期刊
CELL DEATH AND DIFFERENTIATION
卷 18, 期 4, 页码 571-580出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2010.191
关键词
Beclin 1; PI3K; Bcl-2; autophagy; apoptosis; signal transduction
资金
- University of Pittsburgh Department of Surgery
- University of Pittsburgh Cancer Institute
- National Institutes of Health
- National Cancer Institute [P01 CA 101944-04]
Beclin 1, the mammalian orthologue of yeast Atg6, has a central role in autophagy, a process of programmed cell survival, which is increased during periods of cell stress and extinguished during the cell cycle. It interacts with several cofactors (Atg14L, UVRAG, Bif-1, Rubicon, Ambra1, HMGB1, nPIST, VMP1, SLAM, IP3R, PINK and survivin) to regulate the lipid kinase Vps-34 protein and promote formation of Beclin 1-Vps34-Vps15 core complexes, thereby inducing autophagy. In contrast, the BH3 domain of Beclin 1 is bound to, and inhibited by Bcl-2 or Bcl-XL. This interaction can be disrupted by phosphorylation of Bcl-2 and Beclin 1, or ubiquitination of Beclin 1. Interestingly, caspase-mediated cleavage of Beclin 1 promotes crosstalk between apoptosis and autophagy. Beclin 1 dysfunction has been implicated in many disorders, including cancer and neurodegeneration. Here, we summarize new findings regarding the organization and function of the Beclin 1 network in cellular homeostasis, focusing on the cross-regulation between apoptosis and autophagy. Cell Death and Differentiation ( 2011) 18, 571-580; doi: 10.1038/cdd.2010.191; published online 11 February 2011
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据