New roads to FA/BRCA pathway: H2AX

Alex Lyakhovich, Jordi Surrallés

Research output: Contribution to journalReview articleResearchpeer-review

18 Citations (Scopus)


We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by γH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies. ©2007 Landes Bioscience.
Original languageEnglish
Pages (from-to)1019-1023
JournalCell Cycle
Issue number9
Publication statusPublished - 1 May 2007


  • BRCA2
  • DNA repair
  • FANCD2
  • Fanconi anemia
  • Histone H2AX
  • Stalled replication fork


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