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. 2013 Apr 24;41(12):6109–6118. doi: 10.1093/nar/gkt304

Figure 4.

Figure 4.

DNA–PK and ATM-dependent nuclear-wide γH2AX and dose-dependent pan-nuclear pATM (S1981) and pDNA–PKcs (S2056). (A) Confluent human fibroblasts were treated with DMSO, ATM inhibitor (Ai), DNA–PKcs inhibitor (Di) or caffeine and irradiated with three xenon ions (∼18.3 Gy). (B) WT or ATM-deficient human fibroblasts (AT), treated with DMSO or DNA–PKcs inhibitor (Di), and (C) WT MEF, DNA–PK −/− MEF, treated with DMSO or ATM inhibitor (Ai), were irradiated with five nickel ions (∼12.5 Gy). Cells were fixed 1 h after irradiation, and pan-nuclear γH2AX was quantified. (D) Confluent human fibroblasts were irradiated with different numbers of gold ions (∼8.5 Gy/ion), and pan-nuclear pDNA–PKcs (S2056) or pATM (S1981) was quantified 1 h after irradiation. For comparison of pATM and pDNA–PKcs signal intensities, the values were normalized to the intensity in unirradiated cells. (E) Confluent human fibroblasts were treated with DMSO or both ATM and DNA–PKcs inhibitors (Ai + Di) 1 h before until 1 h after irradiation and reseeded 24 h after irradiation with different doses of X-rays or neon ions for the survival assay (N = 3). Solid lines show the linear quadratic (X-rays) or linear (neon) fit for each data set. Error bars denote SD (**P < 0.01, using two-sided U-test, number of analysed cells for immunofluorescence quantification: 84–1228 with an average of 268).