| Project/Area Number |
24659413
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SASAKI SEI 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (60170677)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 水・電解質代謝学 / 水チャネル / 遺伝子改変マウス / アクアポリン / 嚢胞腎 / 小胞体 / トランスジェニックマウス / 免疫染色 |
|---|
| Research Abstract |
The purpose of our study was to clarify pathopysiologival roles of aquaporins in endoplasmic reticulum (ER). AQP11 knockout mice (AQP11-KO) showed polycystic kidney. However, molecular mechanism(s) of the cyst formation remained to be determined. To clarify this, we generated HA-tagged AQP11 BAC transgenic mice (AQP11-TG), and also analyzed AQP11-KO focusing on PKD1 (PC-1)and PKD2 (PC-2). AQP11 was found to be localized in endoplasmic reticulum in the proximal tubules, and impaired glycosylation processing and aberrant membrane trafficking of PC-1 was observed in AQP11 KO mice, suggesting the involvement of AQP11 in proper glycosylation of PC-1 in ER.
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