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2015 Fiscal Year Final Research Report

The regulatory mechanism and the role of CDM family protein in atherosclerosis

Research Project

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Project/Area Number 26870420
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Functional biochemistry
Pathological medical chemistry
Research InstitutionUniversity of Miyazaki (2015)
Kyushu University (2014)

Principal Investigator

Sanematsu Fumiyuki  宮崎大学, 医学部, 助教 (80381094)

Project Period (FY) 2014-04-01 – 2016-03-31
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.

Free Research Field

病態医化学

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Published: 2017-05-10  

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