| Project/Area Number |
24651045
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KANAO Rie 名古屋大学, 環境医学研究所, 助教 (30542287)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 癌 / ゲノム / 放射線 / 遺伝子 / タンパク質 / DNA損傷トレランス / 細胞周期チェックポイント / DNA損傷 / DNA修復 / DNA複製 |
|---|
| Research Abstract |
Human Polh is the responsible gene product of xeroderma pigmentosum variant, a cancer prone syndrome. Polh catalyzes translesion DNA synthesis (TLS) past the most prominent UV-induced DNA lesion, cyclobutane pyrimidine dimer (CPD), very efficiently. On the other hand, Polh is unable to bypass another UV-induced DNA lesion, 6-4 photoproduct, resulting in the activation of cell cycle checkpoint mechanisms. This project aimes to address the relations between TLS and cell cycle checkpoint mechanisms. Expression of Polh or PCNA mutants affected cell cycle checkpoint, suggesting a linkage of TLS and checkpoint mechanisms in human cells.
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