Fig. 3: Loss of TRAF6 in leukemia cells induces the changes in the mitochondrial function parameters.
From: Metabolic reprogramming regulated by TRAF6 contributes to the leukemia progression
A Representative flow cytometry histograms of mitochondrial TMRE levels in HEL cells expressing shTRAF6 or shControl (shCtrl). B Median fluorescent intensity (MFI) of tetramethylrhodamine ethyl ester (TMRE) observed from HEL cells expressing shTRAF6 or shCtrl. Data are presented as the means ± SD from biological replicates (n = 3). Results are representative of two independent assays. C Oxygen consumption rate (OCR) in HEL cells transduced with the inducible shTRAF6. Cells were sequentially treated with oligomycin, fluoro-carbonyl cyanide phenylhydrazone (FCCP), and rotenone/antimycin A at the indicted time points. Data are presented as the means ± SD from technical replicates (n = 4). Results are representative of three independent assays. D Basal respiration, maximal respiration, ATP production and spare respiratory capacities of HEL cells transduced with the inducible shTRAF6 calculated from the data of (C). Data are shown as the means ± SD (n = 4). E Representative flow cytometry histograms of mitochondrial TMRE levels in MLL-AF9;Traf6+/+ and MLL-AF9;Traf6−/− leukemic cells. F MFI of TMRE observed from MLL-AF9;Traf6+/+ and MLL-AF9;Traf6−/− leukemic cells. Data are presented as the means ± SD from biological replicates (n = 6). Results are representative of two independent assays. G OCR in MLL-AF9;Traf6+/+ and MLL-AF9;Traf6−/− leukemic cells. Cells were sequentially treated with oligomycin, FCCP, and rotenone/antimycin A at the indicted time points. Data are presented as the means ± SD from technical replicates (n = 6). Results are representative of two independent assays. H Basal respiration, maximal respiration, ATP production and spare respiratory capacities of MLL-AF9;Traf6+/+ and MLL-AF9;Traf6−/− leukemic cells calculated from the data of (G). Data are shown as the means ± SD (n = 6). **, P < 0.01; ***, P < 0.001.
