Render Target: STATIC
Render Timestamp: 2024-10-31T10:54:27.624Z
Commit: 23cb9f61fe67e1e9093fd644a533c4ff516a6463
XML generation date: 2024-08-01 15:23:33.811
Product last modified at: 2024-09-10T19:45:08.546Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

IRAK-M Antibody #4369

Filter:
  • WB

    Supporting Data

    REACTIVITY H Mk
    SENSITIVITY Endogenous
    MW (kDa) 68
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    IRAK-M antibody detects endogenous levels of total IRAK-M protein. Cross reactivity was not detected with other family members.

    Species Reactivity:

    Human, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy-terminus of human IRAK-M. Antibodies were purified by protein A and peptide affinity chromagraphy.

    Background

    Interleukin-1 (IL-1) receptor-associated kinase (IRAK) is a serine/threonine-specific kinase that can be coprecipitated in an IL-1-inducible manner with the IL-1 receptor (1). The mammalian family of IRAK molecules contains four members (IRAK1, IRAK2, IRAK3/IRAK-M, and IRAK4). The binding of IL-1 to IL-1 receptor type I (IL-1RI) initiates the formation of a complex that includes IL-1RI, AcP, MyD88, and IRAKs (2). IRAK undergoes autophosphorylation shortly after IL-1 stimulation. The subsequent events involve IRAK dissociation from the IL-1RI complex, its ubiquitination, and its association with two membrane-bound proteins: TAB2 and TRAF6. The resulting IRAK-TRAF6-TAB2 complex is then released into the cytoplasm where it activates protein kinase cascades, including TAK1, IKKs, and the stress-activated kinases (3).
    Unlike IRAK1 and IRAK4, IRAK2 and IRAK-M do not have significant kinase activity although they can still activate NF-κB when overexpressed (4). Expression of IRAK-M is more restricted compared to other family members with highest levels of expression occurring in monocytes/macrophages (4). Studies from IRAK-M knockout mice suggest that IRAK-M may play a role as a negative regulator of Toll-like receptor signaling and innate immune responses by preventing the dissociation of IRAK1 and IRAK4 from MyD88 and the subsequent formation of its complex with TRAF6 (5).
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