Journal
CURRENT CANCER DRUG TARGETS
Volume 10, Issue 6, Pages 584-592Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/156800910791859515
Keywords
Apoptosis; Bid; tumorigenesis; DNA damage; stress-response
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Funding
- National Natural Science Foundation of China [30971524]
- Xiamen University
- Research Grants Council of the Hong Kong Special Administrative Region [CUHK 4534/06M]
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Bid, a BH3-only Bcl-2 family member, is proven to be a pivotal molecule for the regulation of tumorigenesis by its multiple functions in promoting apoptosis, survival and proliferation. Growing evidence supports that Bid has double roles with respect to stress-response. In most cases it functions in a truncated form, but the cleavage of Bid may not be an absolute requirement for Bid to be pro-apoptotic. Full-length Bid can also translocate to and activate the mitochondria without cleavage. Bid has emerged as a central player linking death signals through surface death receptors to the core apoptotic mitochondrial pathway. Bid is also involved in DNA damage response, and the phosphorylated Bid may negatively regulate its pro-apoptotic function independent of the BH3 domain. This review surveys recent developments in understanding the molecular mechanisms of Bid activation and its roles in regulating the cross-talk of cell cycle arrest and apoptosis.
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