Unknown

Dataset Information

0

RIP1 negatively regulates basal autophagic flux through TFEB to control sensitivity to apoptosis.


ABSTRACT: 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.

SUBMITTER: Yonekawa T 

PROVIDER: S-EPMC4467854 | biostudies-other | 2015 Jun

REPOSITORIES: biostudies-other

altmetric image

Publications

RIP1 negatively regulates basal autophagic flux through TFEB to control sensitivity to apoptosis.

Yonekawa Tohru T   Gamez Graciela G   Kim Jihye J   Tan Aik Choon AC   Thorburn Jackie J   Gump Jacob J   Thorburn Andrew A   Morgan Michael J MJ  

EMBO reports 20150423 6


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 negativel  ...[more]

Similar Datasets

| S-EPMC5656243 | biostudies-literature
| S-EPMC6411943 | biostudies-literature
| S-EPMC7686991 | biostudies-literature
| S-EPMC5520384 | biostudies-literature
| S-EPMC8184677 | biostudies-literature
| S-EPMC10341959 | biostudies-literature
| S-EPMC6526833 | biostudies-literature
| S-EPMC7141596 | biostudies-literature
| S-EPMC4527287 | biostudies-literature
| S-EPMC4207479 | biostudies-literature