K63-linked polyubiquitination of transcription factor IRF1 is essential for IL-1-induced production of chemokines CXCL10 and CCL5
文献类型：期刊论文
| 作者 | Harikumar, Kuzhuvelil B.3,4; Yester, Jessie W.3,4; Surace, Michael J.3,4; Oyeniran, Clement3,4; Price, Megan M.3,4; Huang, Wei-Ching3,4; Hait, Nitai C.3,4; Allegood, Jeremy C.3,4; Yamada, Akimitsu3,4,5; Kong, Xiangqian1 |
| 刊名 | NATURE IMMUNOLOGY
 |
| 出版日期 | 2014-03 |
| 卷号 | 15期号:3页码:231-238 |
| ISSN号 | 1529-2908 |
| DOI | 10.1038/ni.2810 |
| 文献子类 | Article |
| 英文摘要 | Although interleukin 1 (IL-1) induces expression of the transcription factor IRF1 (interferon-regulatory factor 1), the roles of IRF1 in immune and inflammatory responses and mechanisms of its activation remain elusive. Here we found that IRF1 was essential for IL-1-induced expression of the chemokines CXCL10 and CCL5, which recruit mononuclear cells into sites of sterile inflammation. Newly synthesized IRF1 acquired Lys63 (K63)-linked polyubiquitination mediated by the apoptosis inhibitor cIAP2 that was enhanced by the bioactive lipid SIP. In response to IL-1, cIAP2 and the sphingosine kinase SphK1 (the enzyme that generates S1P) formed a complex with IRF1, which led to its activation. Thus, IL-1 triggered a hitherto unknown signaling cascade that controlled the induction of IRF1-dependent genes that encode molecules important for sterile inflammation. |
| WOS关键词 | NF-KAPPA-B ; REGULATORY FACTOR-I ; SYNERGISTIC ACTIVATION ; GENES ; KINASE ; TRAF2 ; INTERLEUKIN-1 ; EXPRESSION ; APOPTOSIS ; PATHWAY |
| 资助项目 | US National Institutes of Health[1R01AI093718] ; US National Institutes of Health[5R37GM043880] ; US National Institutes of Health[1U19AI077435] ; US National Institutes of Health[R01CA160688] ; US National Institutes of Health[5P30NS047463] ; US National Institutes of Health[P30CA16059] ; National Natural Science Foundation of China[91029704] |
| WOS研究方向 | Immunology |
| 语种 | 英语 |
| WOS记录号 | WOS:000331683100008 |
| 出版者 | NATURE PUBLISHING GROUP |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/277177]  |
| 专题 | 药物发现与设计中心 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 通讯作者 | Kordula, Tomasz |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 200031, Peoples R China; 2.Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA 3.Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Sch Med, Richmond, VA 23284 USA; 4.Virginia Commonwealth Univ, Massey Canc Ctr, Sch Med, Richmond, VA USA; 5.Virginia Commonwealth Univ, Dept Surg, Sch Med, Richmond, VA USA; 6.Washington Univ, Sch Med, Dept Med, Dept Mol Microbiol, St Louis, MO 63110 USA; |
| 推荐引用方式 GB/T 7714 | Harikumar, Kuzhuvelil B.,Yester, Jessie W.,Surace, Michael J.,et al. K63-linked polyubiquitination of transcription factor IRF1 is essential for IL-1-induced production of chemokines CXCL10 and CCL5[J]. NATURE IMMUNOLOGY,2014,15(3):231-238. |
| APA | Harikumar, Kuzhuvelil B..,Yester, Jessie W..,Surace, Michael J..,Oyeniran, Clement.,Price, Megan M..,...&Kordula, Tomasz.(2014).K63-linked polyubiquitination of transcription factor IRF1 is essential for IL-1-induced production of chemokines CXCL10 and CCL5.NATURE IMMUNOLOGY,15(3),231-238. |
| MLA | Harikumar, Kuzhuvelil B.,et al."K63-linked polyubiquitination of transcription factor IRF1 is essential for IL-1-induced production of chemokines CXCL10 and CCL5".NATURE IMMUNOLOGY 15.3(2014):231-238. |
入库方式： OAI收割
来源：上海药物研究所
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