Bid stands at the crossroad of stress-response pathways.
Curr Cancer Drug Targets
; 10(6): 584-92, 2010 Sep.
Article
em En
| MEDLINE
| ID: mdl-20482490
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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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estresse Fisiológico
/
Transformação Celular Neoplásica
/
Proteína Agonista de Morte Celular de Domínio Interatuante com BH3
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Curr Cancer Drug Targets
Assunto da revista:
ANTINEOPLASICOS
/
NEOPLASIAS
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
China