Current Cancer Drug Targets

Ruiwen Zhang 
Texas Tech University Health Sciences Center
1300 Coulter Drive
Amarillo, TX 79106


Bid Stands at the Crossroad of Stress-Response Pathways

Author(s): G. Song, G.G. Chen, T. Hu, P.B.S. Lai.


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

Order Reprints Order Eprints Rights & PermissionsPrintExport

Article Details

Year: 2010
Page: [584 - 592]
Pages: 9
DOI: 10.2174/156800910791859515
Price: $58