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. 2014 Oct 6;143(1):54–63. doi: 10.1093/toxsci/kfu207

FIG 4.

FIG 4.

Effect of ATM, ATR, and DNAPK inhibitors on H2AX phosphorylation in Cr(VI)-treated H460 cells. Asc-restored cells were treated for 3 h with Cr(VI). Histone H2A and tubulin served as loading controls. A, Formation of γH2AX and its ubiquitinated forms by 10 µM Cr(VI) in the presence of ATM-i1 (1 µM KU60019), DNAPK-i1 (30 µM NU7026), and ATR-i1 (3 µM ETP46464). “γH2AX-total” numbers indicate a total normalized intensity of all 3 bands after subtraction of the corresponding Cr-untreated controls. B, Uptake of Cr(VI) by H460 cells in the presence and absence of 3 µM ETP46464 (ATR-i1). Data are means ± SD for 3 independent samples. C, Western blot for γH2AX in H460 cells treated with Cr(VI) in the presence of a second set of inhibitors (ATM-i2—10 µM KU55933, DNAPK-i2—10 µM NU7441, ATR-i2—10 µM VE821). “γH2AX-total” numbers indicate a total normalized intensity of both γH2AX bands from 2 Western blots.