| Project/Area Number |
21221003
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| Research Category |
Grant-in-Aid for Scientific Research (S)
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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 | The University of Tokyo |
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Principal Investigator |
MITANI Hiroshi 東京大学, 新領域創成科学研究科, 教授 (70181922)
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| Co-Investigator(Kenkyū-buntansha) |
NODA Asao (財)放射線影響研究所, 遺伝学部, 副部長 (40294227)
FUJIWARA Tomoko 大阪大学, 医学系研究科, 助教 (70402922)
TAKANO Yoshiro 東京医科歯科大学, 大学院医科歯学総合研究科, 教授 (90126425)
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| Co-Investigator(Renkei-kenkyūsha) |
ODA Shoji 東京大学, 大学院新領域創成科学研究科, 准教授 (50266714)
ASAKA Tomomi 東京大学, 大学院新領域創成科学研究科, 特任研究員 (90555707)
YASUDA Takako 東京大学, 大学院新領域創成科学研究科, 特任研究員 (40450431)
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| Research Collaborator |
漆原 祐介
村田 泰彦
五十嵐 健人
張 添翼
大西 壽子
塩谷 典子
伊藤 加津沙
西谷 彩香
平川 慶
永田 健斗
橋本 知佳
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| Project Period (FY) |
2009-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥99,190,000 (Direct Cost: ¥76,300,000、Indirect Cost: ¥22,890,000)
Fiscal Year 2013: ¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2012: ¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2011: ¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2010: ¥17,030,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥3,930,000)
Fiscal Year 2009: ¥27,950,000 (Direct Cost: ¥21,500,000、Indirect Cost: ¥6,450,000)
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| Keywords | 放射線 / 突然変異 / メダカ / マウス / 細胞死 / 生殖細胞 / 咽頭歯 / DNA修復 |
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| Outline of Final Research Achievements |
A complex network of signaling proteins sense radiation-induced DNA damage and activates the cellular response, which activates cell-cycle checkpoint, DNA repair and apoptosis. The defects in this process lead to mutation, cancer, and cellular death. However, the comparison of mutation frequency among cells in various kind of tissue is very hard to study. In this project, we used mouse and medaka as model animal to analyze the radiation responses in tissue. We reported that the cell lines from radiation-sensitive mutant medaka strain has a defect in the Histone H2AX phosphorylation after irradiation and its low level of DNA-PK activity causes aberrant DNA-PKcs autophosphorylation. We also found novel roles of radiation induced apoptosis in tissue response including testis-ova in p53 deficient mutant medaka. The visualization of mutagenesis and apoptosis in mouse and medaka tissue was developed to detect radiation response in tissue.
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| Assessment Rating |
Verification Result (Rating)
A-
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