| Project/Area Number |
17591286
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | NAGOYA CITY UNIVERSITY |
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Principal Investigator |
MASUDA Kazuhiko Nagoya City University, Graduate School of Medical Sciences, Research Associate, 大学院医学研究科, 助手 (00381799)
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| Co-Investigator(Kenkyū-buntansha) |
MIYOSHI Ichiro Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院医学研究科, 助教授 (10183972)
AGUI Takashi Hokkaido University, Graduate School of Veterinary Medicine, Professor, 大学院獣医学研究科, 教授 (00212457)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | radiation hypersensitivity / responsible gene / linkage analysis / Quantitative trait loci (QTL) / 細胞周期 |
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| Research Abstract |
The LEC rat has been reported to exhibit X-ray hypersensitivity, and Quantitative trait loci (QTL) linkage analysis revealed that the specific region on Chromosomes (Chr) 4 has a very strong linkage to the X-ray hypersensitive phenotype. The present study was performed as the first step to compare between the coding sequences of several genes located on this region of Chr 4 in the wild type rat and the LEC rat, and to try to identify the changes in deduced amino acid sequences. The NP220 (Zfml: Zinc finger, martin like) gene, the DNA-binding nuclear protein, in the LEC rat has a single nucleotide substitution in the coding sequence accompanied by the amino acid substitution from threonine to arginine. To determine which this amino acid substitution was associated with radiation susceptibility, the fibroblast cells derived from the LEC rat, which were transfected the wild type Np220 cDNA, and the transgenic rats, which were carrying it, were constructed, and then, were irradiated. However, the cells and the transgenic rats have not restored the radiation susceptibility, suggesting that the NP220 was unlikely to be responsible gene associated with X-ray hypersensitivity.
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