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 language | English |
|---|---|
| Pages (from-to) | 295-311 |
| Number of pages | 17 |
| Journal | Sub-cellular biochemistry |
| Volume | 40 |
| Publication status | Published - Jan 1 2006 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Biology
- Cell Biology
- Cancer Research
Cite this
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 journal › Review article
}
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.
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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 -