| Project/Area Number |
25340031
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | DSB修復 / M期 / ゲノム不安定化 / XRCC4 / 非相同末端結合 |
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| Outline of Final Research Achievements |
Double-strand break (DSB) is the most severe types of DNA damage. To maintain genomic stability, cells possess several checkpoints and DNA repair mechanisms that respond to DNA damage during the G1, S, and G2 phases. A defect in these processes results in apoptosis, aneuploidy, or translocation. However, mitotic cells are known to suppress DSB repair, although the biological significance of the suppression is unknown. This study showed that DSB repair, which prevents genomic instability in other cell cycle phases, is rather toxic to mitotic cells. During mitosis, phosphorylation of XRCC4, a factor of DSB repair, suppresses DSB repair and plays important roles to prevent aberrant chromosome segregation.
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