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. 2019 Jun 14;34(1):50–62. doi: 10.1038/s41375-019-0497-6

Fig. 6.

Fig. 6

Re-expression of KDM6A suppresses cell growth and sensitizes cells to AraC therapy. ac Immunoblot showing doxycycline inducible re-expression of KDM6A in K562 KDM6A KO #1 PB KDM6A (a), KDM6A mutant THP-1 PB KDM6A (b) and K562 KDM6A KO #1 and #2 PB KDM6A H1146A cells (c) after treatment with 0.5 μg/mL doxycycline for 48 h. Blot is representative of two independent experiments. MW molecular weight, α-Tubulin loading control. d, e Proliferation assay measuring the amount of viable K562 KDM6A KO #1 PB KDM6A (d) and KDM6A mutant THP-1 PB KDM6A cells (e) in the absence or presence of doxycycline (0.5 μg/mL) every 2 days for 8 days. Mean ± s.d. are given for three independent experiments. Unpaired, two-tailed Student’s t-test; *P < 0.05; **P < 0.01; ***P < 0.001. fi AraC dose-response analysis after treatment for 72 h in K562 KDM6A KO #1 PB KDM6A and K562 KDM6A WT #1 (f), KDM6A mutant THP-1 PB KDM6A (g) and K562 KDM6A KO PB KDM6A H1146A cells (h,i) in the absence or presence of doxycycline (0.5 μg/mL). Mean ± s.d. are given for at least three independent experiments. Unpaired, two-tailed Student’s t-test; *P < 0.05; **P < 0.01; ***P < 0.001