Abstract
<p>Figure S1. Inhibition of DNA-PK activity by M3814 overactivates the p53 response to radiation-induced DSBs. Figure S2. The inactive M3814 enantiomer, M3814R, does not enhance the p53 response to IR and M3814. Figure S3. IR plus M3814 treatment induces different cell cycle responses in p53 wild-type and p53-deficient cancer cells. Figure S4. Irradiated p53 wild-type and p53-deficient cells respond differently to M3814. Figure S5. IR plus M3814 treatment induces premature senescence in p53 wild-type cancer cells. Figure S6. Analyses and functional validation of p53 knock-out clones. Figure S7. p53 determines the fate of A549 cancer cells exposed to IR and M3814. Figure S8. p53 is responsible for the strong cell cycle arrest in irradiated HT-1080 cells exposed to IR and M3814.</p>
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