Lack of active key apoptotic caspases delays ER stress–induced cell death. Caspase-3 and caspase-7 DKO and heterozygote MEFs were treated with tunicamycin (1 μg/mL) for the indicated times, and apoptotic loss of mitochondrial membrane potential ΔψM was analyzed by staining with MitoCapture and flow cytometry. (A) Representative plots are shown and the number of cells that have lost their ΔψM is indicated (mean and SEM of 2 independent experiments). The graph shows the number of apoptotic DKO and heterozygote MEFs. P values refer to the comparison of mean apoptosis rates between DKO and heterozygote MEFs, and asterisks indicate significant differences. (B) Immunoblotting with antibodies against BiP, GRP94, and GAPDH (control) carried out on extracts from DKO and heterozygote MEFs after treatment with tunicamycin (1 μg/mL) for the indicated times.