Product: eNOS Antibody
Catalog: AF0096
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Rabbit, Dog
Mol.Wt.: 140kD; 133kD(Calculated).
Uniprot: P29474
RRID: AB_2833277

View similar products>>

   Size Price Inventory
 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

For pricing and ordering contact:
Local distributors

Product Info

Source:
Rabbit
Application:
WB: 1:500-1:3000, IHC 1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Rabbit(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
eNOS Antibody detects endogenous levels of total eNOS.
RRID:
AB_2833277
Cite Format: Affinity Biosciences Cat# AF0096, RRID:AB_2833277.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

cNOS; Constitutive NOS; EC NOS; EC-NOS; ecNOS; Endothelial nitric oxidase synthase; Endothelial nitric oxide synthase; Endothelial nitric oxide synthase 3; Endothelial NOS; eNOS; Nitric oxide synthase 3 (endothelial cell); Nitric oxide synthase 3; Nitric oxide synthase 3 endothelial cell; Nitric oxide synthase endothelial; Nitric oxide synthase, endothelial; NOS 3; NOS III; NOS type III; NOS3; NOS3_HUMAN; NOSIII;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P29474 NOS3_HUMAN:

Platelets, placenta, liver and kidney.

Description:
eNOS endothelial constitutive nitric oxide synthase. Synthesizes nitric oxide (NO) from arginine and oxygen, 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. Induced in humans by caloric restriction. Stimulated by calcium/calmodulin. Inhibited by NOSIP and NOSTRIN.
Sequence:
MGNLKSVAQEPGPPCGLGLGLGLGLCGKQGPATPAPEPSRAPASLLPPAPEHSPPSSPLTQPPEGPKFPRVKNWEVGSITYDTLSAQAQQDGPCTPRRCLGSLVFPRKLQGRPSPGPPAPEQLLSQARDFINQYYSSIKRSGSQAHEQRLQEVEAEVAATGTYQLRESELVFGAKQAWRNAPRCVGRIQWGKLQVFDARDCRSAQEMFTYICNHIKYATNRGNLRSAITVFPQRCPGRGDFRIWNSQLVRYAGYRQQDGSVRGDPANVEITELCIQHGWTPGNGRFDVLPLLLQAPDDPPELFLLPPELVLEVPLEHPTLEWFAALGLRWYALPAVSNMLLEIGGLEFPAAPFSGWYMSTEIGTRNLCDPHRYNILEDVAVCMDLDTRTTSSLWKDKAAVEINVAVLHSYQLAKVTIVDHHAATASFMKHLENEQKARGGCPADWAWIVPPISGSLTPVFHQEMVNYFLSPAFRYQPDPWKGSAAKGTGITRKKTFKEVANAVKISASLMGTVMAKRVKATILYGSETGRAQSYAQQLGRLFRKAFDPRVLCMDEYDVVSLEHETLVLVVTSTFGNGDPPENGESFAAALMEMSGPYNSSPRPEQHKSYKIRFNSISCSDPLVSSWRRKRKESSNTDSAGALGTLRFCVFGLGSRAYPHFCAFARAVDTRLEELGGERLLQLGQGDELCGQEEAFRGWAQAAFQAACETFCVGEDAKAAARDIFSPKRSWKRQRYRLSAQAEGLQLLPGLIHVHRRKMFQATIRSVENLQSSKSTRATILVRLDTGGQEGLQYQPGDHIGVCPPNRPGLVEALLSRVEDPPAPTEPVAVEQLEKGSPGGPPPGWVRDPRLPPCTLRQALTFFLDITSPPSPQLLRLLSTLAEEPREQQELEALSQDPRRYEEWKWFRCPTLLEVLEQFPSVALPAPLLLTQLPLLQPRYYSVSSAPSTHPGEIHLTVAVLAYRTQDGLGPLHYGVCSTWLSQLKPGDPVPCFIRGAPSFRLPPDPSLPCILVGPGTGIAPFRGFWQERLHDIESKGLQPTPMTLVFGCRCSQLDHLYRDEVQNAQQRGVFGRVLTAFSREPDNPKTYVQDILRTELAAEVHRVLCLERGHMFVCGDVTMATNVLQTVQRILATEGDMELDEAGDVIGVLRDQQRYHEDIFGLTLRTQEVTSRIRTQSFSLQERQLRGAVPWAFDPPGSDTNSP

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Bovine
100
Dog
100
Rabbit
100
Horse
0
Sheep
0
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P29474 As Substrate

