BLM and BRCA1-BARD1 coordinate complementary mechanisms of joint DNA molecule resolution.
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The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity.
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PGBD5 promotes site-specific oncogenic mutations in human tumors.
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BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks.
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TopBP1 interacts with BLM to maintain genome stability but is dispensable for preventing BLM degradation.
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