ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts

Shane Deegan; Svetlana Saveljeva; Sanjeev Gupta; David C. Macdonald; Afshin Samali

doi:10.1016/j.bbrc.2014.07.111

ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts

Shane Deegan, Svetlana Saveljeva, Sanjeev Gupta, David C. Macdonald, Afshin Samali

University of Galway

Research output: Contribution to a Journal (Peer & Non Peer) › Article › peer-review

2 Citations (Scopus)

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.

Original language	English
Pages (from-to)	367-373
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	451
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2014.07.111
Publication status	Published - 29 Aug 2014

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Authors
Deegan, S,Saveljeva, S,Gupta, S,MacDonald, DC,Samali, A

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10.1016/j.bbrc.2014.07.111

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title = "ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts",

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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ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts. / Deegan, Shane; Saveljeva, Svetlana; Gupta, Sanjeev et al.
In: Biochemical and Biophysical Research Communications, Vol. 451, No. 3, 29.08.2014, p. 367-373.

Research output: Contribution to a Journal (Peer & Non Peer) › Article › peer-review

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T1 - ER stress responses in the absence of apoptosome

T2 - A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts

AU - Deegan, Shane

AU - Saveljeva, Svetlana

AU - Gupta, Sanjeev

AU - Macdonald, David C.

AU - Samali, Afshin

PY - 2014/8/29

Y1 - 2014/8/29

N2 - 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.

AB - 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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JO - Biochemical and Biophysical Research Communications

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ER -

ER stress responses in the absence of apoptosome: A comparative study in CASP9 proficient vs deficient mouse embryonic fibroblasts

Abstract

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