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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

Irak2  -  interleukin-1 receptor-associated kinase 2

Mus musculus

Synonyms: 6330415L08Rik, AI649099, IRAK-2, Interleukin-1 receptor-associated kinase-like 2, mu-IRAK-2
 
 
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High impact information on Irak2

  • The relative roles of IRAK and IRAK-2 in IL-1 signaling pathways and subsequent cellular responses have not been previously determined [1].
  • Alternative splicing of the Irak2 gene in mice will therefore generate agonistic or antagonistic Irak2 isoforms, which is likely to have consequences for the regulation of TLR signaling [2].
  • The promoter for Irak2c differed from that of the other Irak2 isoforms in that it contained putative NF-kappaB binding sites [2].
 

Biological context of Irak2

  • Herein, we show a detailed analysis of the genomic region encompassing the murine Irak2 gene and the molecular cloning of four isoforms of Irak2 (designated Irak2a, Irak2b, Irak2c, and Irak2d) generated by alternative splicing at the 5'-end of the gene [2].
  • Dominant-negative myeloid differentiation factor 88 (MyD88) or IL-1R-associated kinase (IRAK) 2 diminished LPS-induced apoptosis in YopP-transfected macrophages, suggesting implication of MyD88 and IRAK2 in signaling cell death [3].

References

  1. Interleukin (IL)-1 receptor-associated kinase (IRAK) requirement for optimal induction of multiple IL-1 signaling pathways and IL-6 production. Kanakaraj, P., Schafer, P.H., Cavender, D.E., Wu, Y., Ngo, K., Grealish, P.F., Wadsworth, S.A., Peterson, P.A., Siekierka, J.J., Harris, C.A., Fung-Leung, W.P. J. Exp. Med. (1998) [Pubmed]
  2. The murine IRAK2 gene encodes four alternatively spliced isoforms, two of which are inhibitory. Hardy, M.P., O'Neill, L.A. J. Biol. Chem. (2004) [Pubmed]
  3. Divergence of apoptosis-inducing and preventing signals in bacteria-faced macrophages through myeloid differentiation factor 88 and IL-1 receptor-associated kinase members. Ruckdeschel, K., Mannel, O., Schröttner, P. J. Immunol. (2002) [Pubmed]
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