| Project/Area Number |
25460402
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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 |
Pathological medical chemistry
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| Research Institution | National Institute for Minamata Disease |
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Principal Investigator |
Usuki Fusako 国立水俣病総合研究センター, その他部局等, 部長 (50185013)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMURA Masatake 国立水俣病総合研究センター, 基礎研究部, 室長 (20416564)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMASHITA Akio 横浜市立大学医学部, 分子細胞生物学, 准教授 (20405020)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 環境ストレス / mRNA監視機構(NMD) / eIF2αリン酸化 / NMD抑制 / 早期終止コドン(PTC) / 蛋白質翻訳抑制 / Snhg1 mRNA / eIF2α リン酸化 / 早期終止コドン (PTC) / 小胞体ストレスプレコンディショニング / mTOR pathway / 蛋白質翻訳 / Snhg1 / 早期終止コドン / GAS5 / ストレス蛋白質 |
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| Outline of Final Research Achievements |
Nonsense-mediated mRNA decay (NMD), an mRNA quality surveillance mechanism, was suppressed under environmental stresses and mild endoplasmic reticulum (ER) stress preconditioning. NMD suppression under mild ER stress preconditioning up-regulated the expression of mutant disease-related mRNA carrying premature termination codon (PTC) and restored partially the defect of protein. Mild ER stress preconditioning-induced NMD suppression was caused by phospho-eukaryotic initiation factor 2α- mediated translation suppression and downregulation of some NMD components. Environmental stresses and ER stress preconditioning has potential to affect phenotypes of PTC-related diseases.
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