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Fig. 2 | Clinical Epigenetics

Fig. 2

From: H2AX phosphorylation at the sites of DNA double-strand breaks in cultivated mammalian cells and tissues

Fig. 2

γH2AX release from IR-irradiated cells. a Effect of relatively high IR doses (higher than 10 mGy). After IR action, H2AX histone is rapidly phosphorylated by ATM kinase or, in the absence of ATM, by DNA-PK at the sites of DSBs. γH2AX serves as a docking site for recruitment of DNA repair enzymes. The γH2AX level reaches its maximum at 30–60 min after IR, and after that, γH2AX gradually decreases from chromatin. Twenty-four hours after IR, a small population of cells containing γH2AX foci can still be observed. These foci presumably represent unrepairable DSBs of “complex structure”. Persistent DSBs lead to apoptosis or increase the potential risk of cancer in irradiated tissues. b Effect of low IR doses (less than 10 mGy). DDR is not fully activated after low-dose IR, and DSB repair is inefficient. γH2AX is induced in unirradiated neighboring cells due to the signal transduction from directly irradiated cells (bystander effect). The nature of signaling is not understood, and it has not been shown yet whether γH2AX foci in bystander cells represent physical DSBs

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