eNOS Antibody (YA6099)
(Synonyms: NOS3; Nitric oxide synthase, endothelial; Constitutive NOS; cNOS; EC-NOS; Endothelial NOS; eNOS; NOS type III; NOSIII)
Based on 1 Customer Validation
eNOS Antibody (YA6099) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to eNOS.
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Host:
Rabbit
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Isotype:
IgG/Kappa
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Application:
WB, IHC-P, ICC/IF, IP, ELISA
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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IP
IP: Immunoprecipitation
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|---|---|---|---|---|---|
| Dilution Ratio | 1:1000-1:4000 | 1:1000-1:5000 | 1:200-1:1000 | 1:5000-1:20000 | 1:50-1:200 |
Product Details
eNOS Antibody (YA6099) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to eNOS.
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Host Rabbit
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 133 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 133 kDa
Protein A
Non-conjugated
Unmodified
IgG/Kappa
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
eNOS (NOS3) generates endothelial nitric oxide (NO), a vasoprotective signal that regulates vascular tone, blood pressure, platelet aggregation, leukocyte adhesion, and vascular homeostasis[1][2]. Mechanistically, Akt/PKB activates eNOS through Ser1177 phosphorylation, while agonist-stimulated endothelial cells integrate Ser1177 activation with Thr495 regulation to control NO output[3]. In disease models, eNOS loss or inhibition reduces endothelial NO signaling and increases blood pressure, as shown in eNOS-deficient mice and L-arginine/NOS inhibitor studies[4][5][6]. Compared with related isoforms, eNOS is mostly expressed in endothelial cells, nNOS mediates neuronal signaling, and iNOS produces high-output NO during inflammatory activation[1]. For experimental applications, L-NMMA, L-NIO, and L-NAME inhibit NOS activity and provide pharmacological tools to test endothelial NO-dependent vascular responses[6].
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Subcellular Localization
Cell membrane; Membrane, caveola; Cytoplasm, cytoskeleton; Golgi apparatus
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Expression
Tissue_specificity:Platelets, placenta, liver and kidneys -
Isoforms & Post-Translational Modification
P29474 has 3 isomers: P29474-1: 133275 Da (predicted); P29474-2: 68965 Da (predicted); P29474-3: 67862 Da (predicted).
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 -
Subunit
Homodimer. Interacts with NOSIP and NOSTRIN (PubMed:11149895, PubMed:12446846). Interacts with HSP90AB1 (By similarity) (PubMed:11149895, PubMed:12446846, PubMed:23585225). Forms a complex with ASL, ASS1 and SLC7A1; the complex regulates cell-autonomous L-arginine synthesis and citrulline recycling while channeling extracellular L-arginine to nitric oxide synthesis pathway (By similarity)
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SwissProt ID
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Synonyms
NOS3; Nitric oxide synthase, endothelial; Constitutive NOS; cNOS; EC-NOS; Endothelial NOS; eNOS; NOS type III; NOSIII
Documentation
[1]. Förstermann U, et al. Nitric oxide synthases: regulation and function. Eur Heart J. 2012 Apr;33(7):829-37, 837a-837d. [Content Brief]
[2]. Förstermann U, et al. Endothelial nitric oxide synthase in vascular disease: from marvel to menace. Circulation. 2006 Apr 4;113(13):1708-14. [Content Brief]
[3]. Fleming I, et al. Phosphorylation of Thr(495) regulates Ca(2+)/calmodulin-dependent endothelial nitric oxide synthase activity. Circ Res. 2001 Jun 8;88(11):E68-75. [Content Brief]
[4]. Huang PL, et al. Hypertension in mice lacking the gene for endothelial nitric oxide synthase. Nature. 1995 Sep 21;377(6546):239-42. [Content Brief]
[5]. Shesely EG, et al. Elevated blood pressures in mice lacking endothelial nitric oxide synthase. Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13176-81. [Content Brief]
[6]. Rees DD, et al. Characterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo. Br J Pharmacol. 1990 Nov;101(3):746-52. [Content Brief]
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