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

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

研究成果: Contribution to journalReview article

6 引用 (Scopus)

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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.

元の言語英語
ページ(範囲)295-311
ページ数17
ジャーナルSub-cellular biochemistry
40
出版物ステータス出版済み - 1 1 2006
外部発表Yes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology
  • Cancer Research

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  • これを引用

    Takata, M., Yamamoto, K., Matsushita, N., Kitao, H., Hirano, S., & Ishiai, M. (2006). The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line. Sub-cellular biochemistry, 40, 295-311.