[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. |