| Project/Area Number |
26461244
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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 |
Kidney internal medicine
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HOSOYA Tatsuo 東京慈恵会医科大学, 医学部, 教授 (10125031)
HOSOYAMADA Makoto 帝京大学, 薬学部, 教授 (00291659)
MATSUO Hirotaka 防衛医科大学校, 医学部, 講師 (00528292)
NAKAMURA Makiko 東京薬科大学, 薬学部, 助教 (80447557)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 尿酸輸送体 / 高尿酸血症 / ABCG2 / GLUT9/SLC2A9 / 尿酸トランスポーター / プリン代謝 |
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| Outline of Final Research Achievements |
URAT1/SLC22A12 and GLUT9/SLC2A are urate reabsorptive transporter at proximal tubules, the defects of that result in renal hypouricemia. We reevaluated some mutations of these genes which had been recognized not influencing urate transport via these transporters and demonstrated thaturate uptakes were decreased via the mutants in xenopus oocytes experiments by changing the experimental condition. These results indicated that these mutations influence serum urate levels.
ABCG2 is a urate excretive transporter. Some dysfunctional single nucleotide polymorphisms of the gene increase hyperuricemia risk. We provided some evidence that ABCG2 function is important for serum urate level regulation.
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