Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of genes that regulated by lnc-CXCL2-4-1

ABSTRACT: To demonstrate the regulating function of lnc-CXCL2-4-1 in lung epithelial cells after viral infection, we performed transcriptome sequencing of wild-type and lnc-CXCL2-4-1-silenced A549 cells after influenza A virus (IAV) infection, and then analyzed differentially expressed genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179951 | GEO | 2021/09/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

lnc-Cxcl2 suppressed Cxcl2 expression in mouse lung epithelial cells

Project description:In this study, we performed RNA-seq in GFP-VSV infected mouse lung epithelial cell lines (MLE-12 cells) and found that the expression of a non-coding RNA was increased upon VSV infection in Cxcl2 locus, which we termed it as lnc-Cxcl2. We further detected the function of lnc-Cxcl2 by performing transcriptome analysis in lnc-Cxcl2-deficient MLE-12 cells with and without VSV infection, and found that lnc-Cxcl2 suppressed Cxcl2 expression in MLE-12 cells with and without VSV infection.

2021-09-26 | GSE156949 | GEO

lnc-Cxcl2 suppressed Cxcl2 expression in mouse lung epithelial cells

Project description:lnc-Cxcl2 suppressed Cxcl2 expression in mouse lung epithelial cells

| PRJNA659645 | ENA

Transcriptome analysis of genes that regulated by lnc-CXCL2-4-1

Project description:Transcriptome analysis of genes that regulated by lnc-CXCL2-4-1

| PRJNA745977 | ENA

lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

2018-11-07 | PXD011577 | Pride

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

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

Endogenous pull-downs of human proteins ATP6V1A and AHNAK to validate interactions with influenza A virus proteins M2 and NEP by targeted mass spectrometry in virus-infected cells

Project description:Influenza A Virus (IAV) is a recurring respiratory virus with antiviral therapies of limited use. Understanding host proteins essential for IAV infection can identify targets for alternative host-directed therapies (HDTs). Using affinity purification-mass spectrometry (AP-MS) and global phosphoproteomic and protein abundance analyses with three IAV strains (pH1N1, H3N2, H5N1) in three human cell types (A549, NHBE, THP-1), we mapped 332 IAV-human protein-protein interactions (PPIs) and identified 13 IAV-modulated kinases. Whole exome sequencing of patients who experienced severe influenza revealed several genes, including the structural scaffold protein AHNAK, with predicted loss-of-function variants that were also identified in our proteomic analyses. Of our identified host factors, 54 significantly altered IAV infection upon siRNA knockdown, and two factors, COPB1 and AHNAK, were also essential for productive infection by SARS-CoV-2. Finally, 16 compounds targeting our identified host factors suppressed IAV replication, with two targeting CDK2 and FLT3 showing pan-antiviral activity across influenza and coronavirus families. This study provides a comprehensive network model of IAV infection in human cells, identifying functional host targets for pan-viral HDT. This project includes endogenous IP data from A549 cells and NHBE cells infected with H5N1 IAV validating IAV-host PPIs M2-ATP6V1A and NEP-AHNAK, respectively. M2-ATP6V1A and NEP-AHNAK PPIs were first identified in AP-MS data that is submitted under its own dataset identifier (PXD036077).

2023-07-25 | PXD041663 | Pride

Influenza virus facilitates its infectivity by activating p53 to inhibit the expression of interferon-induced transmembrane proteins (IFITMs)

Project description:Transcriptome analysis of mock or H1N1 IAV PR8 infected p53WT A549 and p53null A549-KO3 cells by Affymetrix GeneChip Human Transcriptome 2.0 Arrays to achieve a set of genes those are regulated by p53 and responsive to IAV infection. Influenza A virus infection activates cellular p53, however it has not been clear whether this process has pro- or anti- viral effects. In this study, using human isogenic p53 wildtype A549 cells and p53null A549-KO3 cells generated from the CRISPR/Cas9 technology, we report that p53null cells exhibit significantly reduced viral propagation property when infected with influenza A virus (H1N1/A/Puerto Rico/8/34). Here, using genome-wide microarray analysis we revealed that p53 regulates the expression of a large set of interferon-inducible genes, some of which are directly associated with viral infectivity and later experimentally validated to be responsible for p53-regulated IAV infectivity.

2018-05-31 | GSE106279 | GEO

microRNA-mediated GALNT3 upregulation facilitates mucin production and viral replication in influenza A virus-infected respiratory epithelial cells

Project description:Viral infections affecting the upper or lower respiratory tract induce mucin production in the epithelial surfaces of the respiratory cells. However, a little is known about how mucins are produced on the surfaces of respiratory epithelial cells and affects viral replication. In the course of the investigation of the cellular responses in the early stage of Influenza A virus (IAV) infection, we found that two miRNAs, miR-221 and miR-17-3p, which target the mRNA of GalNAc transferase 3 (GALNT3), are rapidly down-regulated as early as 1.5 h post-infection. To understand the early host cell responses to the IAV infection, we performed miRNA microarray analysis using a human alveolar adenocarcinoma cell line, A549 cells, infected with influenza A/Puerto Rico/8/34 H1N1 (PR8) virus. We isolated the cellular RNAs at 0.5, 1.5 and 4.5 h post-infection and detected significant changes in the global profile of miRNA expression after infection with IAV. mouse embryonic fibroblasts. Each sample was run in duplicate.

2015-12-08 | E-GEOD-57508 | biostudies-arrayexpress

Global Protein Abundance and Phosphorylation Analyses of Influenza A Virus (IAV)-Infected Human Cells

Project description:Influenza A Virus (IAV) is a recurring respiratory virus with antiviral therapies of limited use. Understanding host proteins essential for IAV infection can identify targets for alternative host-directed therapies (HDTs). Using affinity purification-mass spectrometry and global phosphoproteomic and protein abundance analyses with three IAV strains (pH1N1, H3N2, H5N1) in three human cell types (A549, NHBE, THP-1), we mapped 332 IAV-human protein-protein interactions and identified 13 IAV-modulated kinases. Whole exome sequencing of patients who experienced severe influenza revealed several genes, including the structural scaffold protein AHNAK, with predicted loss-of-function variants that were also identified in our proteomic analyses. Of our identified host factors, 54 significantly altered IAV infection upon siRNA knockdown, and two factors, COPB1 and AHNAK, were also essential for productive infection by SARS-CoV-2. Finally, 16 compounds targeting our identified host factors suppressed IAV replication, with three targeting ATP6V1A, CDK2 and FLT3 showing pan-antiviral activity across influenza and coronavirus families. This study provides a comprehensive network model of IAV infection in human cells, identifying functional host targets for pan-viral HDT. This project includes the global proteomic data (abundance and phosphorylation), the AP-MS data has been submitted separately as its own dataset and has its own dataset identifier.

2023-07-25 | PXD035900 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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