The experimental verification of saturated repair model by using repair reporter genes.
Project/Area Number |
26550025
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Risk sciences of radiation and chemicals
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Research Institution | Kyoto University |
Principal Investigator |
Komatsu Kenshi 京都大学, 放射線生物研究センター, 研究員 (80124577)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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Keywords | 相同組換え修復 / 非相同末端再結合 / 細胞生存曲線の肩 / saturated repair model / DNA修復 / 放射線 / Saturated repair model |
Outline of Final Research Achievements |
Present results confirmed the saturation of DNA repair by using the reporter genes, in which the homologous recombination repair functions within a limited region at a low dose. In contrast, non-homologous end-joining has constant activity irrespective of the radiation dose. As a result, the cells exposed to a low dose can survive due to both functional repair pathways: homologous recombination and non-homologous end-joining, while non-homologous end-joining is sole repair pathway at a higher dose. Thus, biological model based on repair activity of cells became plausible to explain the quasi-threshold of radiation survival curve.
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Report
(3 results)
Research Products
(27 results)
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[Journal Article] Relative contribution of four nucleases, CtIP, Dna2, Exo1 and Mre11, to the initial step of DNA double‐strand break repair by homologous recombination in both the chicken DT40 and human TK6 cell lines2015
Author(s)
Hoa NN, Akagawa R, Yamasaki T, Hirota K, Sasa K, Natsume T, Kobayashi J, Sakuma T, Yamamoto T, Komatsu K, Kanemaki MT, Pommier Y, Takeda S, Sasanuma H
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Journal Title
Genes to Cells
Volume: 20
Issue: 12
Pages: 1059-1076
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Mutations in the FHA-domain of ectopically expressed NBS1 lead to Radiosensitization and to no increase in somatic mutation rates via a partial suppression of homologous recombination2014
Author(s)
Maki Ohara, Yumi Funyu, Shunsuke Ebara, Yuki Sakamoto, Ryota Seki, Kenta Iijima, Akiko Ohishi, Junya Kobayashi, Kenshi Komatsu, Akira Tachibana, and Hiroshi Tauchi
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Journal Title
J. Radiat. Res
Volume: 55
Issue: 4
Pages: 690-698
DOI
Related Report
Peer Reviewed / Open Access
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[Presentation] NBS1物語2015
Author(s)
小松賢志
Organizer
日本放射線影響学会・放射線ワークショップ
Place of Presentation
富山
Year and Date
2015-10-16
Related Report
Invited
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