The regulation of cytoskeletal dynamics in endothelial cells during acute inflammation

急性炎症过程中内皮细胞细胞骨架动力学的调节

• 批准号: 22890104
• 负责人: KATO Hisakazu
• 金额: $ 1.96万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Research Activity Start-up
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-22890104/
• 关键词: 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

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.

在这个研究项目中，我研究了细胞因子诱导的激酶 NUAK2 在内皮细胞中的作用。当内皮细胞中的 NUAK2 被敲低时，观察到肌动蛋白应力纤维的损失和肌球蛋白轻链磷酸化的减少。此外，我还发现了 NUAK2 中的几个自磷酸化位点，这些位点参与其激酶的激活。我将针对 NUAK2 的反义吗啉注射到斑马鱼中，可以对血管进行实时成像，它们显示出致命的表型。这些数据表明 NUAK2-MYPT1 轴参与体外和体内细胞骨架动力学的调节。

项目成果

AMPK controls the speed of microtubule polymerization and directional cell migration through CLIP-170 phosphorylation

• DOI: 10.1038/ncb2060
• 发表时间: 2010-06-01
• 期刊: NATURE CELL BIOLOGY
• 影响因子: 21.3
• 作者: Nakano, Atsushi;Kato, Hisakazu;Takashima, Seiji
• 通讯作者: Takashima, Seiji

Development of anti-HB-EGF immunoliposomes for the treatment of breast cancer

• DOI: 10.1016/j.jconrel.2011.10.010
• 发表时间: 2012-06-10
• 期刊: JOURNAL OF CONTROLLED RELEASE
• 影响因子: 10.8
• 作者: Nishikawa, Kaoru;Asai, Tomohiro;Minamino, Tetsuo
• 通讯作者: Minamino, Tetsuo