Molecular interaction that is important for the maintenance of glomerular filtration barrier and its significance in the signal transduction system
Project/Area Number |
21591017
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Akita University |
Principal Investigator |
WAKUI Hideki 秋田大学, 医学研究科, 准教授 (70240463)
|
Co-Investigator(Kenkyū-buntansha) |
KOMATSUDA Atsushi 秋田大学, 医学部, 講師 (70272044)
|
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: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 細胞・組織 / シグナル伝達 / 生体分子 / 蛋白質 / 内科 / 糸球体濾過バリアー / アクチニン4 / 蛋白尿・ネフローゼ症候群 / アクチニン / 蛋白尿 |
Research Abstract |
Dysfunction of the glomerular filtration barrier in the kidney causes nephrotic syndrome with massive proteinuria. In the present study, RACK1 was identified as a novel molecule that can interact with actinin 4, an important component for the maintenance of barrier function. Since RACK1 is known to be interact with various signal transduction molecules, the actinin 4/RACK1 interaction is considered to be important for the maintenance of barrier function via the signal transduction system. In addition, novel findings in clinical cases with dysfunction of the glomerular filtration barrier were reported.
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Report
(4 results)
Research Products
(10 results)