| Project/Area Number |
26460070
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Biological pharmacy
|
|---|
| Research Institution | Gifu Pharmaceutical University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
原 宏和 岐阜薬科大学, 薬学部, 准教授 (30305495)
足立 哲夫 岐阜薬科大学, 薬学部, 教授 (40137063)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | SOD3 / 銅イオン / Atox-1 / エピジェネティクス / gp91phox / EC-SOD / 細胞内銅イオン / NOX2 / ATP7A |
|---|
| Outline of Final Research Achievements |
We investigated the involvement of intracellular copper homeostasis in SOD3 regulation during monocytic differentiation into macrophage. We confirmed that the alteration of copper homeostasis after phorbol ester (TPA) treatment regulates SOD3 expression. Moreover, Atox-1, a copper chaperone, functions as a transcription factor of SOD3. It raises the possibility that the alteration of copper homeostasis after TPA treatment changes histone modification, especially in histone acetylation. Overall, our results suggest that intracellular copper ion functions as a key molecule for the redox regulation, and better understanding the role of copper ion might lead to improve vascular diseases.
|
