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IL-1β Antibody [H12N7]

Cat.No.: F3067

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:50 - 1:200
    Application
    WB, IHC
    Reactivity
    Human, Mouse
    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
    17 kDa,31 kDa
    Positive Control Human large intestine (chronic colitis of the colon); Human large intestine (ulcerative chronic colitis of the rectum); THP-1 cell (LPS-treated); Raw 264.7 cells (Brefeldin A, 300 ng/mL, last 3 hr of stimulation; LPS, 100 ng/mL, 6 h)
    Negative Control THP-1 cells; Raw 264.7 cells

    Datasheet & SDS

    Biological Description

    Specificity
    IL-1β Antibody [H12N7] detects endogenous levels of total IL-1β protein.
    Clone
    H12N7
    Synonym(s)
    Interleukin-1 beta; IL-1 beta; Catabolin; IL1B; IL1F2
    Background
    Interleukin-1β (IL-1β), the mature pro-inflammatory cytokine cleaved from its 31 kDa precursor by caspase-1 at Asp116-Ala117, functions as a master regulator of innate immunity by binding to IL-1R1 and recruiting IL-1RAcP to form a high-affinity signaling complex that activates MyD88-dependent pathways, primarily IRAK4 and IRAK1, leading to TRAF6 ubiquitination and divergent activation of NF-κB (driving pro-inflammatory gene expression) and MAPK/AP-1 cascades (JNK/p38/ERK, promoting cytokine production). IL-1β adopts a β-trefoil fold with 12 β-strands forming receptor-binding interfaces, where Lys93, Lys94, and Lys117 create a basic patch for IL-1R1 docking and Pro68, Tyr68 stabilize receptor ternary complex formation. IL-1β amplifies acute inflammation by inducing fever through PGE2/COX-2 production acting on hypothalamic EP3R, promoting neutrophil recruitment and survival, stimulating acute phase protein synthesis (CRP, SAA, fibrinogen) in hepatocytes, and driving Th17 polarization while synergizing with IL-6 and TNF-α to sustain chronic inflammation. IL-1β coordinates host defense against infection and injury, whereas pathologically, constitutive activation, often due to NLRP3 inflammasome hyperactivity, drives rheumatoid arthritis (synovial inflammation), type 2 diabetes (β-cell apoptosis), atherosclerosis (plaque instability), and neurodegeneration (microglial activation).
    References
    • https://pubmed.ncbi.nlm.nih.gov/18650393/
    • https://pubmed.ncbi.nlm.nih.gov/18806223/

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