2017 Fiscal Year Final Research Report
Studies on molecules controlling aqaporin-2 trafficking and its mechanism.
| Project/Area Number |
26460267
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Gunma University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
向後 寛 群馬大学, 大学院医学系研究科, 講師 (20282387)
向後 晶子 群馬大学, 大学院医学系研究科, 講師 (20340242)
青木 武生 群馬県立県民健康科学大学, 診療放射線学部, 教授 (70150919)
澤井 信彦 日本医科大学, 医学部, 講師 (70307916)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | アクアポリン2 / リン酸化 / 脱リン酸化 |
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| Outline of Final Research Achievements |
Aquaporin-2 (AQP2) is a water channel protein which traffics between intracellular vesicles and surface plasma membrane in the presence of vasopressin. We analyzed the relationships between phosphorylation-dephosphorylation of serine 269 (S269) and intracellular trafficking both in the rat kidneys and cultured cells. We carefully verified the specificity of the antibody to S269-phophorylated AQP2, which have been previously produced, and confirmed our results that S269 is phosphorylated intracellularly and AQP2 is internalized even if it is phosphorylated. Then, we focused on the dephosphorylation of S269. We expected the importance of calcineurin as a putative phosphatase. We examined whether S269-dephosphorylation would be delayed in the presence of ciclosporin which is a calcineurin inhibitor. However, further consideration of the experimental protocol is required.
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| Free Research Field |
基礎医学
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