Project/Area Number |
10670137
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pathological medical chemistry
|
Research Institution | Nagoya University |
Principal Investigator |
HAMAGUCHI Michinari Nagoya University, School of Medicine, Professor, 医学部, 教授 (90135351)
|
Co-Investigator(Kenkyū-buntansha) |
MATSUDA Satoru School of Medicine, Assistant Prof., 医学部, 講師 (50242110)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | cadherin / Src kinase / signal transduction / cell adhesion / Ras / MAP kinase / Srcキナーゼ |
Research Abstract |
The aim of this study is to clarify the critical signaling pathway for the regulation of cell adhesion that depends on reversible biochemical reaction regulated by c-Src. Based on our previous report that Src kinase can regulate cell adhesion, we planned to clarify the regulation of cell adhesion dependent on cell cycle and NO-signaling. In this study we found that Crk, an adopter molecule that binds c-Src to activate it, suppressed cadherin-dependent cell adhesion via Ras-MEK pathway. In addition we found NO produced by e-NOS could directly activate c-Src kinase.
|