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Irak4  -  interleukin-1 receptor-associated kinase 4

Mus musculus

Synonyms: 8430405M07Rik, 9330209D03Rik, IRAK-4, Interleukin-1 receptor-associated kinase 4, NY-REN-64
 
 
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High impact information on Irak4

  • Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4 [1].
  • Activation of IL-1R-associated kinase-1 (IRAK-1) and IRAK-4 in response to LPS stimulation was inhibited by antioxidants [2].
  • These results suggest that IRAK-4 is an essential component of the IL-18 signaling cascade [3].
  • Because TLR/IL-1R/plant R-containing receptors mediate signal transduction in a similar fashion, we investigated the role of IRAK-4 in IL-18R signaling [3].
  • Among the critical downstream signaling pathways induced by LPS, NF-kappaB activation but not IFN regulatory factor 3 or STAT1 activation was defective in cells lacking IRAK-4 [4].
 

Biological context of Irak4

 

Anatomical context of Irak4

  • We found that stimulation of TLR2, TLR4, or TLR9, but not TLR3, caused a decrease in IRAK-4 protein without affecting its mRNA level in a mouse macrophage cell line, RAW 264 [5].
  • A critical role for the innate immune signaling molecule IRAK-4 in T cell activation [6].
 

Associations of Irak4 with chemical compounds

  • Examination of the IRAK-4 DD crystal structure reveals a single manganese ion coordinated to surface residues lysine-21 and aspartate-24 [7].
 

Other interactions of Irak4

  • These data indicated that TgHSP70 signaling mechanisms were mediated by TLR2, MyD88, and IRAK4, but not by TLR4 [8].
  • Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase C activation through the association with Zap70 [6].

References

  1. Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4. Burns, K., Janssens, S., Brissoni, B., Olivos, N., Beyaert, R., Tschopp, J. J. Exp. Med. (2003) [Pubmed]
  2. Involvement of reactive oxygen species in Toll-like receptor 4-dependent activation of NF-kappa B. Asehnoune, K., Strassheim, D., Mitra, S., Kim, J.Y., Abraham, E. J. Immunol. (2004) [Pubmed]
  3. IL-1 receptor-associated kinase 4 is essential for IL-18-mediated NK and Th1 cell responses. Suzuki, N., Chen, N.J., Millar, D.G., Suzuki, S., Horacek, T., Hara, H., Bouchard, D., Nakanishi, K., Penninger, J.M., Ohashi, P.S., Yeh, W.C. J. Immunol. (2003) [Pubmed]
  4. IL-1R-associated kinase 4 is required for lipopolysaccharide-induced activation of APC. Suzuki, N., Suzuki, S., Eriksson, U., Hara, H., Mirtosis, C., Chen, N.J., Wada, T., Bouchard, D., Hwang, I., Takeda, K., Fujita, T., Der, S., Penninger, J.M., Akira, S., Saito, T., Yeh, W.C. J. Immunol. (2003) [Pubmed]
  5. Prolonged Toll-like receptor stimulation leads to down-regulation of IRAK-4 protein. Hatao, F., Muroi, M., Hiki, N., Ogawa, T., Mimura, Y., Kaminishi, M., Tanamoto, K. J. Leukoc. Biol. (2004) [Pubmed]
  6. A critical role for the innate immune signaling molecule IRAK-4 in T cell activation. Suzuki, N., Suzuki, S., Millar, D.G., Unno, M., Hara, H., Calzascia, T., Yamasaki, S., Yokosuka, T., Chen, N.J., Elford, A.R., Suzuki, J., Takeuchi, A., Mirtsos, C., Bouchard, D., Ohashi, P.S., Yeh, W.C., Saito, T. Science (2006) [Pubmed]
  7. Metal ion-mediated reduction in surface entropy improves diffraction quality of crystals of the IRAK-4 death domain. Lasker, M.V., Kuruvilla, S.M., Gajjar, M.M., Kapoor, A., Nair, S.K. Journal of biomolecular techniques : JBT. (2006) [Pubmed]
  8. Toll-like receptor 4 mediates tolerance in macrophages stimulated with Toxoplasma gondii-derived heat shock protein 70. Mun, H.S., Aosai, F., Norose, K., Piao, L.X., Fang, H., Akira, S., Yano, A. Infect. Immun. (2005) [Pubmed]
 
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