Non-redundant Functions of ATM and DNA-PKcs in Response to DNA Double-Strand Breaks
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Both ATM and DNA-PKcs are recruited at AsiSI-induced DSBs

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Once recruited, both kinases exhibit complementary and non-redundant functions

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DNA-PKcs activity is required for end joining at all AsiSI-induced DSBs

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ATM activity promotes repair accuracy, H2AX phosphorylation, and DSB clustering

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