期刊
EMBO REPORTS
卷 16, 期 6, 页码 700-708出版社
WILEY
DOI: 10.15252/embr.201439496
关键词
autophagy; ERK; RIP1 (RIPK1); TFEB
资金
- NIH [CA 150925]
- Shared Resources from the Cancer Center Support Grant [P30CA046934]
- Cancer League of Colorado Cancer Research Grant from the Cancer League of Colorado, Inc.
- ACS IRG from the American Cancer Society [57-001-53]
In a synthetic lethality/viability screen, we identified the serine-threonine kinase RIP1 (RIPK1) as a gene whose knockdown is highly selected against during growth in normal media, in which autophagy is not critical, but selected for in conditions that increase reliance on basal autophagy. RIP1 represses basal autophagy in part due to its ability to regulate the TFEB transcription factor, which controls the expression of autophagy-related and lysosomal genes. RIP1 activates ERK, which negatively regulates TFEB though phosphorylation of serine 142. Thus, in addition to other pro-death functions, RIP1 regulates cellular sensitivity to pro-death stimuli by modulating basal autophagy.
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