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lüll Endoplasmic reticulum stress-induced cell death mediated by the proteasome Egger L; Madden DT; Rheme C; Rao RV; Bredesen DECell Death Differ 2007[Jun]; 14 (6): 1172-80Cells exposed to sustained endoplasmic reticulum (ER) stress undergo programmed cell death and display features typical of apoptosis, such as cysteine aspartyl protease (caspase) activation, cytochrome c release, and DNA fragmentation. Here, we show that the execution of cell death induced by ER stress is mediated via the proteasome. Inhibition of the proteasome by lactacystin prevented ER stress-induced degradation of Bcl-2, release of cytochrome c, processing of effector caspase-3, and exposure of phosphatidylserine. Owing to the ability of lactacystin to inhibit cytochrome c release, we propose that the pro-apoptotic activity of the proteasome lies upstream of mitochondrial activation. Thus, the proteasome serves as a principal mediator of ER stress-induced cell death in this system.|Acetylcysteine/analogs & derivatives/pharmacology[MESH]|Animals[MESH]|Apoptosis/drug effects/*physiology[MESH]|Blotting, Western[MESH]|Brefeldin A/pharmacology[MESH]|Caspase 3/metabolism[MESH]|Cells, Cultured[MESH]|Chlorhexidine/pharmacology[MESH]|Cytochromes c/metabolism[MESH]|DNA Fragmentation/drug effects[MESH]|Electrophoresis, Polyacrylamide Gel[MESH]|Endoplasmic Reticulum/drug effects/*metabolism[MESH]|Fibroblasts/cytology/drug effects/*metabolism[MESH]|Mitochondrial Membranes/metabolism[MESH]|Models, Biological[MESH]|Phosphatidylserines/metabolism[MESH]|Proteasome Endopeptidase Complex/*metabolism[MESH]|Proteasome Inhibitors[MESH]|Proto-Oncogene Proteins c-bcl-2/metabolism[MESH]|Rats[MESH]|Sulfones/pharmacology[MESH]|Temperature[MESH]|Ubiquitin-Activating Enzymes/genetics/metabolism[MESH] |