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Analysis of the DNA substrate specificity of the human BACH1 helicase associated with breast cancer.
FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein.
Inhibition of BACH1 (FANCJ) helicase by backbone discontinuity is overcome by increased motor ATPase or length of loading strand.
Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability.
Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency.
Loss of nuclear DNA ligase III reverts PARP inhibitor resistance in BRCA1/53BP1 double-deficient cells by exposing ssDNA gaps.
Unveiling the toxicity of single-stranded DNA gaps through a yeast model.
DNA Single Stranded