期刊
ONCOGENE
卷 27, 期 50, 页码 6452-6461出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2008.311
关键词
caspases; mitochondria; caspase-independent cell death; mitochondrial outer membrane permeabilization; cancer
资金
- NIAID NIH HHS [R01 AI047891-10, R01 AI047891] Funding Source: Medline
Apoptosis is dependent upon caspase activation leading to substrate cleavage and, ultimately, cell death. Although required for the apoptotic phenotype, it has become apparent that cells frequently die even when caspase function is blocked. This process, termed caspase-independent cell death (CICD), occurs in response to most intrinsic apoptotic cues, provided that mitochondrial outer membrane permeabilization has occurred. Death receptor ligation can also trigger a form of CICD termed necroptosis. In this review, we will examine the molecular mechanisms governing CICD, highlight recent findings demonstrating recovery from conditions of CICD and discuss potential pathophysiological functions of these processes.
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