Whilst our understanding of NHEJ-mediated repair of high-LET IR-induced DSB is emerging , there is much work to be done in resolving the functional mechanism of NHEJ at highly clustered lesions . How precisely Ku and DNA-PKcs are inhibited at clustered DSBs and how Artemis can function in their functional absence are important , unresolved questions . The role of DNA-PKcs autophosphorylation in the repair of high-LET IR-induced DSBs is also unclear , as is the interplay between NHEJ and other repair
Conflict of interest statement Authors have no competing interests .. Acknowledgements
Work in the AAG laboratory is supported by operating grants from the Canadian Institutes of Health Research and the Alberta Cancer Foundation . AAG is currently the Canada Research Chair for Genome Damage and Instability Disease and this work was undertaken , in part , thanks to funding from the Canada Research Chairs program .
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