Previous studies in vitro have demonstrated that clustered lesions containing base damage and AP sites in opposite strands can be partially processed by the base excision repair enzymes to generate DSBs ( 6 , 7 ) and it has been hypothesized that these clustered lesions maybe biologically highly significant due to the inability of cellular enzymes to completely repair the clustered lesions ( 8 , 9 ).
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DNA repair of clustered lesions in mammalian cells: involvement of non-homologous end-joining.
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