CRL4(DCAF2) negatively regulates IL-23 production in dendritic cells and limits the development of psoriasis
文献类型：期刊论文
| 作者 | Huang, Tao4; Gao, Zhengjun4; Fan, Keqi4; Wang, Fei4; Li, Yiyuan4; Zhong, Jiangyan4; Fan, Heng Y.4; Jin, Jin4,6; Zhang, Yu5; Cao, Qian5 |
| 刊名 | JOURNAL OF EXPERIMENTAL MEDICINE
 |
| 出版日期 | 2018 |
| 卷号 | 215期号:8页码:1999-2017 |
| ISSN号 | 0022-1007 |
| DOI | 10.1084/jem.20180210 |
| 文献子类 | Article |
| 英文摘要 | The E3 ligase CRL4(DCAF2) is believed to be a pivotal regulator of the cell cycle and is required for mitotic and S phase progression. The NEDD8-targeting drug MLN4924, which inactivates cullin ring-finger ubiquitin ligases (CRLs), has been examined in clinical trials for various types of lymphoma and acute myeloid leukemia. However, the essential role of CRL4(DCAF2) in primary myeloid cells remains poorly understood. MLN4924 treatment, which mimics DCAF2 depletion, also promotes the severity of mouse psoriasis models, consistent with the effects of reduced DCAF2 expression in various autoimmune diseases. Using transcriptomic and immunological approaches, we showed that CRL4(DCAF2) in dendritic cells (DCs) regulates the proteolytic fate of NIK and negatively regulates IL-23 production. CRL4(DCAF2) promoted the polyubiquitination and subsequent degradation of NIK independent of TRAF3 degradation. DCAF2 deficiency facilitated NIK accumulation and RelB nuclear translocation. DCAF2 DC-conditional knockout mice displayed increased sensitivity to autoimmune diseases. This study shows that CRL4(DCAF2) is crucial for controlling NIK stability and highlights a unique mechanism that controls inflammatory diseases. |
| 学科主题 | Immunology ; Research & Experimental Medicine |
| WOS关键词 | NF-KAPPA-B ; LYMPH-NODE ; S-PHASE ; C-REL ; ACTIVATION ; PATHWAY ; KINASE ; INFLAMMATION ; NIK ; DEGRADATION |
| 语种 | 英语 |
| WOS记录号 | WOS:000440828500006 |
| 出版者 | ROCKEFELLER UNIV PRESS |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/646]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Dept Rheumatol & Immunol, Chengdu, Sichuan, Peoples R China; 2.Shanghai Jiao Tong Univ, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci,Sch Med, Shanghai, Peoples R China; 3.Collaborat Innovat Ctr Biotherapy, Chengdu, Sichuan, Peoples R China, 4.Zhejiang Univ, Life Sci Inst, Hangzhou, Zhejiang, Peoples R China; 5.Zhejiang Univ, Sir Run Run Shaw Hosp, Coll Med, Hangzhou, Zhejiang, Peoples R China; 6.Zhejiang Univ, Minist Agr, Key Lab Anim Virol, Hangzhou, Zhejiang, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Huang, Tao,Gao, Zhengjun,Fan, Keqi,et al. CRL4(DCAF2) negatively regulates IL-23 production in dendritic cells and limits the development of psoriasis[J]. JOURNAL OF EXPERIMENTAL MEDICINE,2018,215(8):1999-2017. |
| APA | Huang, Tao.,Gao, Zhengjun.,Fan, Keqi.,Wang, Fei.,Li, Yiyuan.,...&,.(2018).CRL4(DCAF2) negatively regulates IL-23 production in dendritic cells and limits the development of psoriasis.JOURNAL OF EXPERIMENTAL MEDICINE,215(8),1999-2017. |
| MLA | Huang, Tao,et al."CRL4(DCAF2) negatively regulates IL-23 production in dendritic cells and limits the development of psoriasis".JOURNAL OF EXPERIMENTAL MEDICINE 215.8(2018):1999-2017. |
入库方式： OAI收割
来源：上海营养与健康研究所
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