期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 16, 期 -, 页码 749-758出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/3717
关键词
Mitochondria; p53; Nontranscriptional; Apoptosis; Interaction; Bcl-2 family; CLIC4; Review
资金
- Southern Illinois University
- NIH [R15CA151094 (RCE)]
- Philip Morris External Research Program
- NATIONAL CANCER INSTITUTE [R15CA151094] Funding Source: NIH RePORTER
It is now well established that p53 is the primary arbiter of stress-response and the principal barrier to neoplastic processes at the cellular level. Perhaps the most potent weapon in p53's tumor suppressive arsenal is apoptosis, enacted as a last resort when all other remedies are exhausted. Initially, the mechanism was thought to be simply activation or repression of Bcl-2 family members by p53. More recently, evidence of a more rapid pathway emerged whereby p53 physically interacts with Bcl-2 family members to tip the balance toward apoptosis. This review details the multiple levels of regulation of mitochondrially-directed apoptosis by p53, including recent findings of how p53 translocation is regulated.
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