Figure 3
Figure 3. XIAP inhibition enhances TRAIL-induced activation of caspases. Jurkat leukemia cells were left untreated or were treated with 0.4 ng/mL TRAIL and/or 10 nM XIAP inhibitor 2, control compound, or DMSO for indicated times. (A) Caspase activation was analyzed by Western blotting. Arrowheads indicate caspase cleavage fragments; the asterisks mark unspecific bands. (B) Caspase activity was determined by FACS analysis as described in “Methods,” and x-fold increase in caspase activity is shown. (C) Jurkat leukemia cells were left untreated (□) or were treated for 72 hours with indicated concentrations of TRAIL and/or 10 nM XIAP inhibitors, control compound, or DMSO and 20 μM zVAD.fmk, 50 μM zDEVD.fmk, or DMSO. Apoptosis was determined by forwardside scatter analysis and flow cytometry. Mean and SD of 3 experiments each performed in triplicate are shown.

XIAP inhibition enhances TRAIL-induced activation of caspases. Jurkat leukemia cells were left untreated or were treated with 0.4 ng/mL TRAIL and/or 10 nM XIAP inhibitor 2, control compound, or DMSO for indicated times. (A) Caspase activation was analyzed by Western blotting. Arrowheads indicate caspase cleavage fragments; the asterisks mark unspecific bands. (B) Caspase activity was determined by FACS analysis as described in “Methods,” and x-fold increase in caspase activity is shown. (C) Jurkat leukemia cells were left untreated (□) or were treated for 72 hours with indicated concentrations of TRAIL and/or 10 nM XIAP inhibitors, control compound, or DMSO and 20 μM zVAD.fmk, 50 μM zDEVD.fmk, or DMSO. Apoptosis was determined by forwardside scatter analysis and flow cytometry. Mean and SD of 3 experiments each performed in triplicate are shown.

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