| Project/Area Number |
20591271
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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 | Toho University (2009-2010)
The University of Tokyo (2008) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IGARASHI Takashi 東京大学, 医学部附属病院, 教授 (70151256)
MIURA Kenichiro 東京大学, 医学部附属病院, 助教 (70408483)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ネフローゼ症候群 / 巣状糸球体硬化症 / ポドサイト / リン酸化 / nepnrin / neph1 / TRPC6 / MYH9 / nephrin / phospholipase C(PLC)-γ1 / 細胞内Ca濃度 / チロシンリン酸化 / シグナル伝達 / NMMHC-IIA / podocyte / FSGS / 細胞内シグナル伝達 / PLC / 細胞内Ca |
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| Research Abstract |
In this study, we demonstrated and reported the following findings.
1) Phosphorylation of adhesion molecules of podocyte, such as neph1 is related to the development of proteinuria.
2) Nephrin binds to PLC-γ1 through its phosphorylation and it evokes the increase of intracellular calcium concentration([Ca2^+] i).
3) In adiition, we demonstrated that nephrin regulated the activity of TRPC6 channel on podocyte cytoplasmic membrane, which also regulate([Ca2^<+]> i).
4) Finally, we analyzed inherited renal disease, i. e. Epstein syndrome, and revealed that its pathogenesis is FSGS, and myosin right chain IIA was decreased in this disease.
These findings are published in, JBC 2008, JBC 2009, KidneyInter 2010, and Mol Cell Biol 2011.
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