research use only

Apolipoprotein E Antibody [L10K14]

Cat.No.: F4857

    Application: Reactivity:

    Usage Information

    Dilution
    1:400
    1:100
    1:25
    1:20 - 1:200
    Application
    WB, IHC, IF, FCM
    Reactivity
    Mouse, Rat, Human
    Source
    Rabbit 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
    49 kDa
    Positive Control Human tonsil tissue; Human liver tissue; Rat cerebral cortex tissue; Mouse thalamus tissue; Rat liver tissue; Mouse liver tissue; Human Kidney cell; Human fetal liver; Rat plasma; Mouse heart; Rat brain; Rat kidney; Mouse cerebral cortex tissue; Mouse brain; Mouse plasma; HepG2 cells
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    Apolipoprotein E Antibody [L10K14] detects endogenous levels of total Apolipoprotein E protein.
    Clone
    L10K14
    Synonym(s)
    SOX10; Transcription factor SOX-10
    Background
    Apolipoprotein E (ApoE) is a 299-amino acid glycoprotein present in three main isoforms (E2, E3, E4) that differ at residues 112 and 158, and it plays a central role in cholesterol and lipid transport through receptor binding in both the plasma, where it associates with VLDL/IDL remnants and HDL, and the central nervous system. SApoE3 features an elongated shape with an N-terminal four-helix receptor-binding domain (residues 1–183) containing Arg/Lys-rich motifs for LDL receptor family interactions, shielded by intramolecular salt bridges and hydrogen bonds from the flexible C-terminal lipid-binding domain (residues 184–299), which interacts with lipids, heparan sulfate proteoglycans, and amyloid-β (Aβ). Lipidation triggers conformational changes that expose the N-terminal domain for high-affinity LDLR/LRP1 binding, enabling remnant clearance, reverse cholesterol transport, and Aβ clearance in the CNS; the E4 isoform’s domain-domain salt-bridge destabilizes this structure, reduces lipidation efficiency, and promotes Aβ aggregation and neurotoxicity. ApoE is crucial for neuronal membrane repair, synaptogenesis, and gliotransmission, with astrocytes and microglia as the main CNS sources. The E4 isoform confers up to a 12-fold increased risk for Alzheimer’s disease by promoting Aβ accumulation, tauopathy, neuroinflammation, and vascular dysfunction, while E2 is protective; current therapies target these isoform-specific structural and functional differences.
    References
    • https://pubmed.ncbi.nlm.nih.gov/25173806/
    • https://pubmed.ncbi.nlm.nih.gov/21873229/

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