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: ジャーナルへの寄稿評論記事

6 引用 (Scopus)

抄録

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

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Fanconi Anemia
Recombinational DNA Repair
BRCA2 Protein
Repair
Cells
Cell Line
DNA
Bone
Genes
Chemical activation
Molecules
Proteins
Biochemical Phenomena
Genomic Instability
DNA Repair
Bone Marrow
Breast Neoplasms

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology
  • Cancer Research

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.

The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line. / Takata, Minoru; Yamamoto, Kazuhiko; Matsushita, Nobuko; Kitao, Hiroyuki; Hirano, Seiki; Ishiai, Masamichi.

:: Sub-cellular biochemistry, 巻 40, 01.01.2006, p. 295-311.

研究成果: ジャーナルへの寄稿評論記事

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, 巻. 40, pp. 295-311.
Takata, Minoru ; Yamamoto, Kazuhiko ; Matsushita, Nobuko ; Kitao, Hiroyuki ; Hirano, Seiki ; Ishiai, Masamichi. / The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line. :: Sub-cellular biochemistry. 2006 ; 巻 40. pp. 295-311.
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abstract = "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.",
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AU - Takata, Minoru

AU - Yamamoto, Kazuhiko

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AU - Kitao, Hiroyuki

AU - Hirano, Seiki

AU - Ishiai, Masamichi

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N2 - 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.

AB - 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.

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