| Project/Area Number |
23590312
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General pharmacology
|
|---|
| Research Institution | Aichi Gakuin University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HATANO Noriyuki 愛知学院大学, 薬学部, 講師 (50454319)
SUZUKI Hiroka 愛知学院大学, 薬学部, 助教 (00581026)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | チャネル / タンパク発現制御 / 炎症 / TRPチャネル / 転写 / タンパク分解 / カチオンチャネル / 細胞異常 / イオンチャネル / ユビキチン |
|---|
| Research Abstract |
In this research project, we have found that TRPA1 channel, a subfamily of TRP cation channel, is substantially induced by inflammatory stimuli in channel-expression and channel-function levels; a transcriptiona factor, which is activated in hypoxia, is involved in the induction and TRPA1 gene promoter has a specific binding site of the factor. Because TRPA1 channel is involved in nociception, the present finding may contribute to developement of novel drugs for inflammatory nociception.
|
