| Project/Area Number |
17K17942
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
Cell biology
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| Research Institution | Osaka University (2020)
Gunma University (2017-2018) |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | ポリグルタミン病 / Nemo-like kinase (NLK) / シグナル伝達 |
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| Outline of Final Research Achievements |
NLK is a protein kinase which is highly expressed in nervous system. Although recent studies using disease model mice showed that NLK positively regulates onset of polyglutamine diseases, the detailed mechanism remains unclear. In this study, we revealed new mechanisms by which NLK promotes polyglutamine diseases. We also tried to generate a chemical inhibitor which can stably inhibits NLK activity in brain to aim for treatment of polyglutamine diseases. In addition, we generated the genetically modified mice lacking NLK kinase activity to estimate the effects of NLK inhibitor in vivo.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究によって、NLKによるポリグルタミン病発症の制御メカニズムの一端を解明することができた。これにより、神経変性の新たなメカニズムが明らかになり、神経科学や細胞生物学の発展に寄与することができた。また、NLK特異的阻害剤の開発が進んだことにより、新たなポリグルタミン病治療戦略へつながる可能性がより高まった。
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