| Project/Area Number |
20890013
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| Research Category |
Grant-in-Aid for Young Scientists (Start-up)
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
SUZUKI Takafumi Tohoku University, 大学院・医学系研究科, 助教 (70508308)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,302,000 (Direct Cost: ¥2,540,000、Indirect Cost: ¥762,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,742,000 (Direct Cost: ¥1,340,000、Indirect Cost: ¥402,000)
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| Keywords | ストレス / 転写因子 / Keap1 / Nrf2 / トランスジェニックマウス / システイン残基 / センサー |
|---|
| Research Abstract |
In this study, we investigated the physiological function of stress sensor Keap1 by mouse genetics. We have found that partial repression of Keap1 leads to activation of transcriptional factor Nrf2, resulting in up-regulation of detoxifying enzymes and anti-oxidant proteins, which is effective for cytoprotection. We have further found that functional Keap1 homodimer is essential for Nrf2 repression, which is disrupted by stress stimuli.
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