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，降解和回收中起关键作用。因此，阐明内吞作用的基本过程很重要。我们已经研究了F-BAR结构域蛋白FCHO2在调节内吞作用中的分子机制，并最近发现其作用是Ubiqutin连接酶NEDD4L的激活。在这里，我们研究了Adaptor分子ARRDC1参与FCHO2/NEDD4L介导的内吞作用过程，并揭示了NEDD4L在质膜上的定位，这对于激活而言至关重要，这对于其激活至关重要，受ARRDC1和FCHO2合作调节。