The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line.

Minoru Takata, Kazuhiko Yamamoto, Nobuko Matsushita, Hiroyuki Kitao, Seiki Hirano, Masamichi Ishiai

Research output: Contribution to journalReview articlepeer-review

6 Citations (Scopus)


Fanconi anemia (FA) is a rare hereditary disorder characterized by bone marrow failure, compromised genome stability, and increased incidence of cancer. FA is caused by abnormalities that occur in components of the FA core complex, a key factor FancD2, breast cancer susceptibility protein BRCA2/FancD1, or BRIP1/FancJ. These proteins are proposed to function in a common biochemical process (FA pathway), however, its precise role is still unclear. In this chapter, we will summarize our genetic analysis on the FA pathway using DT40 cells line. Our data revealed that (1) FA pathway promotes DNA repair mediated by homologous recombination, and likely regulates translesion synthesis, thereby protecting cells against stalled replication forks; (2) BLM helicase can be regarded as an effector molecule of the FA pathway, since its subnuclear localization is regulated by FA pathway; (3) the FA core complex has multiple roles in the activation, relocalization, and DNA repair function of FANCD2.

Original languageEnglish
Pages (from-to)295-311
Number of pages17
JournalSub-cellular biochemistry
Publication statusPublished - 2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology
  • Cancer Research


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