DNA repair is more efficient in undifferentiated embryonal carcinoma cells. (A): Undifferentiated (−RA) and differentiated (+RA) NCCIT cells were irradiated with 4 or 15 Gy IR. The total and phosphorylated ATM, CHK1, CHK2, and p53 were measured by Western blot. (B): IR-induced DNA damage foci in undifferentiated (−RA) and differentiated (+RA) NCCIT cells at 0, 1.5, and 30 hours were localized by immunofluorescence using anti-γH2AX antibody. (C): Quantification of the percentage of cells with 0, <10, and >10 γH2AX foci per nucleus at 0, 1.5, and 30 hours after IR (3 Gy) in undifferentiated (−RA) and differentiated (+RA) NCCIT cells. Data represent means ± SD from two independent experiments. (D): Western blot analysis of γH2AX level at 0, 1.5, and 24 hours after IR (3Gy) in undifferentiated (−RA) and differentiated (+RA) NCCIT cells. Abbreviations: ATM, ataxia-telangiectasia mutated; ATMp, phospho-ATM; CHK1, checkpoint kinase 1; CHK1p, phospho-CHK1; CHK2, checkpoint kinase 2; CHK2p, phospho-CHK2; IR, ionizing radiation; p53p, phospho-p53; RA, retinoic acid.