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• W2000962968 abstract "In this study, we used calnexin-deficient cells to investigate the role of this protein in ER stress-induced apoptosis. We found that calnexin-deficient cells are relatively resistant to ER stress-induced apoptosis. However, caspase 3 and 8 cleavage and cytochrome c release were unchanged in these cells, indicating that ER to mitochondria communication during apoptotic stimulation is not affected in the absence of calnexin. The Bcl-2:Bax ratio was also not significantly changed in calnexin-deficient cells regardless of whether the ER stress was induced with thapsigargin or not. Ca(2+) homeostasis and ER morphology were unaffected by the lack of calnexin, but ER stress-induced Bap31 cleavage was significantly inhibited. Immunoprecipitation experiments revealed that Bap31 forms complexes with calnexin, which may play a role in apoptosis. The results suggest that calnexin may not play a role in the initiation of the ER stress but that the protein has an effect on later apoptotic events via its influence on Bap31 function." @default.
• W2000962968 created "2016-06-24" @default.
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• W2000962968 date "2002-01-26" @default.
• W2000962968 modified "2023-10-14" @default.
• W2000962968 title "Calnexin Deficiency and Endoplasmic Reticulum Stress-Induced Apoptosis" @default.
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• W2000962968 doi "https://doi.org/10.1021/bi015967+" @default.
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