Apoptosis induction by Bid requires unconventional ubiquitination and degradation of its N-terminal fragment

Bcl-2 family member Bid is subject to autoinhibition; in the absence of stimuli, its N-terminal region sequesters the proapoptotic Bcl-2 homology 3 (BH3) domain. Upon proteolytic cleavage in its unstructured loop, Bid is activated, although structural data reveal no apparent resulting conformational...

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Detalhes bibliográficos
Main Authors: Tait, Stephen W.G., de Vries, Evert, Maas, Chiel, Keller, Anna M., D'Santos, Clive S., Borst, Jannie
Formato: Artigo
Idioma:Inglês
Publicado em: The Rockefeller University Press 2007
Assuntos:
Research Articles
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC2373500/
https://ncbi.nlm.nih.gov/pubmed/18166654
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1083/jcb.200707063
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