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. 2003 May 19;197(10):1323–1334. doi: 10.1084/jem.20021952

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Copyright © 2003, The Rockefeller University Press

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Figure 5. — Activation of Bax and Bak by NFX* and CPX through a p53-independent mechanism. (A) Conformational change of Bax and Bak. Cells were stained with monoclonal antibodies recognizing the apoptotic conformation of Bax (6A7) and Bak (Ab-1) 8 h after treatment with NFX* or CPX. (B) Time course of lysosomal and mitochondrial permeabilization induced by NFX* and CPX, as determined by staining with LysoTracker Red and DiOC₆(3) in unfixed cells. (C) Kinetics of NFX*- and CPX-induced lysosomal cathepsin B release, Bax activation (determined as in A), mitochondrial cytochrome c release, and caspase-3 activation, as determined by immunofluorescence of fixed and permeabilized cells. Results are representative of three experiments. (D) Failure of NFX* and CPX to activate p53-dependent transcription. Cells were transfected with a p53-inducible GFP reporter construct, and the percentage of cells expressing GFP was determined by FACS^® analysis. DNA damage by etoposide served as positive control. (E) Failure of pifithrin-α to inhibit NFX*- and CPX-induced cell death. Cells were pretreated for 60 min with the p53 inhibitor pifithrin-α, and the frequency of (DiOC₆(3)^low) and death (PI^high) was determined by cytofluorometry.

Inline graphic — Activation of Bax and Bak by NFX* and CPX through a p53-independent mechanism. (A) Conformational change of Bax and Bak. Cells were stained with monoclonal antibodies recognizing the apoptotic conformation of Bax (6A7) and Bak (Ab-1) 8 h after treatment with NFX* or CPX. (B) Time course of lysosomal and mitochondrial permeabilization induced by NFX* and CPX, as determined by staining with LysoTracker Red and DiOC₆(3) in unfixed cells. (C) Kinetics of NFX*- and CPX-induced lysosomal cathepsin B release, Bax activation (determined as in A), mitochondrial cytochrome c release, and caspase-3 activation, as determined by immunofluorescence of fixed and permeabilized cells. Results are representative of three experiments. (D) Failure of NFX* and CPX to activate p53-dependent transcription. Cells were transfected with a p53-inducible GFP reporter construct, and the percentage of cells expressing GFP was determined by FACS^® analysis. DNA damage by etoposide served as positive control. (E) Failure of pifithrin-α to inhibit NFX*- and CPX-induced cell death. Cells were pretreated for 60 min with the p53 inhibitor pifithrin-α, and the frequency of (DiOC₆(3)^low) and death (PI^high) was determined by cytofluorometry.