TAILIEUCHUNG - báo cáo khoa hoc : Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IjB-f

IjB-f, an essential inflammatory regulator, is specifically induced by Toll-like receptor ligands or interleukin (IL)-1bby post-transcriptional acti-vation mediated via a 165-nucleotide element in IjB-f mRNA. Here, we analyzed the Toll-like receptor–IL-1 receptor signaling components involved in the post-transcriptional regulation of IjB-fwith mutated estro-gen receptor [ER(T2)] fusion proteins. | IFEBS Journal Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IjB-f Tomoyuki Ohba1 2 Yujiro Ariga1 Takashi Maruyama1 2 Nha K. Truong2 Jun-ichiro Inoue3 and Tatsushi Muta1 2 1 Laboratory of CellRecognition and Response Department of DevelopmentalBiology and Neurosciences Graduate Schoolof Life Sciences Tohoku University Sendai Japan 2 Department of Biology Faculty of Science Tohoku University Sendai Japan 3 Division of Cellular and Molecular Biology Department of Cancer Biology Institute of MedicalScience University of Tokyo Japan Keywords interleukin-1 IL-1 interleukin-1 receptor-associated kinase IRAK1 IjB-f post-transcriptional regulation Toll-like receptor Correspondence T. Muta 6-3 Aoba Aramaki Aoba-ku Sendai 980-8578 Japan Fax 81 22 795 6709 Tel 81 22 795 6709 E-mail tmuta@ Received 17 September 2011 revised 18 October 2011 accepted 2 November 2011 doi iKB-f an essential inflammatory regulator is specifically induced by Toll-like receptor ligands or interleukin IL -ip by post-transcriptional activation mediated via a 165-nucleotide element in IKB-f mRNA. Here we analyzed the Toll-like receptor-IL-1 receptor signaling components involved in the post-transcriptional regulation of iKB-f with mutated estrogen receptor ER T2 fusion proteins. Upon 4-hydroxytamoxifen treatment the ER T2 fusion proteins with IL-1 receptor-associated kinase IRAK 1 and IRAK4 elicited specific activation of a reporter gene for the post-transcriptional regulation of IKB-f. The tumor necrosis factor receptor-associated factor TRAF 6-ER T2 protein activated nuclear factor-KB but not post-transcriptional regulation indicating that activation of IRAK1 4 but not of TRAF6 is sufficient to activate the 165-nucleotide element-mediated post-transcriptional mechanism. Interestingly the post-transcriptional mechanism was not activated in TRAF6-deficient cells .

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