research use only

MUC5B Antibody [G14E16]

Cat.No.: F2423

    Application: Reactivity:

    Usage Information

    Dilution
    1:500
    Application
    WB, IHC, ELISA
    Reactivity
    Mouse, Human, Monkey
    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
    Positive Control Murine asthma lung tissue
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    MUC5B Antibody [G14E16] detects endogenous levels of total MUC5B protein.
    Clone
    G14E16
    Synonym(s)
    MUC5; MUC5B; Mucin-5B; MUC-5B; Cervical mucin; High molecular weight salivary mucin MG1; Sublingual gland mucin
    Background
    MUC5B serves as the principal gel-forming mucin secreted by airway submucosal glands and goblet cells, assembling into massive disulfide-linked megapolymers exceeding 1 MDa through N-terminal von Willebrand factor-like D1–D2–D′–D3 domains that dimerize via conserved cysteines, a central ~5760-residue O-glycosylated mucin domain packed with Pro/Thr/Ser repeats and 11 cysteine-rich subdomains forming 4–7 nm beaded bottlebrush motifs from dense glycans, and C-terminal D4–B–C–CK domains enabling covalent multimerization. These linear chains, packaged by sequential ER/Golgi disulfide formation followed by Ca²⁺-induced condensation in acidic secretory granules (pH ~6), undergo exocytosis-triggered rapid uncoiling at neutral pH as calcium dissociates from D3 globular nodes (~10–20 nm), hydrating and expanding over 500-fold into viscoelastic entangled gels that trap microbes, drive mucociliary clearance via MUC5AC synergy, and preserve periciliary layer homeostasis by phase separation and entanglement. MUC5B facilitates leukocyte adhesion, modulates inflammation through glycan-receptor interactions, and regulates fibroblast behavior; the rs35705950 promoter variant boosts transcription, causing hyperpolymerization, impaired phagocytosis, fibroblast recruitment, alveolar remodeling, and progressive fibrosis in idiopathic pulmonary fibrosis (IPF), while contributing to mucus plugs and exacerbations in COPD/asthma via dysregulated secretion and barrier overload.
    References
    • https://pubmed.ncbi.nlm.nih.gov/31758042/
    • https://pubmed.ncbi.nlm.nih.gov/24778189/

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