Site PTM Type Enzyme
K5 Methylation
T33 Phosphorylation
S53 Phosphorylation
Y81 Phosphorylation
C94 S-Nitrosylation
C99 S-Nitrosylation
S102 Phosphorylation
S114 Phosphorylation Q00535 (CDK5)
C184 S-Nitrosylation
C201 S-Nitrosylation
Y210 Phosphorylation
C212 S-Nitrosylation
S260 Phosphorylation
T495 Phosphorylation Q04759 (PRKCQ) , Q13237 (PRKG2) , P05771 (PRKCB) , P17612 (PRKACA) , Q02156 (PRKCE) , O75116 (ROCK2) , P17252 (PRKCA) , P05129 (PRKCG) , P24723 (PRKCH) , Q05655 (PRKCD) , Q13131 (PRKAA1) , P41743 (PRKCI) , Q05513 (PRKCZ)
S508 Phosphorylation
T512 Phosphorylation
S615 Phosphorylation P17612 (PRKACA) , Q9Y243 (AKT3) , P31751 (AKT2) , P31749 (AKT1)
S633 Phosphorylation Q13237 (PRKG2) , P54646 (PRKAA2) , Q13131 (PRKAA1) , P17612 (PRKACA)
S634 Phosphorylation
T636 Phosphorylation
S638 Phosphorylation
Y657 Phosphorylation Q14289 (PTK2B)
C661 S-Nitrosylation
S738 Phosphorylation
K773 Ubiquitination
C802 S-Nitrosylation
K834 Ubiquitination
S836 Phosphorylation
C853 S-Nitrosylation
T854 Phosphorylation
S870 Phosphorylation
K904 Ubiquitination
C976 S-Nitrosylation
C991 S-Nitrosylation
K1035 Ubiquitination
C1048 S-Nitrosylation
C1050 S-Nitrosylation
K1085 Ubiquitination
T1094 Phosphorylation
C1114 S-Nitrosylation
T1175 Phosphorylation
S1177 O-Glycosylation
S1177 Phosphorylation P22612 (PRKACG) , Q9Y478 (PRKAB1) , P31749 (AKT1) , Q13131 (PRKAA1) , P54646 (PRKAA2) , Q13237 (PRKG2) , P17612 (PRKACA)
S1179 Phosphorylation P31749 (AKT1)

Research Backgrounds

Function:

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.

Lacks eNOS activity, dominant-negative form that may down-regulate eNOS activity by forming heterodimers with isoform 1.

PTMs:

Phosphorylation by AMPK at Ser-1177 in the presence of Ca(2+)-calmodulin (CaM) activates activity. In absence of Ca(2+)-calmodulin, AMPK also phosphorylates Thr-495, resulting in inhibition of activity (By similarity). Phosphorylation of Ser-114 by CDK5 reduces activity.

Subcellular Location:

Cell membrane. Membrane>Caveola. Cytoplasm>Cytoskeleton. Golgi apparatus.
Note: Specifically associates with actin cytoskeleton in the G2 phase of the cell cycle; which is favored by interaction with NOSIP and results in a reduced enzymatic activity.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Platelets, placenta, liver and kidney.

Subunit Structure:

Homodimer. Interacts with NOSIP and NOSTRIN. Interacts with HSP90AB1.

Family&Domains:

Belongs to the NOS family.

Research Fields

· Environmental Information Processing > Signal transduction > Calcium signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cGMP-PKG signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Metabolism > Amino acid metabolism > Arginine biosynthesis.

· Metabolism > Amino acid metabolism > Arginine and proline metabolism.

· Metabolism > Global and overview maps > Metabolic pathways.

· Organismal Systems > Immune system > Platelet activation.   (View pathway)

· Organismal Systems > Endocrine system > Estrogen signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Oxytocin signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). Zhou Zhu et al. Micro or nano: Evaluation of biosafety and biopotency of magnesium metal organic framework-74 with different particle sizes. Nano Res 2020 Jan 16 [IF=8.183]

2). Li Z et al. SIRT1 inhibits TGF-β-induced endothelial-mesenchymal transition in human endothelial cells with Smad4 deacetylation. J Cell Physiol 2018 Nov;233(11):9007-9014 (PubMed: 29856490) [IF=5.546]

Application: WB    Species: human    Sample: Umbilical Vein Endothelial Cells

FIGURE 1| TGF‐β induces EndMT in cultured HUVECs. (a) The shape of HUVECs grown in basal media (control) or following exposure to TGF‐β1.TGF‐β1‐treated HUVECs had a fibroblast‐like phenotype, whereas untreated control cells had an endothelial cell phenotype. (b) Immunofluorescent staining of αSMA (red) expression. (c) Relative mRNA expression of endothelial markers CD31, eNOS, VE‐Cadherin, and VWF, and mesenchymal/myofibroblastic markers αSMA, COL1A1, FSP1, SM22α, Zeb‐1, Zeb‐2, TWIST, CNN1, and VIM assessed by qRT‐PCR. (d) The protein levels of CD31,eNOS, αSMA, VIM, FSP1, and CNN1 were determined by Western blot analysis. (e) Cell migration for unstimulated HUVECs versus after treatment with TGF‐β

3). Li Z et al. SIRT1 inhibits TGF-β-induced endothelial-mesenchymal transition in human endothelial cells with Smad4 deacetylation. J Cell Physiol 2018 Nov;233(11):9007-9014 (PubMed: 29856490) [IF=5.546]

4). Lu D et al. Beneficial effects of renal denervation on cardiac angiogenesis in rats with prolonged pressure overload. Acta Physiol (Oxf) 2017 May;220(1):47-57 (PubMed: 27575955) [IF=5.542]

Application: WB    Species: rat    Sample:

Fig. 7. Upregulation of VEGF and VEGFR2 expression as well as activation of eNOS following RDN.

