| Project/Area Number |
16K14743
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Developmental biology
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| Research Institution | Doshisha University |
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Principal Investigator |
Motoyama Jun 同志社大学, 脳科学研究科, 教授 (70321825)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経発生 / マウス / 初期胚 / Shh / 環境因子 / 妊娠糖尿病 / エタノール / 発生 / 分化 / 細胞分裂 / 胚 / 発生・分化 / 先天異常 |
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| Outline of Final Research Achievements |
The action of Shh protein determines the midline of the neural plate during E7.5 to E7.75 in the developing mouse embryos. It has been known that the midline defect is caused by the maternal diabetes. The condition of the high glucose may affect the Shh signaling during midline determination. On the other hand, Shh also functions as activator of differentiation of the neural stem cells into the intermediate neural progenitors during mouse cortical development. During the development of the central nervous system, maternal diabetes increases the risks of developmental disorder, mental retardation, and autism in human. We tried to examine the effects of high glucose condition on the Shh signaling, to understand the etiology of developmental disorder caused by the maternal diabetes.
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