Mouse Endothelial nitric oxide synthase,eNOS ELISA Kit

Code CSB-E08324m
Size 96T,5×96T,10×96T
Trial Size 24T ELISA Kit Trial Size (Only USD$150/ kit)
* The sample kit cost can be deducted from your subsequent orders of 96T full size kits of the same analyte at 1/5 per kit, until depleted in 6 months. Apply now
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Product Details

Target Name
nitric oxide synthase 3 (endothelial cell)
Alternative Names
Nos3 ELISA Kit; EcnosNitric oxide synthase ELISA Kit; endothelial ELISA Kit; EC ELISA Kit; Constitutive NOS ELISA Kit; cNOS ELISA Kit; EC-NOS ELISA Kit; Endothelial NOS ELISA Kit; eNOS ELISA Kit; NOS type III ELISA Kit; NOSIII ELISA Kit
Uniprot No.
Mus musculus (Mouse)
Sample Types
serum, plasma, tissue homogenates
Detection Range
0.312 IU/mL-20 IU/mL
0.078 IU/mL
Assay Time
Sample Volume
Detection Wavelength
450 nm
Research Area
Assay Principle
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
To assess the linearity of the assay, samples were spiked with high concentrations of mouse eNOS in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:1Average %86
Range %82-95
1:2Average %97
Range %91-103
1:4Average %105
Range %98-112
1:8Average %98
Range %94-102
The recovery of mouse eNOS spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 9892-104
EDTA plasma (n=4)10294-106
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
202.995 2.865 2.930 2.728
102.280 2.244 2.262 2.060
51.528 1.546 1.537 1.335
2.50.926 0.940 0.933 0.731
1.250.598 0.578 0.588 0.386
0.6250.445 0.431 0.438 0.236
0.3120.298 0.305 0.302 0.100
00.199 0.204 0.202  
and FAQs
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx

This mouse eNOS ELISA kit employs the quantitative sandwich enzyme immunoassay technique to measure the levels of mouse eNOS in multiple samples, including serum, plasma, and tissue homogenates. It also uses the enzyme-substrate chromogenic reaction to visualize and analyze the analyte levels through the color intensity. The intensity of the colored product is in direct proportion to the eNOS levels in the sample and is measured at 450 nm through a microplate reader.

eNOS, also called NOS3, is usually constitutively expressed in cells in an inactive state and is activated by binding to the CaM protein after the elevation of Ca2+ concentration. NOS3 is highly enriched in endothelial cells (ECs) and contributes to the generation of nitric oxide (NO) to exert vasodilation and regulate the flow of blood throughout the body. It is linked to cardiovascular diseases such as hypertension, atherosclerosis, and diabetes mellitus. Recent studies have shown that NOS3 plays an important role in cancers, such as inhibiting apoptosis and promoting angiogenesis, proliferation, invasiveness, and immunosuppression.

