Investigation of snake venom receptor regulating death of vascular endothelial cells
| Project/Area Number |
13640676
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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 |
動物生理・代謝
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| Research Institution | Nagoya University |
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Principal Investigator |
ARAKI Satohiko Nagoya Univ., Grad.Sch.of Science, Assistant Prof., 大学院・理学研究科, 講師 (80242808)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | vascular / apotosis / hemorrhage / metalloprotease / disintegrin / snake venom |
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| Research Abstract |
Hemorrhagic snake venom induces apoptosis in vascular endothelial cells. In previous investigation, we reported the purification of a vascular apotosis-inducing protein (VAP) from Crotalus atrox. VAPs are a multidomain molecules composed of an N-terminal domain, a metalloproteinase domain, a disintegrin domain and a cysteine-rich domain. In this investigation, the target of Vascular apoptosis-inducing Proteins (VAPs) have been searched and identified. VAP1 is thought to be a highly specific protease, so we searched cleaved proteins from vascular endothelial cells incubated with VAP1. As a result, we found a protein was cleaved by VAP1 in cultured endothelial cells. Biotination to the cells showed the protein, named VAPT, existed on the membrane of the endothelial cells. The antibody of VAPT inhibited the apoptosis induced by VAP1 in vascular endothelial cells. We are further investigating about a apoptosis mechanism involving of VAPs and VAPT. These studies may lead to the clarification of a system of vascular degeneration.
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Report
(3 results)
Research Products
(10 results)
