| Project/Area Number |
23890162
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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 |
General medical chemistry
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 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 |
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| Research Abstract |
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.
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