| Project/Area Number |
25460103
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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 |
Pharmacology in pharmacy
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| Research Institution | Gifu Pharmaceutical University |
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Principal Investigator |
Hara Hideaki 岐阜薬科大学, 薬学部, 教授 (20381717)
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| Co-Investigator(Kenkyū-buntansha) |
TSURUMA Kazuhiro 岐阜薬科大学, 薬学部, 講師 (50524980)
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| Co-Investigator(Renkei-kenkyūsha) |
青木 正志 東北大学, 医学系研究科, 教授 (70302148)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | GPNMB / 記憶 / GluA1 / Na+, K+-ATPase / PI3K/Akt経路 / MEK/ERK経路 / Na+,K+-ATPase / SOD1G93A / 膜タンパク質ライブラリ |
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| Outline of Final Research Achievements |
The aim of this study was to lead to development of effective novel treatment for GPNMB related diseases by investigating whether GPNMB affects to memory and by identifying of novel GPNMB extracellular fragment receptors.
We found that GPNMB promoted hippocampus-dependent memory by increasing expression levels of total GluA1 proteins and phosphorylated GluA1 proteins. Moreover, we also found that GPNMB extracellular fragment bound to Na+, K+-ATPase (NKA) α1 and NKA α3 and activated PI3K/Akt pathway and MEK/ERK pathway via NKA α1 and α3. Therefore, it was suggested that NKA α1 and α3 work as a novel GPNMB extracellular fragment receptor.
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