| Project/Area Number |
15K07948
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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 |
Biological pharmacy
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| Research Institution | Toho University |
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Principal Investigator |
TADA Shusuke 東邦大学, 薬学部, 教授 (00216970)
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| Co-Investigator(Renkei-kenkyūsha) |
TSUYAMA Takashi 東邦大学, 薬学部, 助教 (70436096)
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| Research Collaborator |
NAKAZAKI Yuta
GOTO Yuki
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | Cdt1 / RecQ4 / DNA複製 / ゲノム安定性維持 / 新生鎖伸長反応 / BLM / 非相同末端結合修復 / geminin / ゲノム安定性維持機構 / gemnin / DNA鎖伸長反応 |
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| Outline of Final Research Achievements |
In this research, we explored how functions of Cdt1 and RecQ4, proteins known to play essential roles in DNA replication initiation, give influences on cellular mechanisms to maintain the genome stability. Previously, we have shown that Cdt1 suppresses nascent strand elongation during DNA replication. In this research, we newly obtained results suggesting that this effect is independent of the licensing activity of Cdt1 and does not need re-replication induced by additive Cdt1. Moreover, we showed that BLM, a product of a gene which mutation causes Bloom syndrome, and RecQ5 possibly suppresses severe effects of re-replication due to over expression of Cdt1 in cultured cells. For RecQ4, our results indicate that its N-terminal region inhibits Ku70/80 to bind DNA double strand break sites, and suppresses non-homologous end joining in cell free extracts.
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