期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 67, 期 10, 页码 1567-1579出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-010-0283-0
关键词
Tumor necrosis factor; Apoptosis; Necrosis; Receptor interacting protein kinase 1
资金
- APO-SYS
- Flanders Institute for Biotechnology
- European Union [MRTN-CT-035624, LSHB-CT-2005-019067, HEALTH-F4-2007-200767]
- Interuniversity Poles of Attraction-Belgian Science Policy [IAP6/18]
- Fonds voor Wetenschappelijk Onderzoek-Vlaanderen [G.0133.05, 3G.0218.06]
- Special Research Fund of Ghent University [12.0505.02]
- Flemish government
In this review, we discuss the signal-transduction pathways of three major cellular responses induced by tumor necrosis factor (TNF): cell survival through NF-kappa B activation, apoptosis, and necrosis. Recruitment and activation of caspases plays a crucial role in the initiation and execution of TNF-induced apoptosis. However, experimental inhibition of caspases reveals an alternative cell death pathway, namely necrosis, also called necroptosis, suggesting that caspases actively suppress the latter outcome. TNF-induced necrotic cell death crucially depends on the kinase activity of receptor interacting protein serine-threonine kinase 1 (RIP1) and RIP3. It was recently demonstrated that ubiquitination of RIP1 determines whether it will function as a pro-survival or pro-cell death molecule. Deeper insight into the mechanisms that control the molecular switches between cell survival and cell death will help us to understand why TNF can exert so many different biological functions in the etiology and pathogenesis of human diseases.
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。
推荐
暂无数据