| Project/Area Number |
12358010
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
環境影響評価(含放射線生物学)
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| Research Institution | Nara Medical University |
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Principal Investigator |
OHNISHI Takeo Nara Medical University, Department of Biology, Professor, 医学部, 教授 (60094554)
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| Co-Investigator(Kenkyū-buntansha) |
KOMATSU Kenshi Kyoto University, Radiationbiology Center, Professor, 放生研, 教授 (80124577)
NIWA Ootsura Kyoto University, Radiation Biology Center, Professor, 放生研, 教授 (80093293)
UTSUMI Hiroshi Kyoto University, Research Reactor Institute, Professor, 原子炉, 教授 (20025646)
WATANABE Masami Nagasaki University, School of Pharmaceutical Sciences, Professor, 薬学部, 教授 (20111768)
NORIMURA Toshiyuki University of Occupational & Environmental health, Department of RadiationBiology & Health, Professor, 医学部, 教授 (20039530)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥44,740,000 (Direct Cost: ¥38,200,000、Indirect Cost: ¥6,540,000)
Fiscal Year 2002: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2001: ¥19,500,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥4,500,000)
Fiscal Year 2000: ¥16,400,000 (Direct Cost: ¥16,400,000)
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| Keywords | low dose and low dose-rate radiation / p53 / signal transduction / adaptation / apoptosis / cellcycle / mutation / gnome instability |
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| Research Abstract |
1. Sensor
(1) Chronic irradiation stimulated the decay of accumulated wtp53 by NO-mediated bystander effect, suggesting that this stimulation of the decay may be due to the degradation of p53 by Hdm2 activated by chronic irradiation. (Matsumoto, H.)
(2) We showed here a two-step mechanism for damage recognition, where NBS1 recruits Mrel1 nuclease by interaction to histone H2AX, and then Mrel 1 binds to damaged DNA for initiation of homologous recombination. (Komatsu, K.)
2. Signal transaction
(1) Low-level radiation did not induce signal translation pathway from nucleolus, but did ERK1/2 pathway for phosholizing histon HB. (Watanabe, M.)
(2) In the radioadaptive response of the whole body system in mice, we clarified importance of the window of low dose and the intervals after a conditioning irradiation as an indicator of challenging irradiation-induced apoptosis through a p53 tumor suppressor protein. (Ohnishi, T.)
3. Function
(1) Radiosensitive mouse thymic lymphoma 3SB cell line exhibited apoptotic cell death shortly after exposure to ionizing radiation and showed little dose rate response to radiation-induced apoptosis. (Suzuki, K)
(2) We found that the enhanced cell survival by low-dose rate irradiation owe to not HR but NHEJ repair pathway of DSB repair using the chicken DT40mutant cells. (Utsumi, H.)
(3) Complete repair of genotoxic damage requires the two mechanisms, p53-dependent apoptotic tissue repair as well as the well-known DNA repair. (Norimura, T.)
(4) Molecular nature of mutants induced by low dose of radiation has been compared between somatic tissues and germ line cells, and a significant difference was observed. (Ono, T.)
(5) The frequency of mutation at the maternally derived pink-eyed unstable allele was elevated in the retinal pigment epithelium in Fl mouse born to irradiated sperm, suggesting induction of delayed mutation by DNA damage in sperm. (Niwa, 0.)
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