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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

2015-03-30 | E-GEOD-66661 | biostudies-arrayexpress

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

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

2015-03-30 | E-GEOD-52932 | biostudies-arrayexpress

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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2012-02-15 | E-GEOD-35268 | biostudies-arrayexpress

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

Analysis of global gene expression profiles of hPAF1 deficient A549 cells during infection with H1N1 influenza A virus or vesicular stomatitis virus (VSV)

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2012-02-15 | E-GEOD-35266 | biostudies-arrayexpress

Analysis of global gene expression profiles of hPAF1 deficient A549 cells during stimulation with PR8/∆NS1 influenza virus, IFNβ1 or Poly(I:C)

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

Transcriptomic analysis of Sorghum bicolor responding to combined heat and drought stress

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2014-06-20 | E-GEOD-48205 | biostudies-arrayexpress

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

Project description:We used gene transcript profiling to gain a deeper understanding of the role of FBXW7 in tumor development and to determine the influence of mTOR inhibition by rapamycin on tumor transcriptome and biological functions. In comparison to tumors from p53 single heterozygous (p53+/-) mice, we find that tumors from Fbxw7/p53 double heterozygous (Fbxw7+/-p53+/-) mice show significant deregulation of cholesterol metabolic processes independent of rapamycin treatment, while cell cycle related genes were upregulated in tumors from placebo treated Fbxw7+/-p53+/- mice, but not in tumors from rapamycin treated Fbxw7+/-p53+/- mice. On the other hand, tumors from rapamycin treated Fbxw7+/-p53+/- mice were enriched for genes involved in the integrated stress response, an adaptive mechanism to survive in stressful environments. p53+/â and p53+/âFbxw7+/â mice were generated by crossing p53-/- mice with Fbxw7+/- mice. At 5 weeks of age, mice were exposed whole-body to a single dose of 4 Gy X-ray irradiation. Mice were divided randomly into two groups and treated with rapamycin or placebo. RNA was isolated from thymic lymphomas.

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

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Project description:RNA was extracted from placentas selected based on normotensive pregnancy with low GBA messenger RNA expression and hypertensive pregnancy with relatively high expression of GBA messenger RNA. Total RNA was extracted from placental tissue biopsies stored in RNALater within 2 hours after delivery.

2014-04-01 | E-GEOD-54618 | biostudies-arrayexpress

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