Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA Sequencing Analysis of H1299 cells with Hyperoxia Treatment and Control Cells

ABSTRACT: Purpose: To study the effect of hyperoxia on lung cancer cells, H1299 cells were cultured in 60% O2 for 12 h and 24 h, and RNA-seq was performed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE192839 | GEO | 2023/03/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA Sequencing Analysis of H1299 cells with Hyperoxia Treatment and Control Cells

Project description:RNA Sequencing Analysis of H1299 cells with Hyperoxia Treatment and Control Cells

| PRJNA793435 | ENA

H1299 cells: p53 transcriptional response in hypoxia

Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant. Four-condition experiment: wt p53-transfected H1299 cells treated with normoxia, mut p53-transfected H1299 cells treated with normoxia, wt p53-transfected H1299 cells treated with hypoxia, mut p53-transfected H1299 cells treated with hypoxia. Biological replicates: 1 normoxic sample with wt p53, 1 normoxic sample with mut p53, 3 hypoxic samples with wt p53, 3 hypoxic samples with mut p53.

2014-01-08 | E-GEOD-53893 | biostudies-arrayexpress

Gene expression signatures for hyperoxia in lung cancer cell lines

Project description:Gene profile of normoxia (20% O2) was compared with that of hyperoxia (50% O2) in lung cancer cell lines.

2017-08-17 | GSE102705 | GEO

Meythlation profiling by array to investigate the effect of hyperoxia on DNA methylation in mouse lung tissue

Project description:Hyperoxia has a potential to alter DNA methylation status. We assessed the effect of long term hyperoxia in mouse lung tissue. A total of 24 mice were randomized to hyperoxia (85% O2; 12 animals) or normoxia (21% O2; 12 animals) for 14 days continued with normoxia conditions for all animals for the subsequent 14 days. All mice had free access to food and water and were kept under standard conditions in A-Chambers (O2 – monitor ProOX110, CO2 – monitor ProCO2 P120, BioSpherix). The animals were sacrificed on day 28. Lung tissue was harvested on day 28 after euthanasia with a zolazepam/tiletamine/xylazine/fentanyl cocktail. Tissues samples were snap-frozen in liquid nitrogen immediately after cessation of circulation for the subsequent analysis. Subsequently, DNA methylation profiles in lung tissue were compared by means of methylation microarrays between both groups. We used the Genomic Workbench software (Agilent) to assess the mean methylation status of each DNA fragment (array probe) in each group. We first calculated the normalised, combined Z-scores, representing summation of the left and right Gaussian Z-scores and reflecting the location of a probe log-ratio value in relation to the Gaussian distribution of probes. A strong positive value of the combined Z-score means that a given probe is methylated and strong negative value means that it is unmethylated. Next, we compared the mean combined Z-scores (average methylation patterns) of the probes between hyperoxia and normoxia groups.

2018-02-17 | E-MTAB-6489 | biostudies-arrayexpress

Differential microRNA gene expression between normal and aberrant late lung development induced by hyperoxia in mice

Project description:Newborn mouse pups were exposed either to normoxia (21% O2) or to hyperoxia (85% O2) since the day of birth. Lungs were harvested at P2.5, P3.5, P5.5 and P14.5 and homogenized for a downstream microRNA (miR) microarray in order to compare the differential expression of miRs between normoxia and hyperoxia group. Several miRs appeared to be dysregulated, mainly and with a higher significance, at P5.5 and P14.5.

2017-02-25 | GSE89666 | GEO

H1299 cells: p53 transcriptional response in hypoxia

2014-01-08 | GSE53893 | GEO

Expression profiling of Hyperoxia-Tolerant Drosophila melanogaster

2018-10-23 | GSE12160 | GEO

Expression profiling of Hyperoxia-Tolerant Drosophila melanogaster

Project description:One of the critical substances that mammals highly regulate via the respiratory, cardiovascular and neurologic systems is O2. Both low and high O2 levels can induce major morbidities as well as mortality. Indeed, O2 has been often considered as both an elixir and a poison in humans. In current study, we have used an experimental selection approach to generate Drosophila strains that are tolerant to severe hyperoxic environment. Gene expression profiling is then applied to investigate the mechanisms underlying hyperoxia tolerance in the newly generated strains. 27 isogenic D. melanogaster Lines were pooled and following long-term selection over generations with increased oxygen level in the culture environment. The differences in gene expression were compared between adapted flies and generation matched naive controls by microarray.

2010-07-30 | E-GEOD-12160 | biostudies-arrayexpress

Baby Mice Hyperoxia treatment (G64-N.H-7d14d)

Project description:In this experiment 2 day old baby mice were exposed to hyperoxia (75% O2) continuously for 14 days. Control baby mice were housed in room air (normoxia). Plasma and bronchoalveolar lavage fluid (BALF) were harvested after 14 days of exposure (on Day of life 16)

2014-10-28 | ST000169 | MetabolomicsWorkbench

Exosomes of p53 mutant H1299 cells

Project description:Proteome of exosomes purified from H1299-p53R273H (mutant) and H1299-p53-/- cells, which found the levels of Podocalyxin altered in p53-mutant cells.

2018-12-04 | PXD011241 | Pride

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