Cell Signaling Technology

Product Pathways - NF-kB Signaling

IRAK2 Antibody #4367

Applications Reactivity Sensitivity MW (kDa) Source
W IF-IC H M R Mk Endogenous 62 Rabbit

Applications Key:  W=Western Blotting  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  M=Mouse  R=Rat  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

IRAK2 Antibody detects endogeneous levels of total IRAK2 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 at the carboxy terminus of human IRAK2. Antibodies were purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from Jurkat, Raji and K562 cell lines, using IRAK2 Antibody #4367.

IF-IC

IF-IC

Immunofluorescent staining of HeLa cells, using IRAK2 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 (4,5). Antisense oligonucleotide depletion of IRAK2 can inhibit IL-1 mediated NF-κB activation (6).

  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. Muzio, M. et al. (1997) Science 278, 1612-5.
  6. Guo, F. et al. (1999) Inflammation 23, 535-43.

Application References

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Companion Products

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

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