...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America. >MARCH3 attenuates IL-1 beta-triggered inflammation by mediating K48-linked polyubiquitination and degradation of IL-1RI
【24h】

MARCH3 attenuates IL-1 beta-triggered inflammation by mediating K48-linked polyubiquitination and degradation of IL-1RI

机译：MARCH3 attenuates IL-1 beta-triggered inflammation by mediating K48-linked polyubiquitination and degradation of IL-1RI

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相关主题

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.

著录项

获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号