Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8224650_1.fastq.gz | Fastqsanger.gz | |||
| SRR8224650_2.fastq.gz | Fastqsanger.gz | |||
| SRR8224660_1.fastq.gz | Fastqsanger.gz | |||
| SRR8224660_2.fastq.gz | Fastqsanger.gz | |||
| SRR8224670_1.fastq.gz | Fastqsanger.gz |
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Project description:Chronic hepatitis C virus (HCV) infection is a leading cause of liver cancer. HCV propagation and oncogenicity depend in part on the phosphorylation states of its non-structural protein 5A (NS5A); however, little is known about how hypo- or hyper-phosphorylated NS5A functions. Here, we segregated hypo- from hyper-phosphorylated NS5A in HCV-infected Huh7.5.1 cells with two custom-made specific antibodies and differentiated their interacting proteins with dimethyl labeling-based quantitative proteomics. Bioinformatics analysis revealed that hyper-phosphorylated NS5A preferentially binds the polymerase II-associated factor 1 complex known to alter host gene expression involved in cancer progression. In contrast, hypo-phosphorylated NS5A binds proteins involved in host antiviral response. Moreover, we found that the hypo-phosphorylated NS5A binds DNA-dependent protein kinase catalytic subunit (DNA-PKcs) predicted to phosphorylate NS5A at serine 232, a key amino acid that governs NS5A transition from hypo- to hyper-phosphorylation state. Inhibition of DNA-PKcs with an inhibitor or via gene-specific knockdown significantly reduced serine 232 phosphorylation and NS5A hyper-phosphorylation. Collectively, we have identified a protein kinase that regulates a delicate balance of NS5A between hypo- and hyper-phosphorylation states respectively involved in host antiviral responses and liver cancer progression.
2019-06-17 | PXD012767 | Pride
Project description:Numerous mammalian proto-oncogene and other growth-regulatory transcripts are upregulated in malignancy due to abnormal mRNA stabilization. In hepatoma cells expressing a hepatitis C virus (HCV) subgenomic replicon, we found that the viral nonstructural protein 5A (NS5A), a protein known to bind to viral RNA, also bound specifically to human cellular transcripts that encode regulators of cell growth and apoptosis, and this binding correlated with transcript stabilization. An important subset of human NS5A-target transcripts contained GU-rich elements, sequences known to destabilize mRNA. We found that NS5A bound to GU-rich elements in vitro and in cells. Mutation of the NS5A zinc finger abrogated its GU-rich element-binding and mRNA stabilizing activities. Overall, we identified a molecular mechanism whereby HCV manipulates host gene expression by stabilizing host transcripts in a manner that would promote growth and prevent death of virus-infected cells, allowing the virus to establish chronic infection and lead to the development of hepatocellular carcinoma.
2017-11-01 | GSE102910 | GEO
Project description:We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Goal and objectives: To study the requirement of HCV viral proteins and/or environmental factors (such as alcohol or obesity) in synergistic liver caner development in HCV Core or NS5A Tg mice given alcohol or high-cholesterol high-fat diet, mice were fed alcohol or high-cholesterol high-fat diet and liver tissues from these mice were examined for gene profiles. Alcohol or obesity contributes to synergistic tumor incidence and HCV Core or Ns5a-induced effects. Thus, analysis of gene profiling of these transgenic mice will identify the critical pathways to induce synergistic tumor formation caused by alcohol or obesity.
2014-09-16 | GSE61435 | GEO
Project description:We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Goal and objectives: To study the requirement of HCV viral proteins and/or environmental factors (such as alcohol or obesity) in synergistic liver caner development in HCV Core or NS5A Tg mice given alcohol or high-cholesterol high-fat diet, mice were fed alcohol or high-cholesterol high-fat diet and liver tissues from these mice were examined for gene profiles. Alcohol or obesity contributes to synergistic tumor incidence and HCV Core or Ns5a-induced effects. Thus, analysis of gene profiling of these transgenic mice will identify the critical pathways to induce synergistic tumor formation caused by alcohol or obesity. Liver samples for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain gene profiling data in order to increase understanding the pathways. To perform gene array and proteomic analyses, mice were fed alcohol or high-cholesterol high-fat for 12 months and euthanized after 12 months feeding. Livers were collected at the time of euthanasia.
2014-09-16 | E-GEOD-61435 | biostudies-arrayexpress
Project description:Hepatitis C virus (HCV) exhibits a narrow species tropism, causing robust infections only in humans and experimentally inoculated chimpanzees. The black flying fox orthologue of receptor transport protein 4 (RTP4) was previously shown to be a potent antiviral effector against several ER-replicating RNA viruses, inhibiting viral genome replication. Since the murine but not the human orthologue is a potent inhibitor of HCV we aimed to analyze the potential role for RTP4 in restricting HCV replication in mice. We demonstrate that mouse RTP4 (mmRTP4) functions as a dominant inhibitor of HCV infection. Via interspecies domain-mapping, we identify the zinc-finger domain (ZFD) of murine RTP4 as the essence of its specific HCV inhibition which is consistent with prior work showing that the 3CXXC zinc finger domain of black flying fox RTP4 is necessary and sufficient for antiviral activity. Expression of mouse RTP in HCV-infected Huh7 cells profoundly reduced HCV RNA, NS5A protein production and virion release demonstrating that mmRTP4 can also disrupt already established HCV replication complexes. Bulk RNAseq analysis of HCV-infected samples did not reveal any characteristic antiviral transcriptional signatures following mmRTP4 transduction, indicating that this antiviral activity cannot be readily attributed to induction of an antiviral response. In situ proximity ligation revealed that murine RTP4 associates with the HCV NS5A protein significantly more than human RTP4 during infection. Disrupting RTP4 expression in mice expressing humanized alleles of CD81 and occludin (OCLN) – the species specific cellular factors mediating HCV uptake – did not, however, increase permissiveness irrespective of the immunocompetence of the mice. Collectively, our work provides detailed insights into RTP4’s role in contributing to HCVs narrow host range and will inform downstream development of a more comprehensive small-animal model for this important disease.
2025-06-24 | GSE292032 | GEO
Project description:Polysome profiling of Huh7.5 cells expressing HCV NS5A
| PRJNA198502 | ENA
Project description:Hepatitis C Virus protein NS5A was found to upregulate assembly of cap binding initiation complex eIF4F in Huh7.5 cells. NS5A also was found to associate with translation machinery. To understand consequences of NS5A mediation in host translation, we analyzed mRNA associated with polysome fractions of NS5A expressing Huh7.5 cells and compared them with the corresponding fractions from control cells.
2014-05-01 | GSE46273 | GEO
Project description:Hepatitis C Virus protein NS5A was found to upregulate assembly of cap binding initiation complex eIF4F in Huh7.5 cells. NS5A also was found to associate with translation machinery. To understand consequences of NS5A mediation in host translation, we analyzed mRNA associated with polysome fractions of NS5A expressing Huh7.5 cells and compared them with the corresponding fractions from control cells. Agilent-027114 Genotypic Technology designed Custom Human Whole Genome 8x60k Microarray
2014-05-01 | E-GEOD-46273 | biostudies-arrayexpress
Project description:We performed miRNA array analysis for S-HCV (short-term HCV), L-HCV (long-term HCV) and control (uninfected Huh751), total for 3 samples to identify miRNA candidates in HCV-related HCC.
2023-06-27 | GSE235959 | GEO