research use only

Myelin Proteolipid Protein Antibody [C23K3]

Cat.No.: F2700

    Application: Reactivity:

    Usage Information

    Dilution
    Application
    WB, IHC, IF, FCM
    Reactivity
    Bovine
    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

    Datasheet & SDS

    Biological Description

    Specificity
    Myelin Proteolipid Protein Antibody [C23K3] detects endogenous levels of total Myelin Proteolipid protein.
    Clone
    C23K3
    Synonym(s)
    Myelin proteolipid protein; PLP; Lipophilin; PLP1; PLP
    Background
    Myelin Proteolipid Protein (PLP) is the most abundant protein in central nervous system (CNS) myelin. Synthesized by oligodendrocytes, PLP is a tetraspanin integral membrane protein, with its major isoform DM20 generated through alternative splicing. PLP integrates into the lipid bilayer of compact myelin, stabilizing the multilayered sheath that insulates axons and enables rapid nerve impulse conduction. PLP consists of four transmembrane α-helices connected by two extracellular and two cytoplasmic loops. It exhibits a strong affinity for cholesterol and sphingomyelin-rich lipid rafts, which facilitates its oligomerization into rigid assemblies. These assemblies enhance membrane adhesion and compaction, with key hydrophobic residues in the transmembrane domains enabling tight interlayer stacking, as observed by X-ray diffraction at a periodicity of ~50-60 Å. PLP adheres to extracellular myelin lamellae to prevent cytosolic leakage, supports long-term axonal integrity via metabolic interactions, and is involved in oligodendrocyte signaling pathways, such as integrin complexes, that regulate myelination. Cholesterol-dependent conformational stabilization of PLP’s transmembrane bundles mechanically strengthens myelin’s shear resistance and ion barrier properties. Mutations in the PLP1 gene cause Pelizaeus-Merzbacher disease through ER retention and hypomyelination, while in multiple sclerosis, PLP serves as an autoantigen that can trigger demyelination.
    References
    • https://pubmed.ncbi.nlm.nih.gov/35829923/
    • https://pubmed.ncbi.nlm.nih.gov/36896314/

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