| Project/Area Number |
17K08492
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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 |
General anatomy (including histology/embryology)
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| Research Institution | Hiroshima University |
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Principal Investigator |
Suzuki Atsushi 広島大学, 両生類研究センター, 准教授 (20314726)
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| Co-Investigator(Kenkyū-buntansha) |
竹林 公子 (鈴木) 広島大学, 両生類研究センター, 研究員 (00397910)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 自閉症 / 神経形成 / 誘導因子シグナル / 発生・分化 |
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| Outline of Final Research Achievements |
To understand the embryonic etiology linked to autism spectrum disorders, we analyzed the function of neural specific kinase (Nsk)/Clk2 during neural development of vertebrate embryos. Overexpression of Nsk/Clk2 in Xenopus embryos caused the expansion of neural tissues, while chemical inhibition of Nsk/Clk2 affected neural tissue formation during development. Mechanistically, we found that Nsk/Clk2 promotes neural tissue formation via modulation of the BMP and FGF signaling pathways. In the future, our findings will help the development of better treatments for autism spectrum disorders in human.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果によって、自閉症治療薬の創薬ターゲットであるNsk/Clk2の神経発生における役割と誘導因子シグナルの調節機構が明確になった。今後、Nsk/Clk2が誘導因子シグナル伝達因子（Smad, MAPK）のリン酸化やタンパク質安定性を制御するメカニズムを詳細に解析することで、副作用が少なく効果的な自閉症治療薬の開発に貢献することが期待される。
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