Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-39338
PROVIDER: PRJNA170664 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from glucocorticoid-treated ALL (BCR-ABL patients)
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Project description:This SuperSeries is composed of the following subset Series: GSE39335: Expression data from glucocorticoid-treated ALL (BCR-ABL patients) GSE39338: Expression data from glucocorticoid-treated ALL (CCRF-CEM-C7-14 cells) Refer to individual Series
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Project description:Expression data from glucocorticoid-treated ALL (CCRF-CEM-C7-14 cells)
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Project description:We performed RNA-seq on peripheral blood mononuclear cells (PBMC) from healthy human donors treated with interferon alpha 2a (1000IU/mL) +/- dexamethasone 10^-7M, with the aims of studying interactions between IFN and glucocorticoid induced gene expression, as well as identifying potential transcripts that may be used as a glucocorticoid exposure signature in clinical practice in patients with SLE. Transcripts identified from RNA-seq data were analysed in SLE patient data sets to validate clinical utility. We found that dexamethasone minimally impacts on interferon stimulated gene expression however IFN altered gene transcription of many previously reported glucocorticoid induced genes.
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Project description:A four-dimensional data-independent acquisition(4D-DIA) approach was used to analyse protein expression in glucocorticoid-sensitive (GCS) and glucocorticoid-resistant (GCR) children with ITP. 47 differentially expressed proteins (36 up-regulated and 11 down-regulated) were identified in the GCR group compared with the GCS group.
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Project description:The glucocorticoid receptor (GR) binds the human genome at >10,000 sites, but only regulates the expression of hundreds of genes. To determine the functional effect of each site, we measured the glucocorticoid (GC) responsive activity of nearly all GR binding sites (GBSs) captured using chromatin immunoprecipitation (ChIP) in A549 cells. 13% of GBSs assayed had GC-induced activity. The responsive sites were defined by direct GR binding via a GC response element (GRE) and exclusively increased reporter- gene expression. Meanwhile, most GBSs lacked GC-induced reporter activity. The non-responsive sites had epigenetic features of steady state enhancers and clustered around direct GBSs. Together, our data support a model in which clusters of GBSs observed with ChIP-seq reflect interactions between direct and tethered GBSs over tens of kilobases. We further show that those interactions can synergistically modulate the activity of direct GBSs, and may therefore play a major role in driving gene activation in response to GCs. Glucoroticoid receptor binding site chip-seq libraries were cloned into STARR-seq for massively parallel functioal analysis. The results were confirmed by ChIP-Exo performed on the GR in A549 cells treated with 100 nM dexamethasone for one hour. This dataset [6] contains the ChIP exo data from cells treated with 100 nM DEX.
2016-08-25 | E-GEOD-79429 | biostudies-arrayexpress
Project description:The glucocorticoid receptor (GR) binds the human genome at >10,000 sites, but only regulates the expression of hundreds of genes. To determine the functional effect of each site, we measured the glucocorticoid (GC) responsive activity of nearly all GR binding sites (GBSs) captured using chromatin immunoprecipitation (ChIP) in A549 cells. 13% of GBSs assayed had GC-induced activity. The responsive sites were defined by direct GR binding via a GC response element (GRE) and exclusively increased reporter- gene expression. Meanwhile, most GBSs lacked GC-induced reporter activity. The non-responsive sites had epigenetic features of steady state enhancers and clustered around direct GBSs. Together, our data support a model in which clusters of GBSs observed with ChIP-seq reflect interactions between direct and tethered GBSs over tens of kilobases. We further show that those interactions can synergistically modulate the activity of direct GBSs, and may therefore play a major role in driving gene activation in response to GCs. Glucoroticoid receptor binding site chip-seq libraries were cloned into STARR-seq for massively parallel functional analysis. The results were confirmed by ChIP-Exo performed on the GR in A549 cells treated with 100 nM dexamethasone for one hour. This dataset [8] contains ChIP-seq data for A549 cells treated with DEX or EtOH for 3 hours.
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Project description:These data describe single-cell RNA sequencing in cerebral organoids treated with the glucocorticoid Dexamethasone or with a vehicle control (DMSO) at 90 days in culture.
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