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. 2013 Oct 11;288(47):33654–33666. doi: 10.1074/jbc.M113.518134

FIGURE 3.

FIGURE 3.

Caspase-8 activation contributes to ABT-263-induced apoptosis. A, HCT116 or DLD1 cells were incubated with ABT-263 (24 h) and caspase-8 activity was measured with a luminescent activity assay kit. The mean values are shown from assays performed in triplicate. Error bars, S.D. B and C, ability of ABT-263 to induce caspase cleavage was analyzed in cells with caspase-8 knockdown by siRNA (B) or in caspase-8-deficient I9.2 cells versus parental Jurkat cells (C). D, effect of wild-type (+/+) or Bax knock-out (−/−) status on caspase cleavage was determined in HCT116 cells treated with ABT-263 (48 h). E, effect of a caspase-3 inhibitor, Z-DEVD-FMK (50 μm), on ABT-263-induced caspase-8 and -3 cleavage is shown in HCT116 cells. F, FADD-deficient I2.1 cells versus parental Jurkat cells were treated with ABT-263 + chloroquine (CQ), and caspase cleavage was then examined. G, effect of Bax knockdown by shRNA in DLD-1 cells was determined in cells treated with ABT-263 (2 μm) alone or combined with chloroquine (25 μm) and/or bortezomib (bort, 20 nm).