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Uninfected and human respiratory syncytial virus (RSV)-infected A549 cells, analysed using in-solution protein IEF followed by bottom-up mass spectrometry

ABSTRACT: Proteomic data from uninfected and human respiratory syncytial virus (RSV)-infected A549 cells (24h post infection; five paired biological replicate sets). Data is related to the in-solution protein IEF workflow described in Dave et al. (2014) (PMID: 25106423). Data processed using MaxQuant (version 1.3.0.5).

INSTRUMENT(S): LTQ Orbitrap XL

ORGANISM(S): Homo Sapiens (ncbitaxon:9606) Human Respiratory Syncytial Virus A2 (ncbitaxon:11259)

SUBMITTER: Jeffrey J Gorman

PROVIDER: MSV000079453 | MassIVE | Tue Jan 12 21:17:00 GMT 2016

SECONDARY ACCESSION(S): PXD004737

REPOSITORIES: MassIVE

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A comprehensive proteomic view of responses of A549 type II alveolar epithelial cells to human respiratory syncytial virus infection.

Dave Keyur A KA Norris Emma L EL Bukreyev Alexander A AA Headlam Madeleine J MJ Buchholz Ursula J UJ Singh Toshna T Collins Peter L PL Gorman Jeffrey J JJ

Molecular & cellular proteomics : MCP 20140808 12

Human respiratory syncytial virus is a major respiratory pathogen for which there are no suitable antivirals or vaccines. A better understanding of the host cell response to this virus may redress this problem. The present report concerns analysis of multiple independent biological replicates of control and 24 h infected lysates of A549 cells by two different proteomic workflows. One workflow involved fractionation of lysates by in-solution protein IEF and individual fractions were digested usin ...[more]

PMID: 25106423

Similar Datasets

Uninfected and human respiratory syncytial virus (RSV)-infected A549 cells, analysed using bottom-up mass spectrometry

Project description:Proteomic data from uninfected and human respiratory syncytial virus (RSV) infected A549 cells (24h post infection; four biological replicate sets). Data is related to the fractionation-free workflow described in Dave et al. (2014) (PMID: 25106423). Data is processed using MaxQuant (version 1.3.0.5).

2016-08-08 | MSV000080032 | MassIVE

A549 cells and MSR-A549 cells

Project description:A549 cells and MSR-A549 cells

| PRJNA379619 | ENA

Genome-wide profiling of Glucocorticoid receptor binding in A549, Nalm-6, MEF WT and MEF GCN5/PCAF double knockout (ChIP-seq)

Project description:To identify the sequences responsible for recruitment of Glucocorticoid receptor (GR) to individual loci, we performed ChIP-seq in four cell lines : A549 (ATTC:CCL-185), Nalm-6 (ATCC:CRL-1567), immortalized mouse embryonic fibroblasts (MEFs)(PMID 21131905), and immortalized PCAF-/-; GCN5flox/ MEFs (PMID 21131905) upon glucocorticoid treatment (1.5 hrs, 1M dexamethasone).

2016-11-10 | E-MTAB-5113 | biostudies-arrayexpress

Bottom-up activation of the vocal motor forebrain by the respiratory brainstem.

Project description:Brainstem motor structures send output commands to the periphery and are dynamically modulated by telencephalic inputs. Little is known, however, about ascending brainstem control of forebrain motor structures. Here, we provide the first evidence for bottom-up activation of forebrain motor centers by the respiratory brainstem. We show that, in the avian vocal control system, activation of the brainstem inspiratory nucleus paraambigualus (PAm), a likely homolog of the mammalian rostral ventral respiratory group, can drive neural activity bilaterally in the forebrain vocal control nuclei HVC (used as a proper name) and the robust nucleus of the arcopallium (RA). Furthermore, this activation is abolished by lesions of nucleus uvaeformis (Uva), a thalamic nucleus necessary for song production. We identify a type of bursting neuron within PAm whose activity is correlated, in an Uva dependent manner, to bursting activity in RA, rather than to the respiratory rhythm, and is robustly active during the production of stimulus evoked vocalizations. Because this ascending input results in cross-hemisphere activation, our results suggest a crucial role for the respiratory brainstem in coordinating forebrain motor centers during vocal production.

