Ataxia telangiectasia and DNA-dependent protein kinase (DNA-PK) catalytic subunit-deficient cell lines efficiently form H2AX foci after exposure to ionizing.

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Ataxia telangiectasia and DNA-dependent protein kinase (DNA-PK) catalytic subunit-deficient cell lines efficiently form H2AX foci after exposure to ionizing radiation. Ataxia telangiectasia and DNA-dependent protein kinase (DNA-PK) catalytic subunit-deficient cell lines efficiently form H2AX foci after exposure to ionizing radiation. A, time course of H2AX foci formation after 2 Gy of γ-rays. Cells were grown to near confluence, irradiated, and sampled at the times indicated. Immunofluorescence was carried out using the phospho-specific anti-H2AX antibody (anti-H2AXSer139), and the number of γ-H2AX foci/cell was counted. Error bars represent the SD of the mean between among independent experiments. B, dose response of γ-H2AX foci sampled at 30 min postirradiation. C, the results of experiments in which the DNA-PK inhibitor LY294002 was added 30 min before irradiation. The legend is the same as that for B. 1BR3, AT1BR, AT7BI, F02-98, M059J, and M059K were examined. No induction of foci was observed in either AT1BR or AT7BI. Normal induction of foci was observed in 1BR3 and F02-98 cells, and higher induction of foci was observed in M059J and M059K cells. D, impact of LY294002 on the rate of loss of γ-H2AX foci in mouse embryo fibroblasts. LY294002 was added to the mouse embryo fibroblasts indicated 30 min before irradiation and maintained in medium until sampling. More foci persisted at 120 min postirradiation in DNA-PK−/− cells and in DNA-PK+/+ cells treated with LY294002. Tom Stiff et al. Cancer Res 2004;64:2390-2396 ©2004 by American Association for Cancer Research