2017 Fiscal Year Final Research Report
Analysis of the mechanism of a novel DNA repair reaction in mammalian cells
Project/Area Number |
16K15118
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Biological pharmacy
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Research Institution | Kanazawa University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
若杉 光生 金沢大学, 薬学系, 准教授 (80345595)
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Keywords | ヌクレオチド除去修復 / 紫外線 / DNA損傷 / 色素性乾皮症 |
Outline of Final Research Achievements |
We recently showed that mammalian cells slowly remove UV-induced 6-4 photoproducts from their genome under the nucleotide excision repair (NER)-defective condition. In this study, we have tried to uncover the mechanism of the NER-independent reaction in human cells. We have found that the non-canonical repair reaction requires XPC, but not DDB, both of which are well-known NER factors involved in a damage recognition step. We further found that a proteasomal activity is also required for this reaction only when NER-deficient cells have functional DDB, suggesting the implication of proteasomal degradation mediated by Cul4-DDB1 E3 ligase.
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Free Research Field |
分子細胞生物学
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