2015 Fiscal Year Final Research Report
The regulatory mechanism and the role of CDM family protein in atherosclerosis
Project/Area Number |
26870420
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Functional biochemistry
Pathological medical chemistry
|
Research Institution | University of Miyazaki (2015) Kyushu University (2014) |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Keywords | マクロファージ / 動脈硬化 / マクロピノサイトーシス |
Outline of Final Research Achievements |
Foam cell formation through macropinocytosis in atherosclerosis pathophysiology has been already established. However, detailed mechanism remains to be determined. This study aims to analyze the role of DOCK1/2/5 as Rac activator in foam cell formation. We discovered that the uptake of dextran-FITC was significantly reduced in bone marrow macrophage of DOCK1/2/5 triple knockout mice. Treatment of CPYPP as DOCK 1/2/5 inhibitor in wild type bone marrow macrophage showed the similar result. We found that DOCK1/2/5 function links macropinocytosis formation, suggesting that DOCK1/2/5 participate in foam cell formation. It leads to elucidate their pathogenesis and develop novel therapies.
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Free Research Field |
病態医化学
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