| Project/Area Number |
15K06804
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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 |
Laboratory animal science
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| Research Institution | National Center for Geriatrics and Gerontology |
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Principal Investigator |
TOKUNAGA Akinori 国立研究開発法人国立長寿医療研究センター, 統合加齢神経科学研究部, 室長 (70549451)
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| Co-Investigator(Kenkyū-buntansha) |
濱田 文彦 大分大学, 医学部, 教授 (70252707)
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| Research Collaborator |
TADA Hirobumi
SAJI Tamiko
TAKEI Kimi
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | RNAスプライシング / NMD / 神経発生 / インスリンシグナル / アルツハイマー病 / 神経幹細胞 / PI3K-AKT / 発生工学 |
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| Outline of Final Research Achievements |
In the cranial nervous system, many genes are regulated by RNA modification including splicing, and its breakdown can be a cause of developmental abnormality and neurological disorder. However, its molecular mechanism has not been elucidated. We analyzed the deficient mice of UPF1 gene which is a key component of the RNA surveillance and found that UPF1 is essential for maintenance of neural stem cells and normal nerve differentiation.
Furthermore, since the PI3K-AKT signal responsible for the phosphorylation control of UPF1 is closely related to brain function, we analyzed it using the diabetes model and Alzheimer's disease model which causes abnormality in this signal, we showed that the change in the phosphorylation of PI3K-AKT signal correlates with the progression of brain dysfunction.
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