IRAK Isoform Antibody Sampler Kit #4769
Product Information
Kit Usage Information
Protocols
- 4363: Western Blotting, Immunoprecipitation (Agarose)
- 4367: Western Blotting
- 4369: Western Blotting
- 4504: Western Blotting, Immunoprecipitation (Agarose), Flow
- 7074: Western Blotting
Product Description
Specificity / Sensitivity
Source / Purification
Background
Upon IL-1R/TLR (Toll-Like Receptor) ligation, IRAK1 and IRAK4 are rapidly recruited to the receptor by the adaptor MyD88 (4). IRAK1 is phosphorylated by IRAK4 at Thr209 and Thr387 (5), followed by sequential autohyperphosphorylation in various domains. Unlike IRAK1 and IRAK4, IRAK2 and IRAK-M do not have significant kinase activity although they can still activate NF-κB when overexpressed (6,7). Antisense oligonucleotide depletion of IRAK2 can inhibit IL-1 mediated NF-κB activation (8). Expression of IRAK-M is more restricted compared to other family members with highest levels of expression occurring in monocytes/macrophages (6). Studies from IRAK-M knockout mice suggest that it may play a role as a negative regulator of TLR signaling and innate immune responses by preventing the dissociation of IRAK1 and IRAK4 from MyD88 and the subsequent formation of its complex with TRAF6 (9).
- Dinarello, C.A. (1996) Blood 87, 2095-147.
- Takaesu, G. et al. (2001) Mol Cell Biol 21, 2475-84.
- Janssens, S. and Beyaert, R. (2003) Mol Cell 11, 293-302.
- Gottipati, S. et al. (2008) Cell Signal 20, 269-76.
- Kollewe, C. et al. (2004) J Biol Chem 279, 5227-36.
- Wesche, H. et al. (1999) J Biol Chem 274, 19403-10.
- Muzio, M. et al. (1997) Science 278, 1612-5.
- Guo, F. et al. (1999) Inflammation 23, 535-43.
- Kobayashi, K. et al. (2002) Cell 110, 191-202.
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