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. 2018 Nov 22;38:47–56. doi: 10.1016/j.ebiom.2018.11.025

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© 2018 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 4 — Induction of cytotoxic DSBs by BMN673 and NL101. Representative images of γ-H2AX foci in control, NL101, BMN673 (BMN), and combination treated (COM) MV4-11 (a) and HL-60 (b) cells. (c) Quantification of γ-H2AX foci from immunofluorescent images shown in a and b (*P < .05, **P < .01, One-way ANOVA,combination treatments versus control and single treatments). (d) Western blot analysis of the DNA damage sensors ATM, p-ATM (Ser1981), CHK1, p-CHK1 (Ser317), CHK2 and p-CHK2 (Thr68) in MV4-11 and HL-60 cells. GAPDH served as a loading control.(e)Western blot analysis of PAR at different time points in MV4-11 and HL-60 cells. GAPDH served as a loading control.