The integrated stress response induces a common cell-autonomous death receptor 5-dependent apoptosis switch
Lopez Muniozguren, N.; Zappa, F.; Acosta-Alvear, D.
Show abstract
The integrated stress response (ISR) is a fundamental signaling network that reprograms the transcriptome and proteome to leverage the cells biosynthetic capacity against different stresses. Signaling plasticity is enabled by distinct ISR sensor kinases that detect specific perturbations. The ISR is dichotomous, with tailored homeostatic outputs and a terminal one engaged upon overwhelming stress. Through a chemical-genetics approach that uncouples natural stress inputs from ISR actuation, we show that the ISR engages an input-agnostic, cell-autonomous apoptosis mechanism that requires unconventional signaling by death receptor 5. Our results indicate that a common ISR mechanism eliminates terminally injured cells.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- A phosphorylation of RIPK3 kinase initiates an intracellular apoptotic pathway that promotes corpus luteum regression 96%
- Cytoplasmic mRNA decay represses RNA polymerase II transcription during early apoptosis 96%
- The integrated stress response remodels the microtubule organizing center to clear unfolded proteins following proteotoxic stress 95%
Similar papers in this journal
- Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics 93%
- Cytoplasmic innate immune sensing by the caspase-4 non-canonical inflammasome promotes cellular senescence. 93%
- Tumor growth of neurofibromin-deficient cells is driven by decreased respiration and hampered by NAD+ and SIRT3 92%
Similar papers in this journal
Similar papers in this journal
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.