RIP 1 negatively regulates basal autophagic flux through TFEB to control sensitivity to apoptosis
Copyright policy )RIP 1 negatively regulates basal autophagic flux through TFEB to control sensitivity to apoptosis
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.
- University of Colorado System United States
- University of Colorado Boulder United States
- University of Colorado Anschutz Medical Campus United States
- University of Colorado Denver United States
- University of Colorado Cancer Center United States
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Apoptosis, Fibroblasts, Mice, Gene Expression Regulation, Gene Knockdown Techniques, Receptor-Interacting Protein Serine-Threonine Kinases, Autophagy, Animals, Humans, Phosphorylation, Lysosomes, Cells, Cultured, HeLa Cells, Transcription Factors
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Apoptosis, Fibroblasts, Mice, Gene Expression Regulation, Gene Knockdown Techniques, Receptor-Interacting Protein Serine-Threonine Kinases, Autophagy, Animals, Humans, Phosphorylation, Lysosomes, Cells, Cultured, HeLa Cells, Transcription Factors
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