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. 2006 Mar 23;34(6):1685–1691. doi: 10.1093/nar/gkl108

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© The Author 2006. Published by Oxford University Press. All rights reserved

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Model for ATM activation following PARP inhibition. PARP inhibition results in more collapsed replication forks, probably because of an inability to efficiently repair endogenous SSBs (20). HR is the most important pathway for repair of collapsed replication forks in mammalian cells (32,33) and loss of this pathway results in lethality following PARP inhibition (20). Our data suggests that the HRR pathway involves an ATM signal, which would explain the increased sensitivity to PARP inhibitors in AT cells. In addition our data also imply that a second pathway involving DNA-PK and ATM is required in survival following PARP inhibition, this is most likely to be NHEJ.