| Project/Area Number |
16K18391
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Nagoya University |
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Principal Investigator |
Tsujimura Keita 名古屋大学, 医学系研究科, 特任助教 (60588474)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | MeCP2 / レット症候群 / 発達障害 / miRNA / 軸索形成 / microRNA / 突起伸長 / 極性 / 精神疾患 |
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| Outline of Final Research Achievements |
This research project was performed based on the novel function of MeCP2, Rett syndrome responsible gene product, identified by principal investigator (PI) in the previous study. By conducting experiments using cultured neurons and mice, we found that MeCP2 promotes axon formation through functional small non-coding RNA. Also, we showed that manipulation of function of MeCP2 downstream molecule can restores phenotypes of Rett syndrome model mice. Taken together, these results show novel mechanism of developmental disorders and new avenues for therapy of Rett syndrome.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究成果により、発達障害の原因因子が軸索形成を制御する分子基盤が明らかになった。これらは軸索形成の新たな分子基盤を提示した成果であり、学術的に重要な成果である。また、医学的にも発達障害の病態メカニズムの一端を解明した重要な成果であり、これらの病態機序に基づいた新規の治療法開発につながることが期待される。
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