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Proteome of GPKOW depleted cells with IAV infection, IFN or PPP-RNA treatment

ABSTRACT: The abundance of a protein is defined by its continuous synthesis and degradation, a process known as protein turnover. Here, we systematically profiled the turnover of proteins in influenza A virus (IAV) infected cells using a pulse-chase SILAC-based approach combined with downstream statistical modeling. We identified 1414 virus-affected proteins with turnover changes (tVAPs) out of 7739 detected proteins. In particular, the affected proteins were involved in RNA transcription, splicing and nuclear transport, protein translation and stability, and energy metabolism. Many tVAPs are known IAV-interacting proteins that regulate virus propagation, such as KPNA6, PPP6C and POLR2A. Notably, our analysis identified novel IAV host and restriction factors, such as the splicing factor GPKOW, that exhibit significant turnover rate changes, while their total abundance is not affected. Overall, we show that protein turnover is a critical factor both for virus replication and antiviral defense. The data presented here were used to study GPKOW's function in innate immunity.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Yiqi Huang

LAB HEAD: Andreas Pichlmair

PROVIDER: PXD047060 | Pride | 2025-04-09

REPOSITORIES: Pride

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			Action	DRS
	20150930_QEp5_PhHu_SA_Ph_PU_76_Hela_siGPKOW_41.raw	Raw
	20150930_QEp5_PhHu_SA_Ph_PU_76_Hela_siGPKOW_42rem.raw	Raw
	20150930_QEp5_PhHu_SA_Ph_PU_76_Hela_siGPKOW_43rem.raw	Raw
	20150930_QEp5_PhHu_SA_Ph_PU_76_Hela_siGPKOW_44.raw	Raw
	20150930_QEp5_PhHu_SA_Ph_PU_76_Hela_siScrambled_65.raw	Raw

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Project description:Hepatitis B virus (HBV) causes both acute and chronic liver inflammation. Approximately 600,000 CHB patients each year die of HBV-related diseases such as cirrhosis and liver cancer. Therefore, CHB remains a global health concern. Although there have been anti-HBV agents for treating CHB, they have some limitations including viral-drug resistance and adverse effects. Type III IFN or IFN-λ is promising to use as anti-HBV agents because of its anti-viral activities like type I IFNs. In addition, the expression of its receptor, IFNLR1, is limited only in epithelial cells including hepatocytes. Thus, treatment with IFN-lambda results in less side effects compared to IFN-alpha treatment. IFN-lambdas have been shown to inhibit the replication of several viruses including IAV, DENV, EMCV, HIV, HCV, and HBV; however, there have been no studies on the effects of IFN-λ3, the highest activity among other subtypes, on HBV replication. Therefore, this study aims to determine antiviral activities of IFN-λ3 against HBV replication and to investigate its molecular mechanism responsible for suppressing HBV propagation. The results showed that HBV transcripts and amount of intracellular HBV DNA were decreased in HepG2.2.15 cells, stable HBV-transfected hepatoblastoma cell line, treated with IFN-λ3 in a dose-dependent manner. This indicated that IFN-λ3 could inhibit HBV replication. Next, we performed quantitative proteomics to investigate the proteome changes in HepG2.2.15 treated with IFN-λ3. The proteins that changed their expressions were involved in several biological processes such as defense to viral infection, immune responses, cell-cell adhesion, transcription, translation, and metabolism. We further confirmed the proteomics results by immunoblotting assay. Consistent with MS data, it found that the expression of OAS3, SAMHD1 and STAT1 were increased as a result of IFN-λ3 stimulation. These results indicated that proteomics results were reproducible and reliable. Finally, we proposed 3 possible mechanisms involved in suppressing HBV replication including i.) IFN-λ3 induced anti-viral proteins affecting many steps in HBV life cycle ii.) IFN-λ3 promoted antigen processing and antigen presentation and iii.) IFN-λ3 rescued RIG-I signaling to promote both type I and type III IFN production.

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Proteome of GPKOW depleted cells with IAV infection, IFN or PPP-RNA treatment

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