| Project/Area Number |
12557085
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
IMAI Enyu Osaka University Graduate school of Medicine, Lecturer, 医学系研究科, 講師 (00223305)
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| Co-Investigator(Kenkyū-buntansha) |
TAKENAKA Masaru Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (20222101)
CYUMA Tatsuji JAPAN TOBACCO INC. Pharmaceutical Frontier Research Laboratories Central Pharmaceutical Research Institute, Directo, 医薬探索研究所, 所長(研究職)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 2002: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2000: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | napsin / collagen Type IV / angiotensin I / renin / 遺伝子発現情報 / アンギオテンシン / 新規プロテアーゼ / ゲノム創薬 / 発現遺伝子情報 / アンギオテンシンII / ノックアウトマウス / 遺伝子情報データベース / 近位尿細管 / 腎臓 |
|---|
| Research Abstract |
We cloned a renin-like aspartic proteinase GS4001, which is identified mouse napsin, from mouse proximal tubule.
The mouse napsin cleaved angiotensinogen and generated angiotensin I, while the human counterpart napsin did not cleave the angiotensinogen.
The mouse napsin has a character of matrix metalloproteinase, and cleaved type IV collagen but not type I collagen.
Napsin expression was declined in IgA nephripathy, minimal change nephritic syndrome, crescentic glomerulonephritis. The napsin expression was decreased in mouse BSA-overload model and unilateral ureteral obstruction model.
We attempted to generate a new drug, which activates napsin activity to resolve the interstitial fibrosis.
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