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. 2015 Oct 13;10(10):e0139812. doi: 10.1371/journal.pone.0139812

Fig 5. Effect of TCERG1 on staurosporine-mediated apoptosis involves changes in mitochondrial membrane permeabilization and in the emergence of the active form of Bak.

Fig 5

(A) TCERG1 knockdown decreases the mitochondrial membrane potential dissipation caused by staurosporine. Control and TCERG1-knockdown (KD) Jurkat cells were incubated without (-STAU) or with 0.5 μM staurosporine (+STAU) for 1 h and stained with JC-1 dye. Green fluorescence was measured by flow cytometry, and the data were analyzed using FlowJo software. The bar diagram shows the quantification of JC-1 monomers from two independent experiments (means ± SEM). *, p < 0.05. (B) TCERG1 mRNA interference decreases the mitochondrial membrane potential dissipation caused by oxaliplatin in Jurkat cells. Control and shTCERG1 Jurkat cells were incubated without (-OXALIP) or with 20 μM oxaliplatin (+OXALIP) for 18 h and stained with JC-1 dye. Green fluorescence was measured by flow cytometry, and the data were analyzed using CellQuest and GraphPad software. The bar diagram shows the quantification of JC-1 monomers from two independent experiments (means ± SEM). **, p < 0.01. (C) Changes in Bak-associated fluorescence were quantified by flow cytometry after intracellular staining with the Ab-1 antibody. (D and E) The release of cytochrome c was analyzed by flow cytometry and immunofluorescence. The graphs show data from three independent experiments (means ± SEM). *, p < 0.05, **, p < 0.01.