Regulatory mechanism of EGF Receptor endocytosis by membrane deformingprotein FCHO2

膜变形蛋白FCHO2对EGF受体内吞作用的调控机制

• 批准号: 23890162
• 负责人: SAKAMOTO Yasuhisa
• 金额: $ 2.08万
• 依托单位: Kumamoto 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: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-23890162/
• 关键词: EGF 受容体; エンドサイト-シス; ユビキチン化; エンドサイト―シス; BARドメイン; 細胞膜変形; エンドサイトーシス; EGF受容体

Endocytosis plays a critical role in the signal transduction,degradation, and recycling of EGF receptor. It is thus important to elucidate the basicprocess of endocytosis. We have studied the molecular mechanisms of F-BAR domaincontaining protein FCHO2 in the regulation of endocytosis and recently found its rolein the activation of ubiqutin ligase Nedd4L. Here we studied about the involvement ofadaptor molecule ARRDC1 in the FCHO2/Nedd4L mediated endocytosis process and revealedthat the localization of Nedd4L on plasma membrane, which is essential for its activation, is regulated by ARRDC1 and FCHO2 cooperatively.

内吞作用在EGF受体的信号转导、降解和再循环中起关键作用。因此，阐明内吞作用的基本过程是很重要的。我们已经研究了F-BAR结构域蛋白FCHO 2在内吞调节中的分子机制，最近发现它在泛素连接酶Nedd 4L的激活中起作用。本文研究了FCHO 2/Nedd 4L介导的胞吞过程中衔接分子ARRDC 1的参与，发现Nedd 4L在质膜上的定位是由ARRDC 1和FCHO 2协同调控的，这是Nedd 4L激活的关键。