| Project/Area Number |
26670438
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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 |
Neurology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
WATASE Kei 東京医科歯科大学, 脳統合機能研究センター, 准教授 (30376800)
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| Project Period (FY) |
2014-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | 遺伝子組換えマウス / 神経疾患 / パーキンソン病 / リソソーム / 遺伝子改変 / 神経変性疾患 / モデル動物 |
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| Outline of Final Research Achievements |
Recently a missense mutation in VPS35 (D620N) has been shown to cause an autosomal dominant late-onset form of Parkinson disease (PARK17) but molecular pathogenesis of PARK17 remains elusive. In order to model PARK17 in mice and elucidate its molecular pathogenesis, I have successfully generated the knockin mice carrying the mutation homologous to D620N as well as the mice with an NHEJ-mediated deletion or insertion mutation in the murine Vps35 gene by CRISPR-Cas9 method. Using the same methodology, I have also succeeded in generating knockin mice which express constitutively active form of Tfeb, which is known as a master regulator of lysosomal biogenesis.
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