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Deegan, S,Saveljeva, S,Gupta, S,MacDonald, DC,Samali, A
Biochemical And Biophysical Research Communications
ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts
WOS: 1 ()
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Endoplasmic reticulum (ER) stress Apoptosis Autophagy Unfolded protein response (UPR) Caspase ENDOPLASMIC-RETICULUM STRESS CELL-DEATH AUTOPHAGY PROTEIN ACTIVATION CLEAVAGE KINASES PATHWAY
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. (C) 2014 Elsevier Inc. All rights reserved.
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