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. 2015 May 26;112(23):7201–7206. doi: 10.1073/pnas.1421063112

Fig. 3.

Fig. 3.

Loss of Bok protects cells from ER stress-induced caspase-3/7 activation and annexin V exposure. (A and B) Caspase-3/7 activation in SV40-immortalized WT and Bok−/− cells at 24 h in response to the indicated concentrations of thapsigargin (TG), bortezomib (BTZ), etoposide (ETOP), or staurosporine (STS) (A), and at multiple time points with 10 μM TG, 10 μM BTZ, 10 μM ETOP, or 1 μM STS (B). Bars and lines represent relative fluorescence units (RFU). Dashed lines, vehicle; solid lines, treated. (C) Representative Western blot analysis for activated caspase-3 in SV40-immortalized WT and Bok−/− (KO) MEFs 16 h after treatment with vehicle, 2 μM TG, 1 μM BTZ, 2 μM BFA, 1 μM DTT, 2 μM A23187, 1 μM GELD, 1 μM STS, 1 μM ETOP, and 5 min of 100 J/m2 UV. (D) Percent annexin V-positive/7AAD-negative SV40-immortalized WT and Bok−/− cells treated for 12 h with vehicle, 10 μM TG, 10 μM BTZ, 10 μM ETOP, or 1 μM STS. All experiments were performed at least in triplicate. Error bars represent (A and B) SD or (D) SEM. Significance was calculated using an ANOVA test (**P < 0.005, ****P < 0.0001).