2014 Fiscal Year Final Research Report
Elucidation of the role of ILK in the functional expression of beta3 integrins and investigation of the ILK-related molecules
Project/Area Number |
23591430
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hematology
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Research Institution | National Cardiovascular Center Research Institute |
Principal Investigator |
HONDA Shigenori 独立行政法人国立循環器病研究センター, 研究所, 室長 (00303959)
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Co-Investigator(Renkei-kenkyūsha) |
TOMIYAMA Yoshiaki 大阪大学, 医学研究科, 准教授 (80252667)
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Project Period (FY) |
2011-04-28 – 2015-03-31
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Keywords | インテグリン |
Outline of Final Research Achievements |
β3 integrins are members of the integrin family consisted of αIIbβ3 and αVβ3. αIIbβ3, a major integrin expressed on platelets, is critical for platelet aggregation mediated by bindings of fibrinogen and von Willebrand factor. αVβ3 (vitronectin receptor), an integrin widely expressed on several cell types including blood vessel tissue constitutive cells and tumor cells, play important roles in diverse vascular disease states, tumor proliferation and metastasis. Integrin-linked kinase (ILK) is an important signaling regulator that assembles into the heteroternary complex with adaptor proteins PINCH and parvin (termed the IPP complex). We recently reported that ILK is important for integrin activation in a Chinese hamster ovary (CHO) cell system. In this study, we further investigated the underlying mechanisms for ILK-dependent integrin activation, and we found that the IPP complex rather than ILK alone plays an important role and supports αIIbβ3 activation.
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Free Research Field |
血栓止血学
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