| Project/Area Number |
14572144
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human genetics
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| Research Institution | Kumamoto University |
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Principal Investigator |
TATEISHI Satoshi Kumamoto University, Inst.Mol.Embryol. & Genet., Lecturer, 発生医学研究センター, 講師 (00227109)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | RAD18 / postreplication repair / translesion synthesis / ubiquitin / PCNA / polymerase / ノックアウマウス / DNA修復 / 複製後修復 / Rad18 / ゲノムの安定性 |
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| Research Abstract |
DNA polymerase often stalls at damaged sites on templates, however usually restarts by switching to special DNA polymerases that carry out translesion synthesis (TLS). DNA damaged sites, which is a crucial step for UV-induced TLS. We establish RAD18-/-cell lines and show that pol eta accumulates at replication foci in Rad18 depended manner, resulting in co-localization foci, suggesting that Rad18 recruit pol eta to the site. PCNA is mono-ubiquitinated in Rad18 and hHR6-dependent manner. In vitro, purified Rad18 and Rad6 mono-ubiquitinates PCNA. In our model, Rad18 is a crucial molecule for recruitment and replacement of DNA polymerase eta. We established Rad18-KO mice and observed those pherotypes including sensitivity to radiation.
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