4.3 Review

Mechanisms of RIPK3-induced inflammation

期刊

IMMUNOLOGY AND CELL BIOLOGY
卷 95, 期 2, 页码 166-172

出版社

WILEY
DOI: 10.1038/icb.2016.124

关键词

-

资金

  1. Israel Science Foundation (ISF) [1416/15]
  2. alpha-1 foundation
  3. Recanati Foundation
  4. Varda and Boaz Dotan Research Center

向作者/读者索取更多资源

Receptor-interacting protein kinase 3 (RIP3/RIPK3) is a multifunctional regulator of cell death and inflammation. It controls signalling downstream of the tumor necrosis factor (TNF) receptor family, DNA-dependent activator of IFN-regulatory factors (DAI) and toll-like receptors (TLRs). Today, it is also widely recognized as a component of caspase-independent cell death known as necroptosis, and cytokine production via activation of the inflammasome. Its role in inflammasome activation, in particular, make the interpretation of its role in vivo more complex. In this review, we focus on divergent roles for RIPK3 in cell death and inflammation.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.3
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据