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Characterization of EOLA1 promoter-associated proteome in A549 cells

ABSTRACT: This project utilizes biotin-labeled DNA pull-down followed by LC-MS/MS to identify potential transcription factors regulating EOLA1 expression in human A549 lung epithelial cells. We compared the binding profiles under mock conditions and Influenza A (PR8) virus stimulation.

ORGANISM(S): Homo Sapiens

SUBMITTER: Nan Qi

PROVIDER: PXD077470 | iProX | Wed Apr 22 00:00:00 BST 2026

REPOSITORIES: iProX

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Expression data from A549 cell line infected with influenza A virus (IAV) and treated with/without Itaconate

Project description:Analysis of gene expression in A549 cells infected with influenza A virus or Mock and treated with Itaconic acid (IA), or Dimethyl itaconate (DI) to investigate the effects itaconate have on transcriptional response in A549 cells. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.

2021-10-31 | GSE162260 | GEO

Analysis of global gene expression profiles of hPAF1 deficient A549 cells

Project description:This SuperSeries is composed of the following subset Series: GSE35265: Analysis of global gene expression profiles of hPAF1 deficiency on unstimulated A549 cells GSE35266: Analysis of global gene expression profiles of hPAF1 deficient A549 cells during infection with H1N1 influenza A virus or vesicular stomatitis virus (VSV) GSE35267: Analysis of global gene expression profiles of hPAF1 deficient A549 cells during stimulation with PR8/?NS1 influenza virus, IFN?1 or Poly(I:C) Refer to individual Series

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

Shotgun Proteomic Identification of Amphotericin B Targets in Late Endosomes of Influenza A Virus-Infected A549 Cells

Project description:Amphotericin B (AmB), a polyene macrolide antifungal, is well known for its ability to bind ergosterol and cholesterol; however, its interactions with host proteins remain poorly characterized. In this study, we aimed to identify AmB-binding targets in A549 cells infected with the influenza A virus (H1N1) strain A/PR/8/34 (PR8). We isolated late endosomal fractions and performed a biotin–streptavidin pulldown using a biotinylated AmB probe, with specificity confirmed by competition with excess free AmB. The proteins enriched from these fractions were then analyzed by shotgun LC–MS/MS, revealing a set of late endosomal proteins that specifically interact with AmB during influenza A virus infection.

2026-02-02 | PXD064601 | Pride

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

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Expression data from recoverin positive and negative A549 cell lines

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Promoter Capture Hi-C performed on A549 cells in a SARS-CoV2 infection timecourse

Project description:Here, A549 cells expressing the ACE2 receptor were infected with SARS-CoV2, and pCHi-C was performed at 0 (mock), 8 and 24 hours post-infection. This repository provides the raw pCHi-C sequence reads and downstream processed CHiCAGO data (Rds files).

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

2012-02-15 | GSE35265 | GEO

Small RNA-Seq of influenza A/Puerto Rico/8/1934 (H1N1) virus infected A549 human cells

Project description:To study expression pattern of small nucleolar RNAs (snoRNAs) during influenza A viral infection, human cells A549 were infected with influenza A/Puerto Rico/8/1934 (H1N1) virus. Small RNA-seq analysis of infected cells after 24 h or 48 h incubation was performed on an Illumina NextSeq 500 platform. The same mock-infected cells were used as control. Small RNA fractions (<200 nucleotide length) was used for constructing of cDNA libraries. Differential expressed non-coding RNAs were identified using R package DESeq2.

2022-11-01 | E-MTAB-12088 | 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)

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 A/Puerto Rico/8/1934 influenza virus (H1N1) or vesicular stomatitis virus (VSV). 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-35266 | biostudies-arrayexpress

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