2017 Fiscal Year Final Research Report
Analysis of secondary DNA damage elicited by nucleotide excision repair and the genome maintenance mechanism in mammalian quiescent cells
Project/Area Number |
15K00534
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Risk sciences of radiation and chemicals
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Research Institution | Kanazawa University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
松永 司 金沢大学, 薬学系, 教授 (60192340)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | ヌクレオチド除去修復 / DNA損傷応答 / 二次的DNA損傷 / ssDNAギャップ / DNA二本鎖切断 |
Outline of Final Research Achievements |
In quiescent cells, nucleotide excision repair (NER) process generates multiple types of secondary DNA damage. However, the mechanism of secondary DNA damage formation and their biological meanings are unclear. In this study, we have examined the possible involvement of exonuclease 1 (Exo1) in the processing of ssDNA gap intermediate during NER. We found that Exo1 plays an important role in the processing of NER-induced ssDNA gap intermediates and protects UV-induced cell death in quiescent cells. In addition, we could detect several NER-dependent DNA damage responses in mouse skin, such as H2AX phosphorylation and ATM activation, indicating that NER-dependent formation of secondary DNA damage indeed occurs in vivo as well.
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Free Research Field |
分子細胞生物学
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