Project/Area Number |
20790241
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
General medical chemistry
|
Research Institution | National Institute of Health Sciences |
Principal Investigator |
KATO Reiko National Institute of Health Sciences, 療品部, 主任研究官 (00333469)
|
Project Period (FY) |
2008 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 血管 / リンパ管 / Ras / ERK / シグナル / チロシンキナーゼ / プロテインキナーゼC / VEGF / G-CSF / ホスフォイノシタイド / ノックアウトマウス / 負の制御 / フォスフォリパーゼC / G-CSE |
Research Abstract |
Sprouty/Spred family proteins negatively regulate ERK signaling activated by growth factors and cytokines. We have analyzed gene knockout mice of this family and found that Sproutys negatively regulate angiogenesis, while Spreds regulate lymphangiogenesis. Sprouty4 inhibits vascular endothelial growth factor-A (VEGF-A) induced ERK activation, while Spred1/2 efficiently inhibit VEGF-C, which is essential for lymphangiogenesis. We have identified the difference between Sproutys and Spreds.in the action of VEGFs signal transduction. We also found that human SPRED1 is responsible for neurofibromatosis type I like disease.
|