Studies on molecular mechanisms underlying abnormal differentiation of neural progenitors in a mouse model of Down syndrome
| Project/Area Number |
15K06697
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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 |
Neurophysiology / General neuroscience
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ダウン症 / 神経前駆細胞 / アストロサイト / DYRK1A / STAT / 大脳新皮質 / 中間前駆細胞 / 神経細胞 / 神経発生 |
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| Outline of Final Research Achievements |
Down syndrome, caused by triplication for human chromosome 21, is associated with abnormalities in brain development such as reduced production of neurons and increased generation of astrocytes. Previous studies suggest that both neuronal and astroglial differentiation of progenitors in Down syndrome brains are deregulated and that the deregulation coordinately contributes to impaired brain development. However, very little is known about the molecular mechanisms underlying abnormal differentiation of Down syndrome progenitors. In this study, we identifies DYRK1A-STAT as a signaling pathway responsible for the enhanced astrocytic differentiation of progenitors observed in a Down syndrome mouse model.
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Report
(4 results)
Research Products
(11 results)
