eNOS Antibody (YA5378)
(Synonyms: NOS3; Nitric oxide synthase, endothelial; Constitutive NOS; cNOS; EC-NOS; Endothelial NOS; eNOS; NOS type III; NOSIII)eNOS Antibody (YA5378) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to eNOS.
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Host:
Mouse
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Application:
WB
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Reactivity :
Human, Mouse, Rat, Rabbit
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Formulation:
Supplied in PBS, pH 7.4, containing 0.5%BSA, 0.02% sodium azide as Preservative and 50% Glycerol.
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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 |
WB
WB: Western Blot
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|---|---|
| Dilution Ratio | 1:500-2000 |
Product Details
eNOS Antibody (YA5378) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to eNOS.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat, Rabbit
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Observed Molecular WeightObserved band size: 130-140 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.
Recombinant Protein of eNOS
affinity chromatography.
Non-conjugated
Unmodified
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4, containing 0.5%BSA, 0.02% sodium azide as Preservative and 50% Glycerol.
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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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