| Project/Area Number |
25340036
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
KUBO KIHEI 大阪府立大学, 生命環境科学研究科(系), 教授 (40117619)
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| Co-Investigator(Kenkyū-buntansha) |
Takenaka Shigeo 大阪府立大学, 生命環境科学研究科, 准教授 (10280067)
YAMAMOTO RYOHEI 大阪府立大学, 生命環境科学研究科, 講師 (20457998)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 塩基除去修復 / DSB / MPG / PIKK / RPA2 / タンパク質相互作用 / ノックダウン / Pol beta / APEX / タンパク質間相互作用 / ｐ53 / ATM / AP site / DNA損傷 / ＤＮＡ修復 / マウス胎児線維芽細胞 / ＨｅＬａ細胞 / ノックダウン細胞 / 脱塩基部位 / 修復複合体 / DNA修復制御 / グリコシラーゼ |
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| Outline of Final Research Achievements |
The regulation of initiation of base excision repair (BER) by MPG was investigated using mouse embryonic fibroblasts (MEF). In growth-arrested MEF, the excision of MMS-induced methylated bases was greatly suppressed while the sensitivity was significantly lower as compared with growing cells. The APEX protein content was reduced in growth-arrested MEF or PolB-deficient MEFs. Furthermore, MPG was also decreased in these cells. After the immunoprecipitation with FLAG-tagged MPG, co-precipitated proteins were analyzed by LC/MS/MS and 13 novel proteins were identified. After MMS-treatment, the enhanced interactions with 7 proteins including MLH1, a DnaJ homolog protein and proteasome-related proteins were observed, while the interaction with 5 proteins including Hsc70 were unchanged. Reduced interaction of MPG with RPA2 and increased interaction with p53 suggest that the production of DSB as a result of BER altered protein interaction with MPG via activation of PIKK.
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