Pathogenesis by the analysis of "non" nerve organ of Rett syndrome by the original experimental system with ultrastructure.
| Project/Area Number |
26860813
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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 |
Pediatrics
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| Research Institution | Kagoshima University |
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Principal Investigator |
Irie Rie 鹿児島大学, 医歯学域医学系, 助教 (90381178)
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| Research Collaborator |
Kosai Ken-ichiro 鹿児島大学, 学術研究院 医歯学域医学系 運動機能修復学講座 遺伝子治療・再生医学分野, 教授 (90258418)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 脳・神経 / 脳・神経疾患 / 細胞・組織 / 生理活性 / 解剖学 / 超微形態学 / 発生学 / 形態形成 / 脳神経疾患 / 生理活性物質 |
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| Outline of Final Research Achievements |
We found that morphological changes in non-neuronal organs observed in male deficient MeCP2 gene mice, Rett syndrome (RTT) model mouse, are due to abnormal secretion of certain physiologically active substances. In the cultured cells that MeCP2 gene knockdown cells using RNAi and reproduced the results seen in vivo by biochemical analysis. The genes involved in the biosynthesis of this substance were analyzed by quantitative PCR and we could extract the expression variable gene. Analysis by quantitative PCR must be performed comprehensively and it was not possible to collect sufficient data for analysis of female mice deficient in MeCP 2 gene which is a true RTT model mouse which was the final target.
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Report
(5 results)
Research Products
(3 results)
