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• W2024341906 startingPage "703" @default.
• W2024341906 abstract "Endoplasmic reticulum (ER) stress induces apoptosis by mechanisms that are not fully clear. Here we show that ER stress induced by the Ca(2+)-ATPase inhibitor thapsigargin (THG) activates cytochrome c-dependent apoptosis through cooperation between Bax and the mitochondrial permeability transition (MPT) in human leukemic CEM cells. Pharmacological inhibition of the MPT as well as small interfering RNA (siRNA) knockdown of the MPT core component cyclophilin D blocked cytochrome c release and caspase-dependent apoptosis but did not prevent Bax activation, translocation or N-terminal exposure in mitochondria. siRNA knockdown of Bax also blocked THG-mediated cytochrome c release and apoptosis, but did not prevent MPT activation and resulted in caspase-independent cell death. Our results show that ER-stress-induced cell death involves a caspase and Bax-dependent pathway as well as a caspase-independent MPT-directed pathway." @default.
• W2024341906 created "2016-06-24" @default.
• W2024341906 creator A5053800550 @default.
• W2024341906 creator A5061700569 @default.
• W2024341906 date "2006-12-15" @default.
• W2024341906 modified "2023-10-11" @default.
• W2024341906 title "Bax and the mitochondrial permeability transition cooperate in the release of cytochrome c during endoplasmic reticulum-stress-induced apoptosis" @default.
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• W2024341906 doi "https://doi.org/10.1038/sj.cdd.4402072" @default.
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