Towards a better understanding of corticogenesis by the selective proteolysis of a protein kinase
| Project/Area Number |
24500398
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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 |
Neuroscience in general
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| Research Institution | National Center of Neurology and Psychiatry |
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Principal Investigator |
WAKATSUKI Shuji 独立行政法人国立精神・神経医療研究センター, 神経研究所 疾病研究第五部, 室長 (00378887)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | プロテアソーム / リン酸化シグナル / 神経発生 / 大脳皮質形成 / 小頭症 / 軸索変性 / タンパク質分解 / ユビキチンリガーゼ / 神経科学 / ユビキチンプロテアソームシステム |
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| Outline of Final Research Achievements |
Previously, we reported that ZNRF1 ubiquitin ligase promotes Wallerian degeneration by degrading AKT to induce GSK3B activation. ZNRF1 starts to degrade AKT only after neuronal injury, but the mechanism of ZNRF1 activation in response to invasive stimulations has been unclear. Here we show that oxidative stress activates ZNRF1 by inducing its phosphorylation in neurons. We also found by using in vitro and in vivo models that the pathophysiological significance of ZNRF1-mediated signaling in the regulation of murine corticogenesis, and elucidating the underlying the phosphorylation mediated regulatory mechanism of its catalytic activity is useful for a better understanding of corticogenesis by the selective proteolysis of AKT.
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Report
(4 results)
Research Products
(25 results)
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[Presentation] 軸索を壊すメカニズム2015
Author(s)
若月修二
Organizer
山梨大学若手研究者セミナー
Place of Presentation
山梨 山梨大学医学部臨床小講堂
Year and Date
2015-03-16
Related Report
Invited
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