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Analysis of global gene expression profiles of A549 cells treated with XRN2 siRNA under basal conditions

ABSTRACT: Untransfected (no siRNA), control siRNA or XRN2 siRNA treated A549 cells were analyzed for gene expression differences under basal conditions 3 Biological Replicates per condition

ORGANISM(S): Homo sapiens

SUBMITTER: Ivan Marazzi

PROVIDER: E-GEOD-66662 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Analysis of global gene expression profiles of A549 cells treated with Xrn2 siRNA upon Influenza A/PR/8/34(ΔNS1) Infection

Project description:Untransfected (no siRNA), control siRNA or Xrn2 siRNA treated A549 cells were infected with A/Puerto Rico/8/1934(ΔNS1) for 4 hours 3 Biological Replicates per condition

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Analysis of global gene expression profiles of A549 cells treated with SETX siRNA upon Influenza A/PR/8/34(ΔNS1) Infection

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Analysis of global gene expression profiles of A549 cells treated with SETX siRNA under basal conditions

Project description:Untransfected (no siRNA), control siRNA or SETX siRNA treated A549 cells were analyzed for gene expression differences under basal conditions 3 Biological Replicates per condition

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Analysis of global gene expression profiles of hPAF1 deficient A549 cells

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Analysis of global gene expression profiles of hPAF1 deficiency on unstimulated A549 cells

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 targets the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. More importantly,in the following data sets, we show that hPAF1 plays a crucial role in the antiviral response. Loss of hPAF1C reduces antiviral gene expression and reduces inducible transcription of target genes after stimulation with viral RNA analogue poly(I:C), vesicular stomatitis virus (VSV), exogenous recombinant IFN(beta) and influenza virus (H1N1). This study underscores the importance of hPAF1C in controlling inducible antiviral gene expression. A549 cells were untreated (no siRNA) or treated with control siRNA-treated and hPAF1 siRNA. Total RNA was isolated with the Qiagen RNeasy mini kit. 200ng of total RNA per sample was used to prepare biotin-labeled RNA using MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems) and hybridized to HumanHT-12 v4 Expression BeadChips (Illumina). Data analysis was performed using the GeneSpring GX11.0 software (Agilent Technologies). These samples were then used for comparisons with stimulated cells (See series 1) 3 biological replicates per condition

2012-02-15 | E-GEOD-35265 | biostudies-arrayexpress

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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 targets the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. More importantly,in the following data sets, we show that hPAF1 plays a crucial role in the antiviral response. Loss of hPAF1C reduces antiviral gene expression and reduces inducible transcription of target genes after stimulation with viral RNA analogue poly(I:C), vesicular stomatitis virus (VSV), exogenous recombinant IFN(beta) and influenza virus (H1N1). This study underscores the importance of hPAF1C in controlling inducible antiviral gene expression. Untreated (no siRNA), control siRNA-treated and hPAF1 siRNA-treated A549 cells were stimulated with PR8/∆NS1 influenza virus (MOI 1), IFNβ1 (500U/mL) or Poly(I:C) (2ug/mL). Total RNA was isolated with the Qiagen RNeasy mini kit. 200ng of total RNA per sample was used to prepare biotin-labeled RNA using MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems) and hybridized to HumanHT-12 v4 Expression BeadChips (Illumina). Data analysis was performed using the GeneSpring GX11.0 software (Agilent Technologies). 3 biological replicates per condition

2012-02-15 | E-GEOD-35267 | biostudies-arrayexpress

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Expression profiling reveals transcriptional regulation by Fbxw7/mTOR pathway in radiation-induced mouse thymic lymphomas

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2015-10-31 | E-GEOD-71975 | biostudies-arrayexpress

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