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Development of (a human X-chromosome * hamster) hybrid cell assay system, which is sensitive to tritium exposure.

Development of (a human X-chromosome * hamster) hybrid cell assay system, which is sensitive to tritium exposure.
开发(人类 X 染色体 * 仓鼠)混合细胞测定系统,该系统对氚暴露敏感。
批准号:
09558064
负责人:
KOMATSU Kenshi
金额:
$7.55万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1998

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中文摘要
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英文摘要
HPRT mutation was used to assay the radiation effect, since it is possible to isolate by positeve-negative selection with 6-thioguanin and HAT (hypoxunthin-aminopterin-thymidine). Howeverr, radiation is known frequantly to induce DNA-deletion type mutation, which possibly decrease the HPRT mutation rate. To detect the deletion mutation, we developped HPRT deficient hamster-based hybrid cells, where an intanct human X-chromosome. was transfered our experiments showed that appropriate expression time of these cells is 8-10 days after irradiation. The mutation incidence of theses cells was 450 mutants/ 10^5 survived cells after 4-Gy irradiation and it was contrast with mutantion rate in conventional rodent assay system : 5-50 mutants/10^5 survived cells. Thus, newly developped assay system indicated 10-100 fold highre sesnsitivity than that used to assay for radiation effect. Existance of a transferred human chromosome in their mutant cells were confirmed by FISH ana1ysis, implying mutation induction with the of HPRT gene. Mutation incidences were linearly increased with radiation dose of ^<60>Co-gamma-rays and this dose-relationship showed the approxinately 100-fold high sensitivity, compared with that of conventional HPRT mutation assay. When this incidence was compared with that of tritium-beta rays, the biological effectiveness RBE indicated the consistent value, 1.24, with previous observation. As a results, our studies demonstrated the high sensitivity and usefulness of hamster hybrid cells cantaining an intact human X-chromosome for evaluation of tritium biological effects.
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会议论文
S.Matsuura, et.al.: "Positional cloning of the gene for Nijmegen breakage syndrome" Nature Genet.19. 179-181 (1998)
S.Matsuura 等人:“奈梅亨断裂综合征基因的定位克隆”Nature Genet.19。
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发表时间:
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作者: []
通讯作者:
A.Nakamura,et al.: "Four novel mutations of the Fanconi anemia group A gene (FAA) in Japanese patients" J.Hum.Genet.44. 48-51 (1999)
A.Nakamura 等人:“日本患者中范可尼贫血 A 组基因 (FAA) 的四种新突变”J.Hum.Genet.44。
DOI: --
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作者: []
通讯作者:
Matsuura,S.: "Genetic mapping using microcell-mediated chromosome transfer suggests a locus for Nijmegen Breakage Syndrome at chromosome 8q21-24." Am.J.Hum.Genet.60. 1487-1494 (1997)
Matsuura,S.:“利用微细胞介导的染色体转移进行的基因作图表明,奈梅亨断裂综合征的基因座位于染色体 8q21-24。”
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通讯作者:
K.Matsuura,et al.: "Radiation induction of p53 in cells from Nijmegen breakage syndrome is defective but not similar to ataxia-telangiectasia" Biochem.Biophys.Res.Commun.242. 602-607 (1998)
K.Matsuura 等人:“奈梅亨断裂综合征细胞中 p53 的辐射诱导有缺陷,但与共济失调毛细血管扩张症不相似”Biochem.Biophys.Res.Commun.242。
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通讯作者:
7
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    • 资助金额:
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    Molecular mechanism of radiation/NBS1-associated microcephaly
    • 批准号:
      23651045
    • 项目类别:
      Grant-in-Aid for Challenging Exploratory Research
    • 资助金额:
      $2.58万
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      2011
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    • 项目类别:
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      2006
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