Cell Signaling Technology

Product Pathways - NF-kB Signaling

IRAK-M Antibody #4369

Applications Reactivity Sensitivity MW (kDa) Source
W IF-IC H Mk Endogenous 68 Rabbit

Applications Key:  W=Western Blotting  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

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

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.

Western Blotting

Western Blotting

Western blot analysis of extracts from HL-60, Raji and K562 cell lines, using IRAK-M Antibody.

IF-IC

IF-IC

Immunofluorescent analysis of THP-1 cells differentiated overnight with TPA, using IRAK-M Antibody.

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).

  1. Dinarello, C.A. (1996) Blood 87, 2095-147.
  2. Takaesu, G. et al. (2001) Mol Cell Biol 21, 2475-84.
  3. Janssens, S. and Beyaert, R. (2003) Mol Cell 11, 293-302.
  4. Wesche, H. et al. (1999) J. Biol. Chem. 274, 19403-10.
  5. Kobayashi, K. et al. (2002) Cell 110, 191-202.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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