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RNA-Seq data from A549 cells

Project description:RNA-Seq data from A549 cells

| PRJNA735725 | ENA

Response of A549 cells treated with Aspergillus fumigatus [WT-GC_vs_PrtT-GC]

Project description:Response of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ÎPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF treatment in a protease-dependent manner. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications. 2 independent controls (uninfected A549 cells) as ctrl3_1-2, 2 independent treatments of A549 cells with wild-type A. fumigatus germinating conidia (WT_GC_1-2 ) , 2 independent treatments of A549 cells with inert acrylic beads (Beads 1-2), 3 independent treatments of A549 cells with A. fumigatus prtT mutant germinating conidia (PrtT-GC_1-3).

2010-10-29 | E-GEOD-24984 | biostudies-arrayexpress

Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_PrtT-CF]

Project description:Response of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ÎPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF treatment in a protease-dependent manner. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications. 3 independent controls (uninfected A549 cells) as ctrl2_1-3, 3 independent treatments of A549 cells with wild-type A. fumigatus culture filtrates (WT-CF1_1-3) and 2 independent treatments of A549 cells with A. fumigatus prtT mutant culture filtrates (PrtT-CF_1-2).

2010-10-29 | E-GEOD-24985 | biostudies-arrayexpress

Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_WT-GC]

Project description:Response of A549 cells treated with Aspergillus fumigatus germinating conidia (WT-GC) or culture filtrate (WT-CF) for 8h Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ÎPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF treatment in a protease-dependent manner. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications. 3 independent controls (uninfected A549 cells) as ctrl2_1-3, 2 independent treatments of A549 cells with wild-type A. fumigatus culture filtrates (WT-CF2_1-2) and 2 independent treatments of A549 cells with wild-type A. fumigatus germinating conidia (WT-GC_2-3).

2010-10-29 | E-GEOD-24983 | biostudies-arrayexpress

Transcriptome Analysis of Plasmodium CSP stable expressing or control A549 cells

Project description:To investigate the potential effect of overexpression of Plasmodium yoelii cirumsporozoite protein on A549 cells. Control and CSP stable expression A549 cells were constructed by infected with pLenti vector and pLenti-CSP plasmids and cultured with HBSS for 24h. Total RNA from Control and CSP stable expression A549 cells was extracted using the mirVana miRNA Isolation Kit (Ambion) following the manufacturer’s protocol. RNA integrity was evaluated using the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA). The samples with RNA Integrity Number (RIN) ≥ 7 were subjected to the subsequent analysis. The libraries were constructed using TruSeq Stranded mRNA LTSample Prep Kit (Illumina, San Diego, CA, USA) according to the manufacturer’s instructions. Then these libraries were sequenced on the Illumina sequencing platform (illumina novaseq6000) and 125bp/150bp paired-end reads were generated.

2022-12-31 | GSE189311 | GEO

C4PR_LIV: N-terminomic analysis of SARS-CoV-2-infected ACE2-A549 cells (Unenriched)

Project description:Many events in viral infection are regulated through post-translational modification. In the case of positive-sense RNA viruses such as SARS-CoV-2 which encodes two viral proteases, proteolytic cleavage of both viral and cellular proteins is crucial for productive viral infection. In this work we study proteolysis in the context of SARS-CoV-2 infection of ACE2-A549 and Vero E6 cells, infected at a multiplicity of infection of 1, with samples harvested at 0,6,12 and 24h post-infection. Neo-N-termini and lysine residues were labelled at the protein level with TMTpro reagents prior to tryptic digestion. For unenriched samples, the trypsin-digested material was then fractionated offline, and analysed by LC-MS/MS for the study of total protein abundance over the infection timecourse. For enriched samples, unblocked neo-N-termini generated by tryptic digested were labelled with undecanal and depleted, yielding a sample enriched for blocked neo-N-termini (TMTpro, N-terminal acetylation, and pyroGlu). The enriched samples were similarly fractionated offline and analysed by LC-MS/MS. Please note this is one of several linked datasets. This dataset contains data from ACE2-A549 cells infected with SARS-CoV-2, prior to enrichment.

2021-07-29 | PXD021145 | Pride

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