2014 Fiscal Year Final Research Report
Molecular mechanism on the formation and renewal of slit membranes of glomerular podocyte
Project/Area Number |
24591214
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | Juntendo University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
ICHIMURA Koichiro 順天堂大学, 医学部, 准教授 (10343485)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 腎臓学 / 足細胞 / 糸球体濾過 / 細胞接着 / ネフローゼ |
Outline of Final Research Achievements |
The slit diaphragm (SD) plays an important role in permeability barrier function. We have identified several molecules associated with the formation and renewal of SD. 1) To assess the function of MAGI-1, we analyzed the podocyte-specific MAGI-1 deficient mice and found that the deletion of MAGI-1 caused the decrease of SD molecules at the plasma membrane. In addition, exocytosis of nephrin molecule is inhibited by podocyte-specific deletion of aPKC. Data indicate that both molecules are associated with the turnover of SD. 2) We have found that myosin 1e is tightly associated with the tight junction which moves from the apex to the base of immature podocyte during the development. Myosin 1e is also involved in the SD formation. Recently, we have determined that KIF11 is tightly associated with tight junctions of renal epithelial cells in vivo and in vitro. Calcium switch experiment and silencing of KIF11 indicate that KIF11 is involved in the tight junction formation.
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Free Research Field |
細胞生物学
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