Physiological function of PLCdelta3 in neuronal outgrowth
| Project/Area Number |
20790239
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
General medical chemistry
|
|---|
| Research Institution | Tokyo University of Pharmacy and Life Science |
|---|
Principal Investigator |
KOUCHI Zen Tokyo University of Pharmacy and Life Science, 生命科学部, 研究員 (70322485)
|
|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 細胞内シグナル伝達 / ホスホリパーゼC / 神経突起伸長 / RhoA / 子宮内エレクトロポレーション / 大脳皮質ニューロン / 小脳顆粒細胞 |
|---|
| Research Abstract |
Phospholipase Cd3 (PLCd3) is a key enzyme, which generates two second messengers including IP3 and DAG in phosphatidylinositol signaling and is highly expressed in neuronal tissues. We found that PLCd3 knockdown in cerebral cortex of E14 embryo by in utero electroporation caused the migratory inhibition of cortical neurons in developing cerebral cortex. Furthermore, we demonstrated that neuronal outgrowth was significantly inhibited in cerebellar granule cells or neuroblastoma cells when PLCd3 was transiently knockdowned during differentiation.
|
Report
(3 results)
Research Products
(8 results)
