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埃博拉病毒 VP24 蛋白阻断 p38 丝裂原活化蛋白激酶的磷酸化。

The Ebolavirus VP24 protein blocks phosphorylation of p38 mitogen-activated protein kinase.

机构信息

Department of Pathobiological Sciences, School of Veterinary Medicine, Influenza Research Institute, University of Wisconsin-Madison, WI, USA.

出版信息

J Infect Dis. 2011 Nov;204 Suppl 3(Suppl 3):S953-6. doi: 10.1093/infdis/jir325.

DOI:10.1093/infdis/jir325
PMID:21987775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3189987/
Abstract

Type I interferon (IFN) signaling is mediated through several signaling pathways, including the Janus kinase and signal transducer and activator (JAK-STAT) and p38 mitogen-activated protein (MAP) kinase pathways. The VP24 protein of Ebolavirus is an IFN antagonist, blocking type I IFN signaling through the JAK-STAT pathway. Here, we show that, in 293 cells, VP24 also interferes with the p38 MAP kinase pathway by blocking IFN-β-stimulated phosphorylation of p38-α. Similar inhibition was not observed in HeLa cells, suggesting cell type-specific differences in signal transduction.

摘要

I 型干扰素(IFN)信号转导是通过几条信号通路介导的,包括 Janus 激酶和信号转导及转录激活因子(JAK-STAT)和 p38 丝裂原活化蛋白(MAP)激酶通路。埃博拉病毒的 VP24 蛋白是一种 IFN 拮抗剂,通过 JAK-STAT 通路阻断 I 型 IFN 信号转导。在这里,我们表明,在 293 细胞中,VP24 还通过阻断 IFN-β 刺激的 p38-α磷酸化来干扰 p38 MAP 激酶通路。在 HeLa 细胞中未观察到类似的抑制作用,这表明在信号转导方面存在细胞类型特异性差异。

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本文引用的文献

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Viral tricks to grid-lock the type I interferon system.病毒的诡计:使 I 型干扰素系统陷入僵局。
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Ebola virus VP24 proteins inhibit the interaction of NPI-1 subfamily karyopherin alpha proteins with activated STAT1.埃博拉病毒VP24蛋白抑制NPI-1亚家族核转运蛋白α蛋白与活化的信号转导和转录激活因子1(STAT1)之间的相互作用。
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The VP35 protein of Ebola virus inhibits the antiviral effect mediated by double-stranded RNA-dependent protein kinase PKR.埃博拉病毒的VP35蛋白可抑制由双链RNA依赖性蛋白激酶PKR介导的抗病毒效应。
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