Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene alteration in A549 cells by disinfectant PHMG

ABSTRACT: Polyhexamethyl guanidine is widely used as a disinfectant in various places such as hospitals and restaurants. In order to examine of PHMG cytotoxicity in lung adenocarcinoma A549 cells we treated 5 ug/ml PHMG for 24 h. To investigate cytotoxicity of commonly used bactericidal reagent PHMG, A549 cells were treated 5 ug/ml PHMG for 24 h. After then purified the total RNA from treated and untreated cells using the Rneasy mini kit (Qiagen). The concentration and purity of the total RNA was measured and performed gene array.

ORGANISM(S): Homo sapiens

SUBMITTER: Yong-Sik Kim

PROVIDER: E-GEOD-41156 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene alteration in A549 cells by disinfectant PHMG

Project description:Polyhexamethyl guanidine is widely used as a disinfectant in various places such as hospitals and restaurants. In order to examine of PHMG cytotoxicity in lung adenocarcinoma A549 cells we treated 5 ug/ml PHMG for 24 h.

2012-09-27 | GSE41156 | GEO

Global gene expression profiling of human lung epithelial cells after exposure to nanosilver

Project description:In this study, the effect of AgNPs on the gene expression in the human lung epithelial cell line A549, exposed to 12.1 ug/ml AgNPs (EC20) for 24 and 48 hours was compared with the response to control and silver ion (Ag+) treated cells (1.3 ug/ml) using microarray analysis.

2012-04-16 | E-MEXP-3583 | biostudies-arrayexpress

Transcription profiling of human A549 lung cancer cells treated with compounds from a series of inhibitors developed against the human LIM kinases LIMK1 and LIMK2

Project description:To investigate an unknown mechanism of cytotoxicity, A549 human lung-cancer cells were treated with compounds from a series of inhibitors developed against the human LIM kinases LIMK1 and LIMK2. Compounds 1 and 2 inhibit LIM kinase activity in vitro and affect cell proliferation and survival in vivo. Compounds 3 and 4 inhibit LIM kinases but do not affect cell survival or proliferation. Compounds 5 and 6 affect proliferation and survival but do not inhibit LIM kinases. Nocodazole was included as a comparator because the compounds were known to affect microtubule stability. A treatment of 7 hours was used to examine events prior to apoptosis, while the dose levels captured both cytotoxicity and inhibition of LIMKs (Compounds 1 and 2), LIMK inhibition alone ( Compounds 3 and 4) or cytotoxicity alone (Compounds 5, 6, and Nocodazole).

2008-09-17 | E-TABM-450 | biostudies-arrayexpress

Response of A549 cells treated with Aspergillus fumigatus

Project description:This SuperSeries is composed of the following subset Series: GSE24983: Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_WT-GC] GSE24984: Response of A549 cells treated with Aspergillus fumigatus [WT-GC_vs_PrtT-GC] GSE24985: Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_PrtT-CF] Refer to individual Series

2010-10-29 | E-GEOD-24986 | biostudies-arrayexpress

C646, a Novel p300/CREB-Binding Protein-Specific Inhibitor of Histone Acetyltransferase, Attenuates Influenza A Virus Infection

Project description:Whole-genome data was developed from influenza virus infected A549 cells to better characterize the effect of C646 on influenza virus infection A549 cells were treated with C646 or DMSO for 10 h, and then were infected with A/WSN/33 virus (WSN; H1N1) at a multiplicity of infection (MOI) 2. A549 cells for microarray studies were collected at different times. The gene expression in A549 cells was compared between C646-treated group and DMSO-treated group.

2016-01-07 | E-GEOD-72503 | biostudies-arrayexpress

Comparison of gene expression profiles of A549 cell treated with NRF2 siRNA and control siRNA

Project description:To examine the role of NRF2 in accelerating cell proliferation and to identify the target genes responsible for this function, transcriptome analysis was performed using A549 cells, in which NRF2 is constitutively activated. NRF2 was knocked down by siRNA against NRF2, and the gene expression profile was compared with that of A549 cells treated with control siRNA. To exclude off-target effects, three different siRNAs against NRF2 was independently applied. NRF2 siRNA or control siRNA was transfected into A549 cells. Cells were harvested 24 hours after transfection, and total RNA was purified.

2011-04-01 | E-GEOD-28230 | biostudies-arrayexpress

miRNA expression of lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. miRNA expression of A549 and A549/DDP was then analzyed.

2016-08-16 | E-GEOD-85603 | biostudies-arrayexpress

Integration of metabolomics and transcriptomics to reveal metabolic characteristics and key targets associated with cisplatin resistance in non-small cell lung cancer

Project description:Continuous exposure to cisplatin can induce drug resistance to limit efficacy, however, the underlying mechanisms correlated to cisplatin resistance are still unclear. Drug-sensitive A549 cells and cisplatin-resistant A549/DDP cells were used to explore the potential metabolic pathways and key targets associated with cisplatin resistance by integrating untargeted metabolomics with transcriptomics. The results of comprehensive analyses showed that 19 metabolites were significantly changed in A549/DDP vs A549 cells, and some pathways had a close relationship with cisplatin resistance, such as the biosynthesis of aminoacyl-tRNA, glycerophospholipid metabolism, and glutathione metabolism. Moreover, transcriptomics analysis showed glutathione metabolism was also obviously affected in A549/DDP, which indicated that glutathione metabolism played an import role in the process of drug resistance. Meanwhile, transcriptomics analysis suggested the four enzymes related to glutathione metabolism - CD13, GPX4, RRM2B, and OPLAH - as potential targets of cisplatin resistance in NSCLC. Further studies identified the over-expressions of these four enzymes in A549/DDP. The elucidation of mechanism and discovery of new potential targets may help us have a better understanding of cisplatin resistance.

2019-08-12 | PXD013265 | Pride

RNA-seq data sets of human non small cell lung cancer line A549 treated with feiyanning against untreated controls, during co-culture with macrophages.

Project description:RNA-seq analysis was performed in co-cultured A549 cells with or without feiyanning. A549 cells and macrophages were incubated 48h together in serum-free medium for producing co-cultured A549 cells. Treated groups were supplemented with Chinese traditional medicine Feiyanning.

2023-12-31 | E-MTAB-12420 | biostudies-arrayexpress

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

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