IRAK-M mediates Toll-like receptor/IL-1R-induced NFκB activation and cytokine production

ZhouH.; YuM.; FukudaK.ImJ.YaoP.CuiW.BulekK.ZeppJ.WanY.WhanKimT.YinW.MaV.ThomasJ.GuJ.WangJ.-A.DicorletoP.E.FoxP.L.QinJ.LiX.

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IRAK-M mediates Toll-like receptor/IL-1R-induced NFκB activation and cytokine production

机译：IRAK-M介导toll样受体/ IL-1R-inducedNFκB细胞因子激活和生产

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Toll-like receptors transduce their signals through the adaptor molecule MyD88 and members of the IL-1R-associated kinase family (IRAK-1, 2, M and 4). IRAK-1 and IRAK-2, known to form Myddosomes with MyD88-IRAK-4, mediate TLR7-induced TAK1-dependent NFκB activation. IRAK-M was previously known to function as a negative regulator that prevents the dissociation of IRAKs from MyD88, thereby inhibiting downstream signalling. However, we now found that IRAK-M was also able to interact with MyD88-IRAK-4 to form IRAK-M Myddosome to mediate TLR7-induced MEKK3-dependent second wave NFκB activation, which is uncoupled from post-transcriptional regulation. As a result, the IRAK-M-dependent pathway only induced expression of genes that are not regulated at the post-transcriptional levels (including inhibitory molecules SOCS1, SHIP1, A20 and IκBα), exerting an overall inhibitory effect on inflammatory response. On the other hand, through interaction with IRAK-2, IRAK-M inhibited TLR7-mediated production of cytokines and chemokines at translational levels. Taken together, IRAK-M mediates TLR7-induced MEKK3-dependent second wave NFκB activation to produce inhibitory molecules as a negative feedback for the pathway, while exerting inhibitory effect on translational control of cytokines and chemokines.

机译：toll样受体信号转导通过衔接分子MyD88和成员IL-1R-associated激酶家族(IRAK-1 2米和4)。IRAK-1和IRAK-2形成Myddosomes MyD88-IRAK-4,调解TLR7-induced TAK1-dependent NFκB激活。IRAK-M以前作为一个已知函数消极监管机构阻止了分裂伊拉克共和国的MyD88,从而抑制下游信号。IRAK-M也能够相互作用MyD88-IRAK-4形成IRAK-M Myddosome调解TLR7-induced MEKK3-dependent第二波NFκB激活,分道扬镳转录后调控。只IRAK-M-dependent通路诱导表达的基因是不规范转录后水平(包括抑制分子SOCS1, SHIP1, A20κBα),施加一个整体对炎症的抑制作用响应。IRAK-2 IRAK-M抑制TLR7-mediated细胞因子和趋化因子的生产转化水平。介导TLR7-induced MEKK3-dependent第二波NFκB激活产生抑制分子作为一个负面的反馈途径,发挥抑制作用转化细胞因子和趋化因子的控制。

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来源
《EMBO Journal》 |2013年第4期|583-596|共14页
作者
ZhouH.; YuM.; FukudaK.ImJ.YaoP.CuiW.BulekK.ZeppJ.WanY.WhanKimT.YinW.MaV.ThomasJ.GuJ.WangJ.-A.DicorletoP.E.FoxP.L.QinJ.LiX.;
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作者单位

Department of Molecular Cardiology, Cleveland Clinic Foundation, Cleveland, OH, United States;

Department of Cell Biology, Cleveland Clinic Foundation, Cleveland, OH, United States;

Department of Cardiology, Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, ChinaDepartment of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195, United StatesDepartment of Pediatrics and Molecular Biology, University of Texas, Southwestern Medical Center atDepartment of Biochemistry and Molecular Biology, College of Life Sciences, Peking University;

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正文语种英语
中图分类分子生物学;分子生物学;
关键词
Interleukin-1 Receptor-Associated Kinase 2; Post-Transcriptional Regulation; Interleukin 1 Receptor Associated Kinase 1cytokine productionChemokinesToll-Like ReceptorssignalsIRAK3 gene;

机译：Interleukin-1 Receptor-Associated激酶2,转录后调控;白介素1受体激酶1细胞因子有关productionChemokinesToll-LikeReceptorssignalsIRAK3基因;

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IRAK-M mediates Toll-like receptor/IL-1R-induced NFκB activation and cytokine production

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