| Project/Area Number |
18591095
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
HONDA Shigenori National Cardiovascular Center Research Institute, National Cardiovascular Center Research Institute, Senior Staff (00303959)
|
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| Co-Investigator(Kenkyū-buntansha) |
MIYATA Toshiyuki National Cardiovascular Center Research Institute, 病因部, Director (90183970)
TOMIYAMA Yoshiaki Osaka University Hospital, 医学部附属病院・輸血部, Assistant Professor (80252667)
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| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥3,890,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | integrin / signaling molecule / platelet |
|---|
| Research Abstract |
We established cell line expressing chimeric integrin αIIbα6Bβ3 energy-dependently activated. To obtain signaling defective mutant cells that express inactivated αIIbα6Bβ3, the cell line was treated with a chemical mutagen, EMS. Next, we performed expression cloning in which the mutant clone was transfected with cDNA library, and integrin-linked kinase(ILK) was isolated as a molecule induced activation of inactivated αIIbα6Bβ3 in the mutant. Imunoblot analysis showed that the mutant lacked ILK protein. ILK gene in the mutant contained two different nonsense mutations at a compound heterozygous state. ILK knockdown in a parental cell not treated with EMS significantly suppressed integrin activation.
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