| Project/Area Number |
15K08256
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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 |
General medical chemistry
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| Research Institution | Tohoku Medical and Pharmaceutical University (2016-2017)
Hirosaki University (2015) |
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Principal Investigator |
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| Project Period (FY) |
2015-10-21 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Heme / NRF2 / enhancer RNA / HO-1 / ヘムオキシゲナーゼー１ / ノンコーディングRNA / AKR1C1 / ヒ素応答 / ヘムオキシゲナーゼ-１ / 転写制御 |
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| Outline of Final Research Achievements |
We previously reported that eRNA E2s, a non-coding RNA derived from human heme oxygenase-1 E2 enhancer region, regulates DEM-responsive heme oxygenase-1 gene (HO-1) induction. Whereas it has been documented that most of enhancer RNAs (eRNAs) are cis-acting and modulate the expression of specific gene, we wondered whether eRNA E2s uniquely regulates HO-1 induction or not.
Here we found aldo-keto reductase family 1, member C1 gene (AKR1C1) is one of the eRNA E2s-regulated genes. Diethyl maleate (DEM) and arsenite (As)-responsive gene induction of AKR1C1 was attenuated in eRNA E2s knockdown human cells. In addition, we found As-induced Pol II binding to AKR1C1 promoter region is decreased by eRNA E2s knockdown. Interestingly, AKR1C1 is mapped on chromosome 10, though HO-1 and eRNA E2s is on chromosome 22. Thus, our findings indicate that eRNA E2s functions as a trans-acting regulator of gene induction.
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