Fig. 7: Loss of VDAC2 reduces but does not abolish protection against apoptosis by Ctr-infection.
A Expression levels of VADC2/3 upon Ctr-infection. HeLa cells were infected with Ctr, and expression levels of VDAC2/3 were measured by Western blotting. No antibodies specific exclusively for VDAC2 are available. B HeLa wt or HeLa cells deficient in VDAC2 were infected with Ctr for 24 h and were then treated for an additional 4 h with the Bcl-2/Bcl-XL-inhibitor ABT-737 (1 µM) and the Mcl-1-inhibitor s63845 (500 nM). Apoptosis was measured by staining for cells containing active caspase-3. Data are means/SEM of three independent experiments. ****p < 0.0001, (ns, not significant) p > 0.05, two way Anova for multiple comparisons. C VDAC2-deficient HeLa cells reconstituted with human VDAC2 (hVDAC2), HeLa wt or HeLa cells lacking hexokinase 2 (HK2) were seeded and infected with Ctr for 24 h. Apoptosis was induced by the combination of ABT-737 (1 µM) and S63845 (500 nM) for 4 h and measured by flow cytometry for active caspase-3. Data are means/SEM of three independent experiments. ****p < 0.0001, **p < 0.01, (ns, not significant) p > 0.05, two way Anova for multiple comparisons.
