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 article

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)295-311
Number of pages17
JournalSub-cellular biochemistry
Volume40
Publication statusPublished - Jan 1 2006
Externally publishedYes

Fingerprint

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

Cite this

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.

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

Research output: Contribution to journalReview article

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, vol. 40, pp. 295-311.
Takata M, Yamamoto K, Matsushita N, Kitao H, Hirano S, Ishiai M. The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line. Sub-cellular biochemistry. 2006 Jan 1;40:295-311.
Takata, Minoru ; Yamamoto, Kazuhiko ; Matsushita, Nobuko ; Kitao, Hiroyuki ; Hirano, Seiki ; Ishiai, Masamichi. / The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line. In: Sub-cellular biochemistry. 2006 ; Vol. 40. pp. 295-311.
@article{41faf5cb63964c3786abc307b2d5c239,
title = "The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line.",
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.",
author = "Minoru Takata and Kazuhiko Yamamoto and Nobuko Matsushita and Hiroyuki Kitao and Seiki Hirano and Masamichi Ishiai",
year = "2006",
month = "1",
day = "1",
language = "English",
volume = "40",
pages = "295--311",
journal = "Sub-Cellular Biochemistry",
issn = "0306-0225",
publisher = "Plenum Publishers",

}

TY - JOUR

T1 - The fanconi anemia pathway promotes homologous recombination repair in DT40 cell line.

AU - Takata, Minoru

AU - Yamamoto, Kazuhiko

AU - Matsushita, Nobuko

AU - Kitao, Hiroyuki

AU - Hirano, Seiki

AU - Ishiai, Masamichi

PY - 2006/1/1

Y1 - 2006/1/1

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.

UR - http://www.scopus.com/inward/record.url?scp=34547486820&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34547486820&partnerID=8YFLogxK

M3 - Review article

C2 - 17623912

AN - SCOPUS:34547486820

VL - 40

SP - 295

EP - 311

JO - Sub-Cellular Biochemistry

JF - Sub-Cellular Biochemistry

SN - 0306-0225

ER -