ApoA1 Antibody [L13J2]

Catalog No.: F5020

    Application: Reactivity:
    • Lane 1: Human small intestine, Lane 2: Human plasma
    1/

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    代表番号: 045-509-1970|電子メール:sales@selleck.co.jp

    使用情報

    Dilution
    1:1000
    Application
    WB
    Source
    Mouse Monoclonal Antibody
    Reactivity
    Human
    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
    25 kDa

    Datasheet & SDS

    生物学的記述

    Specificity
    ApoA1 Antibody [L13J2] detects endogenous levels of total ApoA1 protein.
    Clone
    L13J2
    Synonym(s)
    Apolipoprotein A-I; Apo-AI; ApoA-I; Apolipoprotein A1; APOA1
    Background
    Apolipoprotein A-I (ApoA-I) is the primary structural and functional protein of high-density lipoprotein (HDL), synthesized mainly in the liver and intestine to mediate reverse cholesterol transport by facilitating ABCA1-dependent cholesterol efflux from peripheral tissues to the liver for excretion, thereby offering protection against atherosclerosis and cardiovascular disease. The mature 243-amino-acid ApoA-I polypeptide comprises 10 tandem repeats of amphipathic α-helices, with proline residues providing flexibility for lipid binding; its N-terminal region stabilizes the lipid-free form, the central domain (140–170) activates lecithin-cholesterol acyltransferase (LCAT) for cholesterol esterification and HDL maturation, and the C-terminal domain (181–243) enables high-affinity phospholipid binding for nascent HDL formation. ApoA-I serves as a cofactor for LCAT, interacts with ABCA1 and SR-BI receptors to promote lipid efflux, and exhibits strong anti-inflammatory and antioxidant actions by neutralizing lipopolysaccharides and inhibiting vascular adhesion molecule expression. Low ApoA-I levels are an independent risk predictor for coronary artery disease, while APOA1 mutations cause familial HDL deficiency syndromes or hereditary amyloidosis, leading to accelerated atherosclerosis or organ dysfunction from protein deposits, with additional links to Alzheimer’s disease and diabetes through impaired lipid homeostasis and chronic inflammation.
    References

    技術サポート

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