Global quantitative proteomic analysis of human glioma cells profiled host protein expression in response to enterovirus type 71 infection

被引:15
作者
Zhang, Lei-Ke [1 ]
Lin, Tao [2 ]
Zhu, Sheng-Lin [1 ]
Xianyu, Ling-Zhi [2 ]
Lu, Song-Ya [2 ]
机构
[1] Chinese Acad Sci, Wuhan Inst Virol, Wuhan, Peoples R China
[2] Wuhan Univ, Coll Life Sci, State Key Lab Virol, Wuhan 430072, Peoples R China
基金
中国国家自然科学基金;
关键词
Cell biology; EV71; Quantitative proteomics; SILAC; TRAF2; TRAF6; VIRUS; ACTIVATION; TRAF2; ADAPTER; COMPLEX; 3C; IDENTIFICATION; DATABASE; SUBUNIT;
D O I
10.1002/pmic.201500134
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Enterovirus 71 (EV71) is one of the leading causes of hand, foot and mouth disease with neurological complications in some cases. To study the pathogenesis of EV71 infection, large-scale analyses of EV71 infected cells have been performed. However, most of these studies employed rhabdomyosarcoma (RD) cells or used transcriptomic strategy. Here, we performed SILAC-based quantitative proteomic analysis of EV71-infected U251 cells, a human glioma cell line. A total of 3125 host proteins were quantified, in which 451 were differentially regulated as a result of EV71 infection at 8 or 20 hpi or both. Gene Ontology analysis indicates the regulated proteins were enriched in "metabolic process", "biological regulation" and "cellular process", implying that these biological processes were affected by EV71 infection. Furthermore, functional study indicated that TRAF2 and TRAF6 among the up-regulated proteins could inhibit the replication of EV71 at the early phase post infection, and the anti-EV71 function of both proteins was independent of interferon beta. Our study not only provided an overview of cellular response to EV71 infection in a human glioma cell line, but also found that TRAF2 and TRAF6 might be potential targets to inhibit the replication of EV71. All MS data have been deposited in the ProteomeXchange with identifier PXD002454 (http://proteomecentral.proteomexchange.org/dataset/PXD002454).
引用
收藏
页码:3784 / 3796
页数:13
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