Global quantitative proteomic analysis profiles host protein expression in response to Sendai virus infection |
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Authors: | Sheng‐Lin Zhu Xi Chen Liang‐Jie Wang Wei‐Wei Wan Qi‐Lin Xin Wei Wang Gengfu Xiao Lei‐Ke Zhang |
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Affiliation: | 1. State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, P. R. China;2. The Laboratory of Biological Mass Spectrometry, Wuhan Institute of Biotechnology, Wuhan, P. R. China;3. Medical Research Institute, Wuhan University, Wuhan, P. R. China;4. School of Chemistry and Life Sciences, Hubei University of Education, Wuhan, P. R. China |
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Abstract: | Sendai virus (SeV) is an enveloped nonsegmented negative‐strand RNA virus that belongs to the genus Respirovirus of the Paramyxoviridae family. As a model pathogen, SeV has been extensively studied to define the basic biochemical and molecular biologic properties of the paramyxoviruses. In addition, SeV‐infected host cells were widely employed to uncover the mechanism of innate immune response. To identify proteins involved in the SeV infection process or the SeV‐induced innate immune response process, system‐wide evaluations of SeV–host interactions have been performed. cDNA microarray, siRNA screening and phosphoproteomic analysis suggested that multiple signaling pathways are involved in SeV infection process. Here, to study SeV–host interaction, a global quantitative proteomic analysis was performed on SeV‐infected HEK 293T cells. A total of 4699 host proteins were quantified, with 742 proteins being differentially regulated. Bioinformatics analysis indicated that regulated proteins were mainly involved in “interferon type I (IFN‐I) signaling pathway” and “defense response to virus,” suggesting that these processes play roles in SeV infection. Further RNAi‐based functional studies indicated that the regulated proteins, tripartite motif (TRIM24) and TRIM27, affect SeV‐induced IFN‐I production. Our data provided a comprehensive view of host cell response to SeV and identified host proteins involved in the SeV infection process or the SeV‐induced innate immune response process. |
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Keywords: | Innate immune response Quantitative proteomics Sendai virus Virus– host interaction |
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