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Target Background

(From Uniprot)
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. May play a significant role in normal and abnormal limb development.
Gene References into Functions
  1. The results suggest that the interaction between Zeb1, Hdac2, and eNOS is required for early mesendodermal differentiation of naive mouse embryonic stem cells. PMID: 29599503
  2. Decreased NOS3 expression is associated with acute lung injury. PMID: 29074491
  3. 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. PMID: 27915034
  4. 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. PMID: 29311569
  5. 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. PMID: 29967172
  6. endothelial NOS homodimer formation may have a role in the crucial role of ischemia-reperfusion injury in triggering transplant vasculopathy in transplanted aortic grafts PMID: 27883078
  7. 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
  8. 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. PMID: 27910955
  9. Studied effect of eNOS uncoupling in oxidative stress during pulmonary ischaemia-reperfusion injury. PMID: 28481990
  10. 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. PMID: 28690194
  11. LAV-BPIFB4 isoform modulates eNOS signalling through Ca2+/PKC-alpha-dependent mechanism. PMID: 28419216
  12. 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. PMID: 28539820
  13. Reperfusion therapy with recombinant human relaxin-2 (Serelaxin) attenuates myocardial infarct size and NLRP3 inflammasome following ischemia/reperfusion injury via eNOS-dependent mechanism. PMID: 28073832
  14. These observations suggest that DATS promotes revascularization in response to hind-limb ischemia through its ability to stimulate the Akt-eNOS signaling pathway. PMID: 28216514
  15. The increase of oxidative/nitrosative stress induced by NOS-3 overexpression induced DNA damage, p53, CD95/CD95L expression and cell death in hepatocellular carcinoma cells. The effectiveness of the gene therapy has been demonstrated in vitro and in vivo. PMID: 28162288
  16. eNOS deficiency is associated with an upregulation of XOR facilitating the nitrate-nitrite-NO pathway and decreasing the generation of ROS. This interplay between XOR and eNOS is proposed to play a significant role in NO homeostasis and blood pressure regulation. PMID: 27609225
  17. On normal salt diet, renal CuZnSOD and ECSOD proteins were similar but renal MnSOD was lower in hGRK4g486V than Non-T mice and remained low on high salt diet. hGRK4gammawild-type mice were normotensive and hGRK4g142V mice were hypertensive but both were salt-resistant and in normal redox balance. Chronic tempol treatment partially prevented the salt-sensitivity of hGRK4g486V mice. PMID: 28189851
  18. We conclude that pp60(Src) can directly inhibit DDAH II and this is involved in the increased ADMA levels that enhance eNOS uncoupling during the development of acute lung injury (ALI). PMID: 27838434
  19. these data reveal a novel NOS-independent role for BH4 in the regulation of mitochondrial redox signalling and bioenergetic metabolism PMID: 28104455
  20. we show that TRPV4 is activated both by damage associated molecular pattern HMGB1 and collagen in diseased Kupffer cells that in turn activate the endothelial NOS (NOS3) to release nitric oxide (NO). The diffusible NO acts in a paracrine fashion in neighboring hepatocytes to deactivate the redox toxicity induced by CYP2E1 PMID: 27913210
  21. Endothelial cell Gch1 and BH4-dependent eNOS regulation play pivotal roles in maintaining vascular homeostasis in resistance arteries. PMID: 28128438
  22. (-)-Epicatechin counteracts the negative effects that high glucose or simulated type 2 diabetes has on endothelial nitric oxide synthase function. PMID: 26993496
  23. These results suggest that S-glutathionylation of eNOS within the microvascular endothelial cells inhibited NO production and enhanced TLR4 activity, which were implicated in the pathogenesis of necrotizing enterocolitis. PMID: 26845626
  24. Genetic deletion of NOS3 in CAV1-deficient mice restored intraocular pressure and conventional aqueous humor drainage to wild type level. NOS3 and CAV1 interaction is important to intraocular pressure regulation. PMID: 28973370
  25. these data suggest that CD NOS3 may be involved in the diuretic response to a water load in a sex-specific manner; the mechanism of this effect remains to be determined. PMID: 27707708
  26. CAV1 KO mice have elevated IOP and reduced conventional outflow facility when compared with WT mice. CAV2 expression was absent in CAV1 KO mice, but we observed increased expressions of eNOS PMID: 27228562
  27. TNF-alpha does not regulate eNOS activity in murine endothelial cells through serine 116 phosphorylation and Pin1 binding. PMID: 27073025
  28. The eNOS expressed in smooth muscle cells in FAs attenuates alpha-adrenergic vasoconstriction. PMID: 27486092
  29. Thioredoxin-mediated deglutathionylation of eNOS in the coronary artery in vivo protected against reperfusion injury, even in the presence of normal levels of glutathione. PMID: 27587398
  30. Eph-B4 stimulates eNOS phosphorylation in vitro and may mediate vein graft adaptation by regulation of eNOS activity in vivo. PMID: 26817610
  31. Pulse pressure finely regulates eNOS, controlling cerebral artery reactivity. PMID: 26823473
  32. TNF-alpha induces vascular insulin resistance by mechanisms that involve positive modulation of PTEN and inhibition of Akt/eNOS/NO signaling. PMID: 27562094
  33. Beta2AR overexpression enhances endothelial progenitor cells (EPC) functions in vitro and enhances the vascular repair abilities of EPCs in vivo via the beta2AR/Akt/eNOS pathway. PMID: 27194135
  34. the absence of nitric oxide synthases results in a disturbed arginine-nitric oxide metabolism and inadequate fracture healing. PMID: 26555548
  35. Through the abrogation of NAD(P)H oxidase-driven eNOS uncoupling. PMID: 26455387
  36. The in vitro concordance of early Nos3(-/-) disease signatures supports the utility of iPSCs as a cellular model of developmental heart defects PMID: 26344701
  37. Findings do not support the hypothesis that reduced NO production from eNOS contributes to obesity-related adipose tissue inflammation. PMID: 26864812
  38. Normal and high eNOS levels are detrimental in both mild and severe cardiac pressure-overload. PMID: 26436984
  39. eNOS may be necessary to maintain podocyte integrity, especially mitochondrial function PMID: 26119782
  40. Disruption of the eNOS-NO signaling pathway exacerbates peritoneal fibrosis by delaying wound healing. PMID: 25216785
  41. BMP4 has a role in inducing NOX1-dependent eNOS uncoupling in T2DM, which may promote development of novel therapeutics restoring endothelial function in T2DM PMID: 26121233
  42. The eNOS expression was induced with adipocyte differentiation and inhibition of eNOS/NO enhanced lipolysis in vitro and in vivo. PMID: 26317347
  43. Diet-induced obesity leads to l-arginine deficiency and eNOS uncoupling in perivascular adipose tissue. PMID: 26586660
  44. Data show that the transient receptor potential vanilloid type 1 (TRPV1) ligand- induced increase in AMP-activated protein kinase (AMPK) and nitric oxide synthase type III (eNOS) phosphorylation was markedly lower in TRPV1-/- (knockout) than WT aortas. PMID: 22451268
  45. The data identify a novel mechanism for host defense via NOS3 and suggest a potential therapeutic strategy to reduce secondary bacterial pneumonia after influenza. PMID: 25317947
  46. Provide evidence for purinergic glio-endothelial coupling during neuronal activity, highlighting the role of ATP-mediated activation of eNOS via P2Y1 receptors in functional hyperemia. PMID: 26453330
  47. Blood-borne NOS3 attenuates adverse left ventricular remodeling in reperfused myocardial infarction, reducing infarct size and altering expansion and composition of the scar. PMID: 25875863
  48. eNOS gene expression was reduced in the aorta of aged compared to young mice. PMID: 26228838
  49. Thrombotic cerebral infarctions causing cerebral amyloid angiopathy, blood brain barrier damage and dementia were seen in the temporoparietal and retrosplenial granular cortices and hippocampus of eNOS(+/-) mice at 3-6 months but not in eNOS(+/+) mice. PMID: 26104027
  50. eNOS-dependent vascular responses were attenuated in vessels harvested from nitrate-treated mice or when nitrite was acutely added to control vessels. The citrulline-to-arginine ratio in plasma, as a measure of eNOS activity, was reduced in nitrate-treated rodents. PMID: 24224525

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Subcellular Location
Membrane, caveola. Cytoplasm, cytoskeleton. Golgi apparatus. Cell membrane.
Protein Families
NOS family
Database Links
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