and ILK signalling partners including Rho in regulating intrahepatic sinusoidal endothelial cell eNOS expression and function. PMID: 24906011

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  • 亚细胞定位:
    Membrane, caveola. Cytoplasm, cytoskeleton. Golgi apparatus. Cell membrane.
  • 蛋白家族:
    NOS family
  • 组织特异性:
    Expressed constitutively by vascular endothelium. Detected in alveolar and serosal epithelial cells as well as in endothelial cells in one day old rat. In adult lung, detected in rare endothelial cells.
  • 数据库链接:

    KEGG: rno:24600

    STRING: 10116.ENSRNOP00000013058

    UniGene: Rn.44265