期刊
CELL RESEARCH
卷 18, 期 3, 页码 343-349出版社
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2008.31
关键词
TNF; necrosis; Nox1; TRADD; RIP1; ROS; INK
类别
资金
- NATIONAL CANCER INSTITUTE [ZIASC010376, Z01SC010376, Z01BC010783, ZIABC010783] Funding Source: NIH RePORTER
- Intramural NIH HHS Funding Source: Medline
Death receptors, including the TNF receptor-1 (TNF-RI), have been shown to be able to initiate caspase-independent cell death. This form of necrotic cell death appears to be dependent on the generation of reactive oxygen species. Recent data have indicated that superoxide generation is dependent on the activation of NADPH oxidases, which form a complex with the adaptor molecules RIP1 and TRADD. The mechanism of superoxide generation further establishes RIP1 as the central molecule in ROS production and cell death initiated by TNF alpha and other death receptors. A role for the sustained JNK activation in necrotic cell death is also suggested. The sensitization of virus-infected cells to TNF alpha indicates that necrotic cell death may represent an alternative cell death pathway for clearance of infected cells.
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