2001 Fiscal Year Final Research Report Summary
DNA repair research using DNA double-strand break repair-gene knockout mutants
| Project/Area Number |
11480139
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
UTSUMI Hiroshi RESEARCH REACTOR INSTITUTE, Kyoto University, RPOFESSOR, 原子炉実験所, 教授 (20025646)
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| Co-Investigator(Kenkyū-buntansha) |
YASUHIRA Shinji RESEARCH REACTOR INSTITUT Kyoto University, ASSOCIATE PROFESSOR, 原子炉実験所, 助手 (90311729)
TANO Keizo RESEARCH REACTOR INSTITUT Kyoto University, ASSOCIATE RPOFESSOR, 原子炉実験所, 助教授 (00183468)
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| Project Period (FY) |
1999 – 2001
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| Keywords | Knockout mutant / DNA double-strand break / sublethal damage repair / homologous recombination / non-homologous end-joining |
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| Research Abstract |
Split-dose recovery has been observed under a variety of experimental conditions in many cell systems and believed to be the repair of sublethal damage. It is considered to be one of the most widespread and important cellular responses in clinical radiotherapy. To study the molecular mechanism of this repair, we analyzed the knockout mutants KU70', RAD54',and KU70'/RAD54' of the chicken B-cell line, DT4. Rad54 ParticiPates in the recombinational repair of DNA double-strand breaks, while KU Protein' are involved in non-homologous end-joining. The result showed that sublethal damage repair ls due to double-strand break repair via or mediated by homologous recombination, and that these breaks constitute niS!f^nation and that these breaks constitute sublethal damage. Recently, we found that DNA-PKcs-knockout DT40 cells had also a biphasic survival curte but were sensitive even in hgih dose region than parental DT40 cells contrary to KU70/' cells. Moreover, DNA-PKcs/ Ku70-double-knockout DT40 cells were the very same in survival curve as KU70'/ cells suggesting the same as the phenotypes of KU70/' Cells' Rad Proteins might compete with Ku70 in channeling the broken DNA ends into alternative repair pathways in late S-G_2 phase.
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