Sutudy for substances responsible for renal failure death in xanthine oxidoreductase knockout mice
| Project/Area Number |
18K08222
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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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| Review Section |
Basic Section 53040:Nephrology-related
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
細山田 真 帝京大学, 薬学部, 教授 (00291659)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 腎不全 / 腎毒性 / プリン代謝関連物質 / HPRT / キサンチンオキシドレダクターゼ / ウリカーゼ / ノックアウトマウス |
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| Outline of Final Research Achievements |
As a research result, since the hypoxanthine transporter gene A knockout mouse alone did not attenuate the excretion of urinary oxypurine, an A gene-Xor double knockout mouse was created. The generated mice survived for one week longer than the HPRT highly active Xor-KO mice, and the amount of urinary oxypurine excreted was halved. We also confirmed that SLC23A3 is a hypoxanthine transporter in the human kidney.
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| Academic Significance and Societal Importance of the Research Achievements |
国内外でHPRT高活性マウスを用いた研究はなく、他にXOR-KOマウスを生存させた報告もないことから、私たちがプリン代謝関連酵素の活性を変えることで腎障害を回避することに世界で初めて成功したことになる。慢性腎臓病における腎障害の進行因子としてプリン代謝を検討した研究はなく、腎障害の新規バイオマーカーの発掘と腎障害進行の新たなメカニズムの解明を目指す点から、本研究は新規性の高い研究という位置づけにある。
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Report
(5 results)
Research Products
(4 results)
