Abstract
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.
Keywords: Apoptosis, Bid, tumorigenesis, DNA damage, stress-response
Current Cancer Drug Targets
Title: Bid Stands at the Crossroad of Stress-Response Pathways
Volume: 10 Issue: 6
Author(s): G. Song, G.G. Chen, T. Hu and P.B.S. Lai
Affiliation:
Keywords: Apoptosis, Bid, tumorigenesis, DNA damage, stress-response
Abstract: 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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Cite this article as:
Song G., Chen G.G., Hu T. and Lai P.B.S., Bid Stands at the Crossroad of Stress-Response Pathways, Current Cancer Drug Targets 2010; 10 (6) . https://dx.doi.org/10.2174/156800910791859515
DOI https://dx.doi.org/10.2174/156800910791859515 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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