2016 Fiscal Year Final Research Report
Analysis of regulatory mechanism of sustained integrin alphaIIbbeta3 activation.
Project/Area Number |
26461403
|
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 |
Kato Hisashi 大阪大学, 医学系研究科, 助教 (20705214)
|
Co-Investigator(Renkei-kenkyūsha) |
Tomiyama Yoshiaki 大阪大学, 医学部附属病院・輸血部, 准教授 (80252667)
|
Research Collaborator |
Ichii Michiko 大阪大学, 大学院医学系研究科・血液・腫瘍内科, 寄付講座助教 (30633010)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | インテグリンαIIbβ3 / Inside-Outシグナル / CalDAG-GEFI |
Outline of Final Research Achievements |
Platelet fibrinogen receptor integrin αIIbβ3 is essential for hemostasis and its activation state is tightly regulated by inside-out signaling. So far, the detailed mechanism how inside-out signaling induces activation of αIIbβ3 is still obscure. In this study, we determined the molecules which are important for inside-out signaling in the megakaryocytic cell line CMK and the patient with CalDAG-GEFI deficiency who has been suffering severe bleeding problems. However, platelets with CalDAG-GEFI deficiency showed mildly impaired αIIbβ3 activation. And we found the delayed αIIbβ3 activation in CalDAG-GEFI deficient platelets is related to severe bleeding symptoms. Our results indicate the importance of CalDAG-GEFI and αIIbβ3 activation kinetics for normal hemostasis (Blood 2016).
|
Free Research Field |
血栓止血
|