Journal
CELL DEATH AND DIFFERENTIATION
Volume 24, Issue 9, Pages 1478-1487Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2017.82
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Funding
- FONDECYT [3150113, 1140549]
- FONDAP program [15150012]
- Millennium Institute [P09-015-F]
- European Commission RD MSCA-RISE [734749]
- Michael J Fox Foundation for Parkinson's Research - Target Validation grant [9277]
- FONDEF [ID16I10223, D11E1007]
- US Office of Naval Research-Global (ONR-G) [N62909-16-1-2003]
- U.S. Air Force Office of Scientific Research [FA9550-16-1-0384]
- ALSRP Therapeutic Idea Award [AL150111]
- Muscular Dystrophy Association [382453]
- CONICYT-Brazil [441921/2016-7]
- CONICYT fellowship
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In the last decade, the endoplasmic reticulum (ER) has emerged as a central organelle regulating the core mitochondrial apoptosis pathway. At the ER membrane, a variety of stress signals are integrated toward determining cell fate, involving a complex cross talk between key homeostatic pathways including the unfolded protein response, autophagy, calcium signaling and mitochondrial bioenergetics. In this context, key regulators of cell death of the BCL-2 and TMBIM/BI-1 family of proteins have relevant functions as stress rheostats mediated by the formation of distinct protein complexes that regulate the switch between adaptive and proapoptotic phases under stress. Here, we overview recent advances on our molecular understanding of how the apoptotic machinery integrates stress signals toward cell fate decisions upstream of the mitochondrial gateway of death.
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