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IL-6 Antibody [F4K18]

Cat.No.: F3023

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:100
    1:200 - 1:400
    1:400
    Application
    WB, IP, IF, FCM
    Reactivity
    Mouse
    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
    24 kDa
    Positive Control Raw 264.7 cells (LPS, 100 ng/ml, 6 h)
    Negative Control Raw 264.7 cells

    Datasheet & SDS

    Biological Description

    Specificity
    IL-6 Antibody [F4K18] detects endogenous levels of total IL-6 protein.
    Clone
    F4K18
    Synonym(s)
    Interleukin-6; IL-6; B-cell stimulatory factor 2 (BSF-2); CTL differentiation factor (CDF); Hybridoma growth factor; Interferon beta-2 (IFN-beta-2); IL6; IFNB2
    Background
    Interleukin-6 (IL-6), a pleiotropic glycoprotein cytokine with a four-helix bundle structure and a conserved disulfide bond between Cys44 and Cys50, serves as a central mediator of acute phase responses and immune regulation by binding its α-receptor (IL-6R) to form a high-affinity complex with gp130, which then triggers JAK1/JAK2-mediated tyrosine phosphorylation of gp130 and recruits STAT3 (Tyr705) for nuclear translocation and transcriptional activation of target genes. IL-6 possesses site I/II/III interfaces where key residues such as Phe171, Arg167, and Pro33 mediate receptor docking, with classic signaling via membrane-bound IL-6R driving anti-inflammatory and hepatocyte effects (such as C-reactive protein and fibrinogen induction), while trans-signaling through soluble IL-6R promotes pro-inflammatory responses via activation of MAPK/ERK, PI3K/Akt, and SHP2 pathways. IL-6 stimulates hepatic acute phase protein synthesis, drives B-cell differentiation into plasma cells with IgM and IgG production, induces Th17 polarization while inhibiting Treg differentiation, and coordinates monocyte-to-macrophage transition during infection and injury. IL-6 balances innate and adaptive immunity as well as hematopoiesis, while pathologically, chronic elevation leads to rheumatoid arthritis with synovial inflammation and joint destruction via RANKL-mediated osteoclastogenesis, supports plasma cell survival and proliferation in multiple myeloma, and contributes to cancer cachexia through STAT3-mediated metabolic reprogramming.
    References
    • https://pubmed.ncbi.nlm.nih.gov/32864098/
    • https://pubmed.ncbi.nlm.nih.gov/32765502/

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