N3893
Anti-Nitric Oxide Synthase, Endothelial (1185-1205) antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
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Synonym(s):
Anti-eNOS
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 135 kDa
species reactivity
bovine, mouse, rat, human
technique(s)
immunohistochemistry (frozen sections): 1:100 using acetone-fixed, frozen tissue sections of mouse heart
microarray: suitable
western blot: 1:10,000 using bovine lung endothelial cell extract
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... NOS3(4846)
mouse ... Nos3(18127)
rat ... Nos3(24600)
Related Categories
General description
Endothelial nitric oxide synthase (eNOS) is a 135 kDa protein and is an isoform of NOS. eNOS expression is not limited to the endothelium of blood vessels, it is also expressed in the epithelium of several tissues, including the bronchial tree. It is also localized in neurons in the brain, especially the pyramidal cells of the hippocampus.
The gene encoding endothelial nitric oxide synthase (eNOS) is localized on chromosome 7q35-36 and has 26 exons.
Immunogen
synthetic peptide corresponding to nitric oxide synthase (NOS) of bovine endothelial origin (eNOS, amino acids 1185-1205 with an N-terminally added lysine) conjugated to KLH. The immunogen sequence is highly conserved in human eNOS.
Application
Anti-Nitric Oxide Synthase, Endothelial (1185-1205) antibody produced in rabbit has been used in immunoblotting and immunohistochemistry.
Biochem/physiol Actions
Endothelial nitric oxide synthase (eNOS) has been studied as a modulator of vascular function and it is involved in the production of nitric oxide. Defects in the enzyme expression have been shown to be associated with coronary artery disease.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
常规特殊物品
Certificates of Analysis (COA)
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Mónica Martínez-Moreno et al.
FEBS letters, 579(14), 3159-3163 (2005-06-01)
We have performed the recombinant expression and purification of the reductase domain of endothelial nitric oxide synthase (eNOS) and used it as a bait in search for interacting proteins present in endothelial cells. Using mass spectrometry of the bound proteins
Contribution of oxidative stress and prostanoids in endothelial dysfunction induced by chronic fluoxetine treatment
Simplicio JA, et al.
Vascular Pharmacology, 73(2), 124-137 (2015)
Katia Colombo Marchi et al.
Alcohol and alcoholism (Oxford, Oxfordshire), 51(5), 522-534 (2016-07-07)
Investigate the role of NADPH oxidase on ethanol-induced hypertension and vascular oxidative stress. Male Wistar rats were treated with ethanol (20% v/v). Apocynin (10 mg/kg/day, i.p.) prevented ethanol-induced hypertension. The increased contractility of endothelium-intact and endothelium-denuded aortic rings from ethanol-treated
María Teresa Soto-Navarrete et al.
Frontiers in cardiovascular medicine, 9, 928362-928362 (2022-08-26)
Bicuspid aortopathy occurs in approximately 50% of patients with bicuspid aortic valve (BAV), the most prevalent congenital cardiac malformation. Although different molecular players and etiological factors (genetic and hemodynamic) have been suggested to be involved in aortopathy predisposition and progression
L G Fryer et al.
Diabetes, 49(12), 1978-1985 (2000-12-16)
Glucose transport in skeletal muscle is stimulated by two distinct stimuli, insulin and exercise. The mechanism by which exercise stimulates glucose transport is not known, although it is distinct from the insulin-mediated pathway. Recently, it has been shown that AMP-activated
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