5). Liao L et al. Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H2O2-Induced HUVECs. Oxid Med Cell Longev 2021 Aug 3;2021:9919466. (PubMed: 34394836) [IF=5.076]

6). Zhang M et al. Human Tissue Kallikrein 1 Is Downregulated in Elderly Human Prostates and Possesses Potential In Vitro Antioxidative and Antifibrotic Effects in Rodent Prostates. Oxid Med Cell Longev 2021 Apr 30;2021:8877540. (PubMed: 34007408) [IF=5.076]

Application: WB    Species: rat    Sample: prostate

Figure 6|: KLK1 could upregulate NO/cGMP signal and inhibit fibrosis in the prostate of aged rats.(c, f, and i) Representative Western blot results of eNOS, DDAH2, COX-2, PTGIS, TGF-β1, RhoA, and ROCK1 in prostates of all three groups.

7). Cai BB et al. Acid sphingomyelinase downregulation alleviates vascular endothelial leptin resistance in rats. Acta Pharmacol Sin 2019 Dec 17 (PubMed: 31848475) [IF=5.064]

Application: WB    Species: Rat    Sample: rat aortic endothelial cells (RAECs)

Fig. 4 ASM downregulation increased eNOS/NO signaling in RAECs. RAECs were incubated with 0.3 mM PA for 24 h and then transfected with ASM siRNA, or RAECs were transfected with Ob-Rb siRNA for 48 h and then treated with 10 μM AMI and 10 μM IMI for 24 h. Then, 100 nM leptin was added for 15 min prior to the collection of the cells. Summarized data showing the effects of ASM downregulation on the ratio of p-eNOS (Ser1177)/eNOS (a), eNOS activity (b), NO release (c), Ob-Rb expression (d), and the ratios of p-STAT3/STAT3 (e) and p-Akt/Akt (f) in RAECs. *P < 0.05 vs. vehicle control (Vehl Scr); #P < 0.05 vs. the PA alone-treated group; ΔP < 0.05 vs. the Ob-Rb siRNA alone-transfected group. Representative Western blot gels and summarized data showing the ratios of p-STAT3/STAT3 and p-Akt/Akt in RAECs that were pretreated with 10 μM cryptotanshinone for 24 h and then incubated with 0.3 mM PA for 24 h (g, h) or transfected with Ob-Rb siRNA for 48 h (i, j). *P < 0.05 vs. vehicle control (Vehl Scr); #P < 0.05 vs. the SCH772984 alone-treated group. The co-immunoprecipitation assay was used to test the interaction between p-STAT3 and p-Akt in RAECs treated with PA (k) or transfected with Ob-Rb siRNA (l). The data are the means ± SEMs from three experiments.

8). Xue M et al. Corin plays a protective role via upregulating MAPK and downregulating eNOS in diabetic nephropathy endothelial dysfunction. FASEB J 2020 Jan;34(1):95-106. (PubMed: 31914697) [IF=4.966]

Application: WB    Species: Human    Sample: HK‐2 cells

FIGURE 4 The effect of Corin deficiency in HK‐2 cells on EA.hy926 cells endothelial function and the mechanism. A, The wound healing scratch assay showed the effect of culture supernatants of HK‐2 cells on EA.hy926 cells migration at 0 and 24 h in Ctrl, NC‐siRNA, Corin‐siRNA, and Corin‐siRNA + ANP groups (original magnification 100×). B‐E, The ERK, P38, JNK, and their phosphorylation forms protein levels of EA.hy926 cells treated with culture supernatants of HK‐2 cells were measured by western blot (n = 6 for each group). F,G, The eNOS and p‐eNOS protein levels of EA.hy926 cells treated with culture supernatants of HK‐2 cells were measured by western blot (n = 6 for each group). Data are presented as mean ± SEM. *P < .05 and **P < .01

9). Lu Y et al. Protective effects of Danzhi jiangtang capsule on vascular endothelial damages induced by high-fat diet and palmitic acid. Biomed Pharmacother 2018 Nov;107:1631-1640 (PubMed: 30257381) [IF=4.545]

10). Gao Y et al. Ginsenoside Re inhibits PDGF-BB-induced VSMC proliferation via the eNOS/NO/cGMP pathway. Biomed Pharmacother 2019 May 10;115:108934 (PubMed: 31082773) [IF=4.545]

Load more

Restrictive clause

 

Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.