Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA121317 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA CD36+ EPCs were generated from CD34+ stem cells, and transduced with B19V NS1 or control-lentivirus for 12, 24,and 48 hours. Each sample has triplicates. There are 18 samples analyzed.
2010-11-03 | E-GEOD-18906 | biostudies-arrayexpress
Project description:B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA
2010-11-03 | GSE18906 | GEO
Project description:The goal of our present work was to understand the influence parvovirus B19 infection may have on the thyroid hormone signaling pathway, as well as the nuclear receptors (NR) pathway overall. We demonstrated that B19 infection of CD36+ erythroid progenitor cells leads to downregulation of the thyroid hormone receptor α isoform. In addition to that we have shown that B19 infection modulates the expression of other members of the NR superfamily such as estrogen and retinoid receptors. CD36+ cells (StemCell Technologies) were mock-infected or infected with B19, 48 hours post infection cells were collected, total RNA was isolated, and cDNA was obtained as described above. TaqMan® array human nuclear receptors fast 96-well plates obtained from Applied Biosystems (Carlsbad, CA) were utilized in order to assess the differences of 92 nuclear receptors’ expression in mock- and B19-infected CD36+ cells. Relative quantity (RQ) values were calculated using the 2-ΔΔCt method.
2012-11-04 | E-GEOD-42005 | biostudies-arrayexpress
Project description:Human parvovirus B19 (B19V) infection can cause transient aplastic crisis, persistent viremia, and pure red-cell aplasia. In fetuses, B19V infection can result in non-immune hydrops fetalis and fetal death. To systematically investigate the interaction between B19V and erythoid progenetor cells (EPC), microarray was applied to systematically analyze the dynamic transcriptome of CD36+ EPCs during B19V infection.
2017-12-07 | GSE103460 | GEO
Project description:The goal of our present work was to understand the influence parvovirus B19 infection may have on the thyroid hormone signaling pathway, as well as the nuclear receptors (NR) pathway overall. We demonstrated that B19 infection of CD36+ erythroid progenitor cells leads to downregulation of the thyroid hormone receptor α isoform. In addition to that we have shown that B19 infection modulates the expression of other members of the NR superfamily such as estrogen and retinoid receptors.
2012-11-04 | GSE42005 | GEO
Project description:We construct two stable UT7/Epo-S1 cell lines which could be inducible expressing B19 NS1 and NS1 TAD2 domain mutation proteins. After treated with or without doxycycline induction, we extract the total RNA for RNA-seq analysis.
2017-03-01 | GSE83525 | GEO
Project description:Viral infection is commonly associated with virus-driven hijacking of host proteins. We describe a novel mechanism by which influenza virus impacts host cells through the interaction of influenza NS1 protein with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 target the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. In the following data sets, we show that NS1 colocalizes with hPAF1 on the chromatin of infected cells and that siRNA-mediated reduction of hPAF1 expression results in reduced recruitment of NS1 to the chromatin.
2013-07-01 | GSE35774 | GEO
Project description:Viral infection is commonly associated with virus-driven hijacking of host proteins. We describe a novel mechanism by which influenza virus impacts host cells through the interaction of influenza NS1 protein with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 target the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. In the following data sets, we show that NS1 colocalizes with hPAF1 on the chromatin of infected cells and that siRNA-mediated reduction of hPAF1 expression results in reduced recruitment of NS1 to the chromatin. Examination of different histone modifications in infected cells and RNA-Seq and GRO-Seq transcript measurements.
2013-07-01 | E-GEOD-35774 | biostudies-arrayexpress
Project description:The NS1 protein of influenza virus counters host antiviral defences primarily by antagonizing the type I interferon (IFN) response. Both the N-terminal dsRNA-binding domain and the C-terminal effector domain are required for optimal suppression of host responses during infection. To better understand the regulatory role of the NS1 effector domain, we used an NS1-truncated mutant virus derived from human H1N1 influenza isolate A/Texas/36/91 (Tx/91) and assessed global transcriptional profiles from two independent human lung cell-culture models.
2012-07-10 | GSE39200 | GEO
Project description:The NS1 protein of influenza A virus (IAV) is a multifunctional virulence factor. Mouse adaptive mutations in the NS1 protein of the human isolate A/Hong Kong/1/1968(H3N2) (HK) have been previously reported to increase virulence, viral fitness, and interferon antagonism, but differ in binding to post-transcriptional processing factor CPSF30. Because nuclear trafficking is a major genetic determinant of influenza virus host adaptation, we assessed subcellular localization and host gene expression of NS1 adaptive mutations. Recombinant HK viruses with adaptive mutations in the NS1 gene were assessed for NS1 protein subcellular localization in mouse and human cells using confocal microscopy and cellular fractionation. HK-wt virus NS1 partitioned equivalently between the cytoplasm and nucleus in human cells but was defective in cytoplasmic localization in mouse cells. The adaptive mutations either increased the proportion or abundance of NS1 in the cytoplasm, and/or the nucleus. NS1 mutations that increased cytoplasmic distribution identified a putative second nuclear export signal (NES) spanning aa positions 98-106 LSEDWFMLM, (mutation sites in bold); with the strongest effect seen for mutation M106I. The putative NES in the NS3 protein was associated with cytoplasmic localization. The host gene expression profile of the adaptive mutants was determined by microarray analysis of infected mouse cells to show either high or low gene regulation (HGR or LGR) phenotypes that mapped to the amino-terminal and the carboxy-terminal regions respectively. The HGR and LGR mutations were predominantly down regulating versus up regulating respectively. The greatest effect on host gene expression in the HGR group correlated with the ability of the NS1 protein to bind CPSF30. To our knowledge this is the first report of roles of adaptive NS1 mutations that affect intracellular localization and regulation of host gene expression.
2013-06-22 | GSE48217 | GEO