Novel functions, membrane receptor and mechanisms for angiostatin
| Project/Area Number |
23590099
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Mukogawa Women's University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Akinori 岩手医科大学, 薬学部, 准教授 (40260319)
SATO Keisuke 九州保健福祉大学, 薬学部, 教授 (00315293)
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| Co-Investigator(Renkei-kenkyūsha) |
SAKANAKA Mariko 武庫川女子大学, 薬学部, 助教 (00425109)
SHINYA Tomohiro 九州保健福祉大学, 薬学部, 助教 (60551299)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アンギオスタチン / 血管新生 / 血管内皮細胞 / 受容体 / eNOS / COX-2 |
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| Research Abstract |
We identified membrane protein p130 as a novel receptor for angiostatin (AS). Extracellular region of p130 including vWF-like domains binds AS. AS inhibited VEGF-induced NO production, COX-2 expression in vascular endothelial cells and migration of endothelial cells. We found that p130 might mediate such effects of AS. Our data suggest that AS impairs HSP90 association with eNOS, and that AS abrogates JNK activation. In addition, p130 forms a complex with VE-cadherin and beta-catenin in endothelial cells.
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Report
(4 results)
Research Products
(13 results)
