The Fanconi anemia pathway promotes homologous recombination repair in DT40 cell line.
作者： Minoru Takata , Kazuhiko Yamamoto , Nobuko Matsushita , Hiroyoki Kitao , Sciki Hirano
DOI: 10.1007/978-1-4020-4896-8_17
关键词:
摘要: Fanconi anemia (FA) is a rare hereditary disorder characterized by bone marrow failure, compromised genome stability, and increased incidence of cancer. FA caused abnormalities that occur in components the core complex, key factor FancD2, breast cancer susceptibility protein BRCA2/FancD1, or BRIP1/FancJ. These proteins are proposed to function common biochemical process (FA pathway), however, its precise role still unclear. In this chapter, we will summarize our genetic analysis on pathway using DT40 cells line. Our data revealed (1) promotes DNA repair mediated homologous recombination, likely regulates translesion synthesis, thereby protecting against stalled replication forks; (2) BLM helicase can be regarded as an effector molecule pathway, since subnuclear localization regulated pathway; (3) complex has multiple roles activation, relocalization, FANCD2.
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