2021 Fiscal Year Research-status Report
新規DNA相同組み換え機構に基づく細胞選択的合成致死誘導の開発
| Project/Area Number |
20K08071
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| Research Institution | Yamagata University |
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Principal Investigator |
田嶋 克史 山形大学, 医学部, 非常勤講師 (80292423)
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| Co-Investigator(Kenkyū-buntansha) |
安田 武嗣 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所 放射線障害治療研究部, 主幹研究員 (60332269)
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | RAD52 / DNA repair / BRCA2 / homologous recombination |
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| Outline of Annual Research Achievements |
Mutants of RAD52 were produced. The mutation amino acids are suggested to be responcible for binding to single-strand DNA. A mutant RAD52 (K102A) inhibited proliferation of cells with knock-down of BRCA2 by siRNA.
This mutation (K102A) also disturbed both homologous-recombination (HR) and single-strand anealing (SSA) assays as repair mechanisms for the DNA double strand breaks (DSBs).
In contrast, the mutation of K133A could not inhibit proliferation of cells in spite of the BRCA2 silencing. This mutant had not effects on SSA but on HR. These mutants could not localize at DSB sites in cellss after irradation. In conclusion, the regutaion of RAD52 including acetylation, may be responsible for synthetic lethalty for cells accompanying with the BRCA2-dysfunctions.
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| Current Status of Research Progress |
Current Status of Research Progress
3: Progress in research has been slightly delayed.
Reason
COVID-19によりface to faceの情報交換ができないため
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| Strategy for Future Research Activity |
実験補助員の確保と実験実施を加速させる。研究計画の変更はない。
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| Causes of Carryover |
研究実施者の雇用確保とCOVID-19による研究者間の打ち合わせができなかったため。
研究実施者の雇用は目途が立ち、人流制限も緩和されたので、今後の研究実施は可能と推察している。
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