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The BRCA1-associated protein BACH1 is a DNA helicase targeted by clinically relevant inactivating mutations.
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.
Human MutL-complexes monitor homologous recombination independently of mismatch repair.
FANCJ uses its motor ATPase to destabilize protein-DNA complexes, unwind triplexes, and inhibit RAD51 strand exchange.
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.
FANCJ/BACH1 acetylation at lysine 1249 regulates the DNA damage response.
BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ.
Assessing the link between BACH1 and BRCA1 in the FA pathway.
BACH1 is a DNA repair protein supporting BRCA1 damage response.
Inhibition of BACH1 (FANCJ) helicase by backbone discontinuity is overcome by increased motor ATPase or length of loading strand.
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.
Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome.
Hereditary breast cancer and the BRCA1-associated FANCJ/BACH1/BRIP1.
Fanconi anemia group J helicase and MRE11 nuclease interact to facilitate the DNA damage response.
Basic-Leucine Zipper Transcription Factors
FANCJ localization by mismatch repair is vital to maintain genomic integrity after UV irradiation.
Crosstalk between BRCA-Fanconi anemia and mismatch repair pathways prevents MSH2-dependent aberrant DNA damage responses.
FANCJ at the FORK.
Basic Leucine Zipper Transcription Factors