| Project/Area Number |
21890144
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Tottori University |
|---|
Principal Investigator |
KITATANI Kazuyuki Tottori University, 医学部・附属病院, 助教 (40539235)
|
|---|
| Project Period (FY) |
2009 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
|---|
| Keywords | 酸性グルコセレブロシダーゼ / セラミド / 炎症 / p38 / スフィンゴ脂質 / ゴーシェ病 / GBA1 / サイトカイン |
|---|
| Research Abstract |
Acid-β-glucocerebrosidase (GBA1) contributes to the formation of ceramide and signal that suppresses p38δ activation and IL6 formation. In this project, the PI uncovered that p38δ is involved in inducing the formation of proteases including MMP1 and MMP13. Moreover, in GBA1-deficient Gaucher disease model, the activation of inflammatory kinase p38 was significantly increased. Taken together, GBA1-ceramide pathway is suggested to account for suppressing p38δ-mediated inflammatory responses.
|
