| Project/Area Number |
22890104
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
KATO Hisakazu 大阪大学, 大学院・医学系研究科, 特任研究員 (30589312)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,068,000 (Direct Cost: ¥2,360,000、Indirect Cost: ¥708,000)
Fiscal Year 2011: ¥1,469,000 (Direct Cost: ¥1,130,000、Indirect Cost: ¥339,000)
Fiscal Year 2010: ¥1,599,000 (Direct Cost: ¥1,230,000、Indirect Cost: ¥369,000)
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| Keywords | 組織・細胞 / 生体分子 / 循環器・高血圧 / 血管内皮細胞 / タンパク質キナーゼ / タンパク質脱リン酸化酵素 / 炎症性サイトカイン / 細胞遊走 |
|---|
| Research Abstract |
In this research project, I examined the role of cytokine-induced kinase NUAK2 in endothelial cells. When NUAK2 was knocked down in endothelial cells, loss of actin stress fiber and decrease in phosphorylation of myosin light chain were observed. Furthermore, I identified several auto-phosphorylation sites in NUAK2, which involved in activation of its kinase. I injected antisense morpholino against NUAK2 into the zebrafish allowing live imaging of blood vessels, and they showed lethal phenotypes. These data suggest that NUAK2-MYPT1 axis involves in the regulation of cytoskeletal dynamics in vitro and in vivo.
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