4.7 Review

Roles of RIPK3 in necroptosis, cell signaling, and disease

期刊

EXPERIMENTAL AND MOLECULAR MEDICINE
卷 54, 期 10, 页码 1695-1704

出版社

SPRINGERNATURE
DOI: 10.1038/s12276-022-00868-z

关键词

-

资金

  1. National Research Foundation of Korea [2021R1A4A1031856, 2022R1A2B5B03001824]
  2. Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea [HR21C1003]
  3. Northeastern State University Faculty Research Committee
  4. Oklahoma Health Research grant from the Oklahoma Center for the Advancement of Science and Technology [HR20]
  5. Oklahoma Center for Advancement of Science and Technology [HR20-067]
  6. National Research Foundation of Korea [2022R1A2B5B03001824, 2021R1A4A1031856] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

This article discusses the roles of RIPK3 in cell signaling and necroptosis, as well as the pathways that trigger RIPK3 activation and cell death. The significance of this research lies in revealing the association of necroptosis with inflammation and the immune system, and exploring the potential role of RIPK3 in diseases.
Receptor-interacting protein kinase-3 (RIPK3, or RIP3) is an essential protein in the programmed and regulated cell death pathway called necroptosis. Necroptosis is activated by the death receptor ligands and pattern recognition receptors of the innate immune system, and the findings of many reports have suggested that necroptosis is highly significant in health and human disease. This significance is largely because necroptosis is distinguished from other modes of cell death, especially apoptosis, in that it is highly proinflammatory given that cell membrane integrity is lost, triggering the activation of the immune system and inflammation. Here, we discuss the roles of RIPK3 in cell signaling, along with its role in necroptosis and various pathways that trigger RIPK3 activation and cell death. Lastly, we consider pathological situations in which RIPK3/necroptosis may play a role.

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

4.7
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