| Project/Area Number |
24591422
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KASHIWAGI Hirokazu 大阪大学, 大学院医学系研究科, 講師 (10432535)
TODOKORO Seiji 大阪大学, 大学院医学系研究科, 助教 (80403062)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | インテグリンαIIbβ3 / CMK / inside-out signaling / talin-1 / kindlin-3 / 血小板 / タリン / キンドリン / Inside-out signaling / CMK細胞 / インテグリンαIIｂβ3 |
|---|
| Outline of Final Research Achievements |
Platelet integrin αIIbβ3 plays a crucial role in thrombosis as well as hemostasis. In this study, we have investigated the regulatory mechanism for αIIbβ3 function employing novel CMK cell system.
We demonstrated that agonist stimulation, talin-1, and kindlin-3 were crucial for αIIbβ3 activation in CMK cells: overexpression of talin head domain is sufficient for the activation of αIIbβ3 exogenously expressed on CHO cells, but not for endogenous αIIbβ3 expressed on CMK cells in the absence of agonists.
In addition, employing several talin mutants, we strongly suggested that interaction between talin-1 and membrane proximal region of β3 plays a crucila role in αIIbβ3 activation.
|
