γ疱疹病毒趋化因子结合蛋白与CXCL8的N端结合。
The gammaherpesvirus chemokine binding protein binds to the N terminus of CXCL8.
作者信息
Webb Louise M C, Clark-Lewis Ian, Alcami Antonio
机构信息
Department of Medicine, Division of Virology, University of Cambridge, Cambridge, United Kingdom.
出版信息
J Virol. 2003 Aug;77(15):8588-92. doi: 10.1128/jvi.77.15.8588-8592.2003.
Abstract
Viruses encode proteins that disrupt chemokine responses. The murine gammaherpesvirus 68 gene M3 encodes a chemokine binding protein (vCKBP-3) which has no sequence similarity to chemokine receptors but inhibits chemokine receptor binding and activity. We have used a panel of CXCL8 analogs to identify the structural requirements for CXCL8 to bind to vCKBP-3 in a scintillation proximity assay. Our data suggest that vCKBP-3 acts by mimicking the binding of chemokine receptors to CXCL8.
摘要
病毒编码可破坏趋化因子反应的蛋白质。小鼠γ疱疹病毒68基因M3编码一种趋化因子结合蛋白（vCKBP - 3），它与趋化因子受体没有序列相似性，但能抑制趋化因子受体的结合和活性。我们使用了一组CXCL8类似物，通过闪烁邻近分析来确定CXCL8与vCKBP - 3结合的结构要求。我们的数据表明，vCKBP - 3通过模拟趋化因子受体与CXCL8的结合来发挥作用。
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