Project/Area Number |
15590251
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General medical chemistry
|
Research Institution | Wakayama Medical University |
Principal Investigator |
YOKOTE Hideyuki Wakayama Medical University, Molecular medicine, Assistant professor, 付置研究所, 助手 (60316122)
|
Co-Investigator(Kenkyū-buntansha) |
SAKAGUCHI Kazushige Wakayama Medical University, Molecular medicine, professor, 付置研究所, 教授 (60178548)
JING Xuefeng Wakayama Medical University, Molecular medicine, Assistant professor, 付置研究所, 助手 (70316123)
奥野 悦生 和歌山県立医科大学, 付置研究所, 助教授 (20124886)
|
Project Period (FY) |
2003 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | FGFR / Eph / Neural stem cell |
Research Abstract |
We hypothesized that neural stem cell growth, differentiation and chemotaxsis are regulated by molecular interaction between FGFR and Eph. Our study is focused on elucidation of a novel signaling mechamism through FGFR-EphA4 complex. Our summary of findings are described bellow. (1)Physiological significance of FGFR-EphA4 interaction Ephrin stimulation of differentiated P19 cellls expressing both FGFR and EphA4 promoted FGFR-EphA4 complex formation and then activated EphA4 trans-phosphorylated FGFR. Futhermore, colocalization of FGFR and EphA4 on P19 cells and neural stem cells was shown by immunocytochemical study, indicating that FGFR interacts with EphA4 phisiologically. (2)FGFR-EphA4 complex formation increased FRS2-Ras-MAPK signaling through FGFR FRS2 is well known as a down strem molecule activated by FGFR. We found a complex formation of FRS2-FGFR-EphA4 in mouse neural stem cells and this interaction increasesd Ras-MAPK signaling. Our results suggested that FGFR-EphA4 interaction was important for neurogenesis and regeneration.
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