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Human MutL-complexes monitor homologous recombination independently of mismatch repair.
Assessing the link between BACH1/FANCJ and MLH1 in DNA crosslink repair.
An MLH1 mutation links BACH1/FANCJ to colon cancer, signaling, and insight toward directed therapy.
The FANCJ/MutLalpha interaction is required for correction of the cross-link response in FA-J cells.
Targeting the FANCJ-BRCA1 interaction promotes a switch from recombination to poleta-dependent bypass.
Adaptor Proteins, Signal Transducing
Crosstalk between BRCA-Fanconi anemia and mismatch repair pathways prevents MSH2-dependent aberrant DNA damage responses.
Adaptor Proteins Signal Transducing