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FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein.

The BRCA1 associated C-terminal helicase (BACH1, designated FANCJ) is implicated in the chromosomal instability genetic disorder Fanconi anemia (FA) and hereditary breast cancer. A critical role of FANCJ helicase may be to restart replication as a component of downstream events that occur during the repair of DNA cross-links or double-strand breaks. We investigated the potential interaction of FANCJ with replication protein A (RPA), a single-stranded DNA-binding protein implicated in both DNA replication and repair. FANCJ and RPA were shown to coimmunoprecipitate most likely through a direct interaction of FANCJ and the RPA70 subunit. Moreover, dependent on the presence of BRCA1, FANCJ colocalizes with RPA in nuclear foci after DNA damage. Our data are consistent with a model in which FANCJ associates with RPA in a DNA damage-inducible manner and through the protein interaction RPA stimulates FANCJ helicase to better unwind duplex DNA substrates. These findings identify RPA as the first regulatory partner of FANCJ. The FANCJ-RPA interaction is likely to be important for the role of the helicase to more efficiently unwind DNA repair intermediates to maintain genomic stability.

Pubmed ID: 17596542


  • Gupta R
  • Sharma S
  • Sommers JA
  • Kenny MK
  • Cantor SB
  • Brosh RM



Publication Data

October 1, 2007

Associated Grants

  • Agency: Intramural NIH HHS, Id:

Mesh Terms

  • Basic-Leucine Zipper Transcription Factors
  • Cell Line
  • DNA Damage
  • DNA Helicases
  • DNA-Binding Proteins
  • Fanconi Anemia
  • Fanconi Anemia Complementation Group Proteins
  • Humans
  • Kinetics
  • Mutation
  • Protein Binding
  • RNA, Small Interfering
  • Replication Protein A