| Project/Area Number |
25460387
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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 |
Pathological medical chemistry
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| Research Institution | Oita University (2014-2015)
Kyoto University (2013) |
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Principal Investigator |
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| Research Collaborator |
HANADA Reiko
TERANISHI Hitoshi
Penninger Josef
Martinez Javier
Weitzer Stefan
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | RNA代謝 / 遺伝子改変動物 / 神経変性疾患 / 分子病態学 |
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| Outline of Final Research Achievements |
CLP1 and NOL9 are the novel RNA kinase family molecules involved in RNA metabolism. In this project, we investigated the in vivo function and the relevance to a human disease of these molecules using these genetically modified mice. Previously, we have reported that the CLP1 kinase function dead mutant mice were shown to display a progressive neurodegenerative disease. Then, we further surveyed the human genome of patients with neurodegenerative diseases and identified a CLP1 homozygous missions mutation (R140H) in Turkish five families. Now the CLP1 mutation (R140H) associated neurodegenerative disease is classified as the pontocerebellar hypoplasia type 10. We newly established NOL9 kinase function dead mutant mice in this project. We would like to clarify the whole picture about the role of RNA kinase family molecules in vivo.
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