| Project/Area Number |
10044295
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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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 | HIROSHIMA UNIVERSITY |
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Principal Investigator |
KOMATSU Kenshi Research Institute for Radiation Biology and Medicine, Hiroshima University, Professor, 原爆放射能医学研究所, 教授 (80124577)
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| Co-Investigator(Kenkyū-buntansha) |
TAUCHI Hiroshi Research Institute for Radiation Biology and Medicine, Hiroshima University, Research Associate, 原爆放射能医学研究所, 助手 (70216597)
MATSUURA Shinya Research Institute for Radiation Biology and Medicine, Hiroshima University, Assosiate Professor, 原爆放射能医学研究所, 助教授 (90274133)
HEUVEL Vande University Hospital Nijmegen Oediatric I, Research A
SMEETS Domin University Hospital Nijmegen Human Genet, Associate
WEEMACS Corr University Hospital Nijmegen Oediatric I, Associate
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥7,700,000 (Direct Cost: ¥7,700,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1998: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Keywords | NBS / AT / NBS1 / ATM / ionizing radiation / dsb / linkage analysis / p53 / p53 / MDM2 / p21 / ナイミーヘン染色体不安定症候群 / NBSI / Xrs2 / ア-Tバリアント / 二重鎖切断 / 放射線感受性 / YAC / ポジショナルクローニング |
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| Research Abstract |
We have investigated phenotypes and genotypes of cells from patients with Nijmegen breakage syndrome.
1. NBS cells partially repressed the induction of p53 and phosphorylation of p53 (ser-15) after irradiation.
2. NBS cells showed the defect in apoptic response to radiation.
3. For the perpose of prenatal diagnosis, we analyzed mutation in NBS gene of patients and haplotype of parental DNA.
4. We investigated mechanism of NBS1 in chromosomal stability, radiation sensitivity and signal transduction, which include ATM, Histon H2AX, p53, NBS, hMre11, Ku.
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