期刊
EMBO REPORTS
卷 19, 期 2, 页码 234-243出版社
WILEY
DOI: 10.15252/embr.201744046
关键词
apoptosis; BCL-2 family; BCL-xL mobility; E2F1
资金
- Ministere de la Recherche et de l'Enseignement Superieur
- Ligue contre le cancer [R13137]
- MCRC-CRUK training award
- Wellcome Trust
- Region Pays de la Loire (CIMATH2)
- ARC [R15083NN]
- INCA PLBio [R12134NN]
- Ligue contre le cancer 44
E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity.
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