| Project/Area Number |
13557010
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
General medical chemistry
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TAKEDA Shunichi Kyoto University, Faculty of Medicine, Professor, 医学研究科, 教授 (60188191)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Daisuke Kirin Brewery Co., LTD. Basic Technology Institute Researcher, 基盤技術研究所, 研究員
YAMAZOE Mitsuyoshi Kyoto University, Faculty of Medicine, Assistant Professor, 医学研究科, 助手 (00284745)
SONODA Eiichiro Kyoto University, Faculty of Medicine, Associate Professor, 医学研究科, 助教授 (50281093)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,800,000 (Direct Cost: ¥13,800,000)
Fiscal Year 2002: ¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 2001: ¥8,000,000 (Direct Cost: ¥8,000,000)
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| Keywords | DNA damage / DNA replication / Translesion DNA synthesis / Homologous DNA recombination / DNA polymerase / DT40 / Sister chromatid exchange / 相同DM組換え / 相同DNA組み換え / DNA修復 / チェックポイント / DT40細胞 / 遺伝子治療 |
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| Research Abstract |
During each cell cycle replication forks inevitably stall at damaged DNA. The ability to overcome DNA lesions is an essential feature of the replication machinery. A large variety of specialized polymerases have recently been discovered that enable cells to replicate past various forms of damage. Alternatively homologous recombination can be used to restart DNA replication across the lesion. Genetic studies have shed light on the impact of these two post replication repair pathways in bacteria and yeast. In vertebrates, however, a genetic approach to study post replication repair has been compromised because most of the genes involved appear to be essential for embryonic development. We have taken advantage of the chicken cell line DT40 to perform a genetic analysis of translesion synthesis and homologous recombination and to characterize genetic interactions between these two pathways in vertebrates. In this article we aim to summarize our current understanding of post replication repair in DT40 in the perspective of results from other model systems.
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