The key function of IRAK-4 in the inflammation signal pathway mediated by Toll-like receptors

LI Fan; RUI Yao-Cheng

Message Board

Respected readers, authors and reviewers, you can add comments to this page on any questions about the contribution, review, editing and publication of this journal. We will give you an answer as soon as possible. Thank you for your support!

Name

E-mail

Phone

Title

Content

Verification Code

interleukin-1 receptor-associated kinase 4 (IRAK-4) is a key molecular which participates in the innate immune processes. It belongs to the IRAK family with the other three members: IRAK-1, IRAK-2, and IRAK-M. However, It has been found that IRAK-4 plays a more important role in the inflammatory signal pathway mediated by TLRs/IL-1Rs through the deep investigation of the IRAK-4 kinase activity and the positive/negative regulation mechanism of the inflammatory reactions. The activities of IRAK-4 and the crucial function of IRAK4 in the TLRs/IL-1Rs mediated pathways of inflammatory signal transmission were summarized.

The key function of IRAK-4 in the inflammation signal pathway mediated by Toll-like receptors

Department of Pharmacology, The Second Military Medical University, Shanghai 200433,China

Received Date: 2010-09-20

Rev Recd Date: 2010-10-21

Key words:

Abstract: interleukin-1 receptor-associated kinase 4 (IRAK-4) is a key molecular which participates in the innate immune processes. It belongs to the IRAK family with the other three members: IRAK-1, IRAK-2, and IRAK-M. However, It has been found that IRAK-4 plays a more important role in the inflammatory signal pathway mediated by TLRs/IL-1Rs through the deep investigation of the IRAK-4 kinase activity and the positive/negative regulation mechanism of the inflammatory reactions. The activities of IRAK-4 and the crucial function of IRAK4 in the TLRs/IL-1Rs mediated pathways of inflammatory signal transmission were summarized.

HTML

Reference (14)

[1]	Rekhter M, Staschke K, Estridge T, et al. Genetic ablation of IRAK-4 kinase activity inhibits vascular lesion formation[J]. Biochem Biophys Res Commun, 2008, 367(3)：642.
[2]	Kim TW, Staschke K, Bulek K, et al. A critical role for IRAK4 kinase activity in Toll-like receptor-mediated innate immunity[J]. The Journal of Experimental Medicine, 2007, 204(5)：1025.
[3]	Lye E, Mirtsos C, Suzuki M, et al. The role of interleukin 1 receptor-associated kinase-4 (IRAK-4) kinase activity in IRAK-4-mediated signaling[J]. The Journal of Biological Chemistry, 2004, 279(39)：40653.
[4]	Qin JZ, Jiang ZF, Qian YC, et al. IRAK4 kinase activity is redundant for interleukin-1 (IL-1) receptor-associated kinase phosphorylation and IL-1 responsiveness[J]. The Journal of Biological Chemistry, 2004, 279(25)：26748.
[5]	Song KW, Talamas FX, Suttmann RT, et al. The kinase activities of interleukin-1 receptor associated kinase (IRAK)-1 and 4 are redundant in the control of inflammatory cytokine expression in human cells[J]. Molecular Immunology, 2009,46：1458.
[6]	Hatao F, Yamamoto M, Muroi M, et al. MyD88-induced downregulation of IRAK-4 and its structural requirements[J]. FEMS Immunol Med Microbial, 2008, 53：260.
[7]	Hatao F, Muroi M, Hiki N, et al. Prolonged Toll-like receptor stimulation leads to down-regulation of IRAK-4 protein[J]. Leukoc.Biol, 2004, 76：904.
[8]	Suzuki N, Suzuki S，Yeh WC， et al. IRAK-4 as the central TIR signaling mediator in innate immunity[J]. Trends in Immunology, 2002, 23(10)：503.
[9]	Cheng H, Addona T, Keshishian H, et al. Regulation of IRAK-4 kinase activity via autophosphorylation within its activation loop[J]. Biochemical and Biophysical Research Communications, 2007, 352：609.
[10]	Kuglstatter A, Villasen AG, Shaw D, et al. Cutting Edge: IL-1 receptor-associated kinase 4 structures reveal novel features and multiple conformations[J]. The Journal of Immunology, 2007, 178：2641.
[11]	Lasker MV, Gajjar MM, Nair SK,et al. Cutting Edge: Molecular structure of the IL-1R-associated kinase-4 death domain and its implications for TLR signaling[J]. The Journal of Immunology, 2005, 175：4175.
[12]	Suzuki N, Suzuki S, Millar DG, et al. A critical role for the innate immune signaling molecule IRAK-4 in T cell activation[J]. Science, 2006, 311(5769)：1927.
[13]	Chandrasekar B, Mummidid S, Valente AJ, et al. The pro-atherogenic cytokine interleukin-18 induces CXCL16 expression in rat aortic smooth muscle cells via MyD88, interleukin-1 receptor associated kinase, tumor necrosis factor receptor associated factor 6, c-Src, phosphatidylinositol 3 kinase, Akt, c-Jun N- terminal kinase, and activator protein-1 signaling[J]. J Biol Chem, 2005, 280(28)：26263.
[14]	Pacquelet S, Johnson JL, Ellis BA, et al. Cross-talk between IRAK-4 and the NADPH oxidase[J]. Biochem. J, 2007, 403：451.

Message Board

The key function of IRAK-4 in the inflammation signal pathway mediated by Toll-like receptors

Abstract

References

Proportional views

通讯作者: 陈斌, bchen63@163.com

Article Metrics

Related

Proportional views