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Updated: Apr 26, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
Published on: March 5, 2018
ER stress responses in the absence of apoptosome: a comparative study in CASP9 proficient vs deficient mouse
Shane Deegan1, Svetlana Saveljeva1, Sanjeev Gupta2
1Apoptosis Research Centre, NUI Galway, Ireland; School of Natural Sciences, NUI Galway, Ireland.
Abstract:
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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