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Gene Review

IRAK3  -  interleukin-1 receptor-associated kinase 3

Homo sapiens

Synonyms: ASRT5, IL-1 receptor-associated kinase M, IRAK-3, IRAK-M, IRAKM, ...
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Disease relevance of IRAK3


High impact information on IRAK3

  • The induction of IRAK-M by hyaluronan and tumor cells was abolished by incubation with anti-CD44 or anti-TLR4 blocking Abs [1].
  • Altogether, our findings indicate that deactivation of human monocytes in the presence of tumor cells involves IRAK-M up-regulation, and this effect appears to be mediated by hyaluronan through the engagement of CD44 and TLR4 [1].
  • Furthermore, down-regulation of IRAK-M expression by small interfering RNAs specific for IRAK-M reinstates both TNF-alpha mRNA expression and protein production in human monocytes re-exposed to a tumor cell line [1].
  • By contrast, another IRAK family member, IRAK-M, negatively regulates this pathway, and is up-regulated in cultures of endotoxin-tolerant monocytes and in monocytes from septic patients within the timeframe of tolerance [1].
  • IRAK-M was induced in monocytes upon coculturing with different tumor cells, as well as by fixed tumor cells and medium supplemented with the supernatant from tumor cell cultures [1].

Biological context of IRAK3

  • Conclusions: This study showed that the mechanism of endotoxin tolerance exists in the intrahepatic biliary tree and is possibly induced by the expression of IRAK-M in the intrahepatic biliary epithelium, suggesting that the endotoxin tolerance is important in maintaining innate immune biliary homeostasis [4].
  • These IRAK-M molecules show 71% sequence identity, a comparable cellular expression, and functional similarities with respect to signal transduction capacity and kinase activity, suggesting functional homology in signalling in human and mouse cells [5].
  • To investigate whether polymorphisms in these genes were associated with asthma or asthma-related phenotypes, we screened these genes for polymorphisms by direct sequencing of 24 asthmatics and identified 19 variants in IRAK-M and 12 variants in SIGIRR [6].
  • None of the alleles or haplotypes of IRAK-M and SIGIRR were associated with asthma susceptibility or asthma-related phenotype [6].

Anatomical context of IRAK3


Associations of IRAK3 with chemical compounds


Regulatory relationships of IRAK3

  • Furthermore, the expression of IRAK-M induced by GSNO was inhibited by the presence of a blocking antibody raised against TNF-alpha [7].

Other interactions of IRAK3

  • The latter include induction of IRAK-M and suppressor of cytokine-signaling-1 (SOCS-1), phosphoinositide-3-kinase (PI3K) signaling, and increased or maintained expression of inhibitor-kappaB (IkappaB) isoforms [8].


  1. Tumor cells deactivate human monocytes by up-regulating IL-1 receptor associated kinase-M expression via CD44 and TLR4. del Fresno, C., Otero, K., Gómez-García, L., González-León, M.C., Soler-Ranger, L., Fuentes-Prior, P., Escoll, P., Baos, R., Caveda, L., García, F., Arnalich, F., López-Collazo, E. J. Immunol. (2005) [Pubmed]
  2. Upregulation of TNF-alpha production signaling pathways in monocytes from patients with advanced cirrhosis: possible role of Akt and IRAK-M. Tazi, K.A., Quioc, J.J., Saada, V., Bezeaud, A., Lebrec, D., Moreau, R. J. Hepatol. (2006) [Pubmed]
  3. Induction of IRAK-M is associated with lipopolysaccharide tolerance in a human endotoxemia model. van 't Veer, C., van den Pangaart, P.S., van Zoelen, M.A., de Kruif, M., Birjmohun, R.S., Stroes, E.S., de Vos, A.F., van der Poll, T. J. Immunol. (2007) [Pubmed]
  4. Endotoxin tolerance in human intrahepatic biliary epithelial cells is induced by upregulation of IRAK-M. Harada, K., Isse, K., Sato, Y., Ozaki, S., Nakanuma, Y. Liver Int. (2006) [Pubmed]
  5. Identification and characterization of murine IRAK-M. Rosati, O., Martin, M.U. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  6. An association study of asthma and related phenotypes with polymorphisms in negative regulator molecules of the TLR signaling pathway. Nakashima, K., Hirota, T., Obara, K., Shimizu, M., Jodo, A., Kameda, M., Doi, S., Fujita, K., Shirakawa, T., Enomoto, T., Kishi, F., Yoshihara, S., Matsumoto, K., Saito, H., Suzuki, Y., Nakamura, Y., Tamari, M. J. Hum. Genet. (2006) [Pubmed]
  7. Nitric oxide activates the expression of IRAK-M via the release of TNF-alpha in human monocytes. del Fresno, C., Gómez-García, L., Caveda, L., Escoll, P., Arnalich, F., Zamora, R., López-Collazo, E. Nitric Oxide (2004) [Pubmed]
  8. Molecular mechanisms of endotoxin tolerance. Fan, H., Cook, J.A. J. Endotoxin Res. (2004) [Pubmed]
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