| Project/Area Number |
25430118
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
Miyoshi Hiroshi 聖マリアンナ医科大学, 医学部, 講師 (80322519)
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| Co-Investigator(Kenkyū-buntansha) |
ENOMOTO Atsushi 名古屋大学, 医学研究科, 准教授 (20432255)
YUZAWA Satoru 九州大学, 医学研究院, 助教 (40515029)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | ダイナミン / Girdin / エンドサイトーシス / 浸潤・転移 / 細胞運動 |
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| Outline of Final Research Achievements |
The activation mechanism of dynamin GTPase by Girdin was investigated by X-ray crystallography and confocal laser scanning microscopy.
We showed that the actin-binding protein girdin is a regulator of cargo-selective CME. Girdin interacts with dynamin 2, a GTPase that excises endocytic vesicles from the plasma membrane, and functions as its GTPase activating protein. Interestingly, girdin depletion leads to the defect in clathrin-coated pit formation in the center of cells. Also, we find that girdin differentially interacts with some cargoes, which competitively prevents girdin from interacting with dynamin 2 and confers the cargo selectivity for CME.
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