Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MEXP-1072

ABSTRACT: Transcription profiling by array of human A549 epithelial cells infected with poliovirus

PROVIDER: E-MEXP-1072 | ExpressionAtlas | 2025-01-22

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MEXP-1072-analysis-methods.tsv	Tabular
	E-MEXP-1072-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-1072-configuration.xml	Xml
	E-MEXP-1072-percentile-ranks.tsv	Tabular
	E-MEXP-1072-zoomifications-log.tsv	Tabular

Items per page:

1 - 5 of 64

Similar Datasets

Host microRNA molecular signatures associated with human H1N1 and H3N2 influenza A viruses

Project description:In this study, we performed a miRNA global profiling in human lung epithelial cells (A549) infected by two different subtypes of human influenza A viruses (H1N1 and H3N2). A549 cells were either mock-infected or infected at a multiplicity of infection (MOI) of 1 with H1N1 or H3N2 viruses, and total RNAs were isolated at 24 hours post-infection (hpi). An MOI of 1 was performed to ensure that 100% of the cells were infected at 24 hpi, a strategy that we have previously validated and used for a transcriptional profiling study of infected cells (Josset et al. , 2010). The purified RNAs were subjected to reverse transcription using a pool of miRNA RT primers (Human pool A v2.1, Applied Biosystems) and subsequently amplified and quantified by RT-qPCR in a TaqMan array MicroRNA card (Applied biosystems).

2013-04-03 | E-GEOD-42003 | biostudies-arrayexpress

Host microRNA molecular signatures associated with human H1N1 and H3N2 influenza A viruses

Project description:In this study, we performed a miRNA global profiling in human lung epithelial cells (A549) infected by two different subtypes of human influenza A viruses (H1N1 and H3N2).

2013-04-03 | GSE42003 | GEO

Dual-action host-guest chemistry suppresses PAO1 virulence in A549 cell line model

Project description:Our study showed that selected pillararene was able to decrease the level of cell death and demage caused to human A549 epithelial cells by Pseudomonas aeruginosa PAO1 infection. To further understand the protective effects of pillararene during bacterial infections, we analyzed total mRNA isolated from the A549 epithelial cells. Our study showed that pillararene alone had minimal effect on A549 epithelial cells. The addition of PAO1 to A549 cells greatly altered expression levels. The addition of pillararene to infected A549 epithelial cells displayed a concentration-dependent reduction in the inflammatory response.

2023-02-27 | GSE182847 | GEO

Retinoic Acids Exposure Alters TGFbeta1 -Induced Epithelial Mesenchymal Transition via Wnt5b expression.

Project description:Idiopathic pulmonary fibrosis (IPF) is a refractory and lethal interstitial lung disease; EBV has previously been localised to alveolar epithelial cells of IPF patients. The molecular process of the epithelial mesenchymal transition (EMT) in IPF remains still unknown. Using an oligonucleotide array analysis, we observed dysregulated expression of members of non-canonical Wnt family in EBV infected A549 after TGF?1 exposure. TGF?1 exposure induced EMT increasing ?-Smooth Muscle Actin (ACTC) and Wnt5b gene expression, but decreasing E-cadherin and DKK1. When data were analyzed as a function of Wnt5b in EMT, significance differences in ACTC and E-cadherin gene expression, active TGF?1 protein levels and collagen deposition could be detected. Treatment with 9-cis Retinoic Acid (9-cisRA) significantly inhibited Wnt5b expression in both EBV infected and non-infected A549, followed by decreased collagen deposition and active TGF?1 protein level. Specific non-canonical Wnt-signalling genes are dysregulated in EBV infected cells and A549 treated with TGF?1; while, 9-cisRA treatment appears to attenuate EMT process in vitro. Keywords: EBV infection, EMT and non-canonical Wnt pathway in A549 detected by oligonucleotide array

2006-08-05 | GSE5457 | GEO

Proteomic characterization of the interplay of Staphylococcus aureus and human alveolar epithelial cells during infection - S. aureus proteins

Project description:Since infectious diseases caused by Staphylococcus aureus are still a major threat for human health we aimed to gain a detailed understanding of the molecular interplay of pathogen and host upon internalization by proteome analyses. In the present study we infected human alveolar epithelial A549 cells with S. aureus HG001 pMV158GFP and separated intact bacteria from host cell debris or infected from non-infected A549 cells prior to proteome analysis by cell sorting thus facilitating detailed analyses. During the first 6.5 h in the intracellular milieu S. aureus displayed reduced growth rate, induction of the stringent response, and adaptation to microaerobic conditions as well as cell wall stress. Interestingly, both truly infected host cells and those only potentially exposed to secreted S. aureus proteins but not infected displayed differences in the proteome pattern compared to A549 cells which had never been in contact with S. aureus. However, adaptation reactions were more pronounced in infected compared to non-infected A549 cells. Additional cytokine measurements revealed elaborated levels of pro-inflammatory cytokines in supernatants of the infection setting compared to pure host cell cultures which might mediate communication among the host cells and trigger adaptation even in cells not infected with S. aureus.

2015-08-05 | PXD002384 | Pride

Proteomic characterization of the interplay of Staphylococcus aureus and human alveolar epithelial cells during infection - host cell proteins

2015-08-05 | PXD002388 | Pride

Differential Mitochondrial proteomics analysis of A549 cells infected with H5 and H9 subtypes of avian influenza viruses

Project description:The temporal response of primary human alveolar adenocarcinoma epithelial cells (A549) infected with H5N1 influenza virus and H9N2 influenza A viruswere evaluated using the proteomics approaches (2D-DIGE combined with MALDI-TOF-MS/MS) at 24 hours post of the infection .

2020-03-06 | PXD017921 |

microRNA (miRNA) expression profiling of A549 with H5N1 Influenza A Virus (hm/06)infection

Project description:To study miRNA expression profiles during highly pathogenic avian influenza virus infection, we conducted global miRNA expression profiling in human lung epithelial cells (A549) with or without H5N1 IAV infection. .

2014-09-25 | GSE61701 | GEO

Differential miRNA expression profiling of A549 cells infected with influenza A virus

Project description:To further understand the roles of miRNA during influenza A virus infection, we performed miRNA profiling in human alveolar adenocarcinoma cell lines, A549 cells, infected with influenza A virus A/Beijing/501/2009(H1N1) and A/goose/Jilin/hb/2003(H5N1).

2017-03-22 | GSE96857 | GEO

Gene Expression Data from Influenza A Virus-Infected and Mock-infected A549 Human Aveolar Epithelial Carcinoma Cells with Exposure to Mouse Eosinophils.

Project description:Eosinophils are terminally differentiated granulocytes that participate in innate immunity against Influenza A Virus (IAV). Here, we investigate transcriptional changes that occur in IAV-infected human A549 aveolar epithelial carcinoma cells with and without direct or indirect exposure to mouse bone marrow-derived eosinophils (BMdEos). Global changes in the transcriptome of A549 cells due to Influenza A virus-infection and/or direct and indirect eosinophil exposure were assessed using ThermoFisher/Affymetrix Clariom™ S Human microarrays.

2021-03-31 | GSE163224 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data