identification of proteins interacting with causative molecules for hereditary nephrotic syndrome and analysis of pathogenesis of it.
| Project/Area Number |
21591387
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Okayama University |
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Principal Investigator |
AYA Kunihiko 岡山大学, 岡山大学病院, 講師 (20379762)
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| Co-Investigator(Kenkyū-buntansha) |
OUCHIDA Mamoru 岡山大学, 大学院・医歯薬学総合研究科, 准教授 (80213635)
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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|---|
| Keywords | 小児腎・泌尿器学 / 蛋白尿 / 輸送蛋白 / 細胞内輸送 / 質量分析 / ネフリン / ポドシン / ネフローゼ症候群 / ネフローゼ / 遺伝子 / nephrin / 先天性 |
|---|
| Research Abstract |
We identified transport protein x bounded to podocin, important molecule for proteinuria, with immunoprecipitation and LC/MS. The double staining with endothelial marker and anti-x antibody indicated that protein x was expressed in podocyte. When protein x was suppressed with siRNA in cells, podocin expression along cell membrane was much lower than control and cell shape was changed. Overexpression of protein x improved expression of mutated podocin along cell membrane. These data indicated protein x play role in membrane trafficking of podocin.
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Report
(4 results)
Research Products
(20 results)
