ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts
2014
Deegan, Shane | Saveljeva, Svetlana | Gupta, Sanjeev | MacDonald, David C | Samali, Afshin
Cells respond to endoplasmic reticulum (ER) stress through the unfolded protein response (UPR), autophagy and cell death. In this study we utilized casp9+/+ and casp9−/− MEFs to determine the effect of inhibition of mitochondrial apoptosis pathway on ER stress-induced-cell death, UPR and autophagy. We observed prolonged activation of UPR and autophagy in casp9−/− cells as compared with casp9+/+ MEFs, which displayed transient activation of both pathways. Furthermore we showed that while casp9−/− MEFs were resistant to ER stress, prolonged exposure led to the activation of a non-canonical, caspase-mediated mode of cell death.
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