Fig. 6 Caspase-3– and -7–deficient cells maintain mitochondrial membrane polarity following intrinsic or extrinsic apoptotic stimuli. Caspase-3– and -7–deficient.

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Fig. 6 Caspase-3– and -7–deficient cells maintain mitochondrial membrane polarity following intrinsic or extrinsic apoptotic stimuli. Caspase-3– and -7–deficient cells maintain mitochondrial membrane polarity following intrinsic or extrinsic apoptotic stimuli. (A) TMRE staining and (B) quantification of mean TMRE signal in NALM6 WT and caspase-3/7 knockout cells treated with ABT263 (5 μM) for the indicated time points. TMRE flow cytometry measurements (A and C) and quantification plot (B and D) of NALM6 WT and caspase-3/7 knockout cells treated with Birinapant (50 nM) and TNF (10 ng/ml) for the indicated time points. Cytochrome c release measurement by flow cytometry (E) and its corresponding quantification graph (F) of NALM6 WT and caspase-3/7 knockout cells untreated (control) or treated with ABT263 (5 μM). Flow cytometry graphs are representative images of three independent experiments. Quantification graphs show the mean from three independent experiments ± SEM. (G) Graphical model of feedback activation by caspase-3 and -7 upon apoptotic stimulation. Histograms show representative data from at least three independent experiments performed in duplicate, with the mean from these ± SEM presented in the line or bar graphs. Scott McComb et al. Sci Adv 2019;5:eaau9433 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).