March3 attenuates il-1 beta-triggered inflammation by mediating k48-linked polyubiquitination and degradation of il-1ri
文献类型：期刊论文
| 作者 | Lin, Heng1,2; Gao, Deng1; Hu, Ming-Ming1; Zhang, Man2; Wu, Xiao-Xia2; Feng, Lu1; Xu, Wen-Hua1; Yang, Qing1; Zhong, Xuan2; Wei, Jin1 |
| 刊名 | Proceedings of the national academy of sciences of the united states of america
 |
| 出版日期 | 2018-12-04 |
| 卷号 | 115期号:49页码:12483-12488 |
| 关键词 | March3 Il-1 Listeria monocytogenes Polyubiquitination Inflammation |
| ISSN号 | 0027-8424 |
| DOI | 10.1073/pnas.1806217115 |
| 通讯作者 | Shu, hong-bing(shuh@whu.edu.cn) |
| 英文摘要 | The proinflammatory cytokine il-1 beta plays critical roles in inflammatory and autoimmune diseases. il-1 beta signaling is tightly regulated to avoid excessive inflammatory response. in this study, we identified the e3 ubiquitin ligase membrane-associated ring-ch-type finger 3 (march3) as a critical negative regulator of il-1 beta-triggered signaling. overexpression of march3 inhibited il-1 beta-triggered activation of nf-kappa b as well as expression of inflammatory genes, whereas march3 deficiency had the opposite effects. march3-deficient mice produced higher levels of serum inflammatory cytokines and were more sensitive to inflammatory death upon il-1 beta injection or listeria monocytogenes infection. mechanistically, march3 was associated with il-1 receptor i (il-1ri) and mediated its k48-linked polyubiquitination at k409 and lysosomal-dependent degradation. furthermore, il-1 beta stimulation triggered dephosphorylation of march3 by cdc25a and activation of its e3 ligase activity. our findings suggest that march3-mediated il-1ri degradation is an important mechanism for attenuating il-1 beta-triggered inflammatory response. |
| WOS关键词 | NF-KAPPA-B ; DOWN-REGULATION ; RECEPTOR ; ACTIVATION ; FAMILY ; IRAK ; ADAPTER ; UBIQUITINATION ; TRAFFICKING ; STABILITY |
| WOS研究方向 | Science & Technology - Other Topics |
| WOS类目 | Multidisciplinary Sciences |
| 语种 | 英语 |
| WOS记录号 | WOS:000452124700051 |
| 出版者 | NATL ACAD SCIENCES |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2373212 |
| 专题 | 武汉病毒研究所 |
| 通讯作者 | Shu, Hong-Bing |
| 作者单位 | 1.Wuhan Univ, Dept Infect Dis, Med Res Inst, Zhongnan Hosp,Sch Med, Wuhan, Hubei, Peoples R China 2.Wuhan Univ, Coll Life Sci, Wuhan 430072, Hubei, Peoples R China 3.Chinese Acad Sci, Wuhan Inst Virol, State Key Lab Virol, Wuhan 430071, Hubei, Peoples R China |
| 推荐引用方式 GB/T 7714 | Lin, Heng,Gao, Deng,Hu, Ming-Ming,et al. March3 attenuates il-1 beta-triggered inflammation by mediating k48-linked polyubiquitination and degradation of il-1ri[J]. Proceedings of the national academy of sciences of the united states of america,2018,115(49):12483-12488. |
| APA | Lin, Heng.,Gao, Deng.,Hu, Ming-Ming.,Zhang, Man.,Wu, Xiao-Xia.,...&Shu, Hong-Bing.(2018).March3 attenuates il-1 beta-triggered inflammation by mediating k48-linked polyubiquitination and degradation of il-1ri.Proceedings of the national academy of sciences of the united states of america,115(49),12483-12488. |
| MLA | Lin, Heng,et al."March3 attenuates il-1 beta-triggered inflammation by mediating k48-linked polyubiquitination and degradation of il-1ri".Proceedings of the national academy of sciences of the united states of america 115.49(2018):12483-12488. |
入库方式： iSwitch采集
来源：武汉病毒研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。