| Project/Area Number |
26860180
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | NRF2 / FDH / グルタチオン / ヒストン脱メチル化 / ホルムアルデヒド / GSH / 酸化ストレス / ストレス防御 |
|---|
| Outline of Final Research Achievements |
We analyzed molecular mechanisms of maintenance system for nuclear redox balance to support the epigenome regulation. Using gene-deleted cells and gene-knockout mice, we successfully showed that NRF2 and FDH cooperatively function through the regulation of GSH in the protection from oxidative damage in liver. We also found that formaldehyde increased in the Nrf2::Fdh double mutant cells, compared to respective single mutant cells. To examine the importance of NRF2-FDH-GSH system in cancer cells, we successfully established a model cancer cell line, which rigorously form tumors in allograft experiments in NRF2-dependent manner.
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