| Project/Area Number |
25670600
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular surgery
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| Research Institution | Dokkyo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ANZAI NAOHIKO 獨協医科大学, 医学部, 教授 (70276054)
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| Co-Investigator(Renkei-kenkyūsha) |
JUTABHA PROMSUK 獨協医科大学, 医学部, 助教 (90541748)
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| Research Collaborator |
TSUCHIYA GO 獨協医科大学, 医学部, 大学院生
HORI TAKAYUKI 獨協医科大学, 医学部, 大学院生
OHNO YUTA 獨協医科大学, 医学部, 研究生
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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 |
¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 動脈屈曲症候群 / 遺伝子変異 / トランスポーター / グルコーストランスポーター / GLUT10 |
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| Outline of Final Research Achievements |
The aim of this study is to clarify the mechanism of onset for hereditary cardiovascular diseases and finding novel target for developing novel therapeutics by analyzing protein function of glucose transporter 10 (GLUT10) which is known as a cause of arterial tortuosity syndrome (ATS), particularly from the point of substrate transport. We performed the transport studies using Xenopus oocytes expression system and found that GLUT10 mediates the uptake of both glucose and adenosine significantly. But unfortunately, we could not proceed our further study due to the very low expression of GLUT10 protein in Xenopus oocytes and we could not reached a goal although we tried to overcome such problem that sometime happens in Xenopus oocytes system.
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