| Project/Area Number |
21591376
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Chiba Cancer Center (Research Institute) |
|---|
Principal Investigator |
NAKAMURA Yohko 千葉県がんセンター(研究所), 研究局, 主席研究員 (60260254)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TATSUMI Yasutoshi 千葉県がんセンター(研究所), 研究局, 研究員 (00450578)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
NAKAGAWARA Akira 千葉県がんセンター(研究所), センター長 (50117181)
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | 神経芽腫 / BMCC1 / 神経細胞の増殖と分化 / 神経細胞死 / TrkA / ノックアウトマウス / ノックアウマウス |
|---|
| Research Abstract |
Here, we analyzed the molecular function of BMCC1, a novel gene we had identified, and found that BMCC1 is inactivated by phoshorylation with NGF-activated TrkA. This BMCC1 suppression resulted in the activation of Cdc42, and subsequently it was essential for differentiation of neuronal cells. In combination with our previous finding that BMCC1 promoted the NGF-depletion-induced apoptosis of neuronal cells, the findings from this study might be important for understanding the mechanisms of NGF-regulated neuronal cell fate and spontaneous regression of neuroblastoma. Furthermore, we generated a BMCC1 knockout mouse for the first time in the world. This might become a powerful tool for analyzing in vivo function of BMCC1.
|
