eNOS/NOS Type III Antibody [L17A10]

Catalog No.: F0871

For research use only.

    Application: Reactivity:

    Experiment Essentials

    WB
    Recommended SDS-PAGE separating gel concentration: 5%.
    Exposure time of at least 60s is recommended.

    Usage Information

    Dilution
    1:2500 - 1:10000
    Application
    WB, IF
    Reactivity
    Human
    Source
    Mouse Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    140 kDa
    Positive Control Human endothelial cell
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    eNOS/NOS Type III Antibody [L17A10] detects endogenous levels of total eNOS/NOS Type III protein.
    Subcellular Location
    Cell membrane, Cytoplasm, Cytoskeleton, Golgi apparatus, Membrane
    Uniprot ID
    P29474
    Clone
    L17A10
    Synonym(s)
    Nitric oxide synthase 3; Constitutive NOS (cNOS); EC-NOS; NOS type III (NOSIII); Nitric oxide synthase; endothelial (Endothelial NOS; eNOS); NOS3
    Background
    eNOS/NOS Type III, also known as (Endothelial nitric oxide synthase, NOS3) is a constitutively expressed dimeric enzyme predominantly localized in vascular endothelial cells, where it plays a central role in cardiovascular homeostasis by producing nitric oxide (NO), a potent vasodilator. Structurally, eNOS is composed of an N-terminal oxygenase domain, which binds heme, zinc, tetrahydrobiopterin (BH4), and L-arginine, and a C-terminal reductase domain, which contains binding sites for NADPH, FAD, and FMN, with the two domains connected by a calmodulin-binding region; dimerization and cofactor binding are essential for its catalytic activity. Expression of eNOS, though constitutive, is also found in other cell types such as cardiomyocytes, platelets, and certain neurons, and is tightly regulated at transcriptional, posttranscriptional, and posttranslational levels. Functionally, eNOS synthesizes NO from L-arginine in a calcium/calmodulin-dependent manner, and this NO diffuses into vascular smooth muscle cells to activate soluble guanylate cyclase (sGC), increasing cyclic GMP levels and stimulating protein kinase G (PKG)-mediated phosphorylation events that lower intracellular calcium, promote vasodilation, inhibit platelet aggregation, and thereby maintain vascular tone, blood pressure, and endothelial health.
    References
    • https://pubmed.ncbi.nlm.nih.gov/26428312/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
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