Zhou Mao-Tian, Qin Yue, Li Mi, Chen Chen, Chen Xi, Shu Hong-Bing, Guo Lin
From the ‡State Key Laboratory of Virology, College of Life Sciences;
From the ‡State Key Laboratory of Virology, College of Life Sciences; §Medical Research Institute, Wuhan University;
Mol Cell Proteomics. 2015 Sep;14(9):2535-49. doi: 10.1074/mcp.M115.048413. Epub 2015 Jun 29.
Compared with whole-cell proteomic analysis, subcellular proteomic analysis is advantageous not only for the increased coverage of low abundance proteins but also for generating organelle-specific data containing information regarding dynamic protein movement. In the present study, peroxisome-enriched fractions from Sendai virus (SeV)-infected or uninfected HepG2 cells were obtained and subjected to quantitative proteomics analysis. We identified 311 proteins that were significantly changed by SeV infection. Among these altered proteins, 25 are immune response-related proteins. Further bioinformatic analysis indicated that SeV infection inhibits cell cycle-related proteins and membrane attack complex-related proteins, all of which are beneficial for the survival and replication of SeV within host cells. Using Luciferase reporter assays on several innate immune-related reporters, we performed functional analysis on 11 candidate proteins. We identified LGALS3BP and CALU as potential negative regulators of the virus-induced activation of the type I interferons.
与全细胞蛋白质组分析相比，亚细胞蛋白质组分析不仅有利于增加低丰度蛋白质的覆盖范围，还有利于生成包含动态蛋白质运动信息的细胞器特异性数据。在本研究中，从感染或未感染仙台病毒（SeV）的HepG2细胞中获得了富含过氧化物酶体的组分，并进行了定量蛋白质组学分析。我们鉴定出311种因SeV感染而发生显著变化的蛋白质。在这些改变的蛋白质中，有25种是免疫反应相关蛋白。进一步的生物信息学分析表明，SeV感染会抑制细胞周期相关蛋白和膜攻击复合物相关蛋白，所有这些都有利于SeV在宿主细胞内的存活和复制。通过对几个先天免疫相关报告基因进行荧光素酶报告基因测定，我们对11种候选蛋白进行了功能分析。我们鉴定出LGALS3BP和CALU是病毒诱导的I型干扰素激活的潜在负调节因子。
