E-GEOD-21048
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA126431
PROVIDER: E-GEOD-21048 | ExpressionAtlas | 2015-09-15
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-21048-analysis-methods.tsv | Tabular | |||
| E-GEOD-21048-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-21048-configuration.xml | Xml | |||
| E-GEOD-21048-percentile-ranks.tsv | Tabular | |||
| E-GEOD-21048.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 89 |
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Project description:Prednisolone-induced differential gene expression in liver of mice carrying the wild type or a dimerization-defective glucocorticoid receptor
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Project description:Glucocorticoids control expression of a large number of genes after binding to the glucocorticoid receptor (GR). Transcription may be regulated either by binding of the GR dimer to DNA regulatory elements or by protein-protein interactions of GR monomers with other transcription factors. Although the type of regulation for a number of individual target genes is known, the relative contribution of both mechanisms to the regulation of the entire transcriptional program remains elusive. To study the importance of GR dimerization in regulation of gene expression, we performed gene expression profiling in liver of prednisolone-treated wild type (WT) and genetically engineered mice that have lost the ability to form GR-dimers (GRdim). Mice carrying a wild type (WT) glucocorticoid receptor or a dimerization-defective glucocorticoid receptor (GRdim) were treated subcutaneous with vehicle or prednisolone (1mg/kg) and sacrificed 150 minutes later. From the livers of these mice total RNA was extracted, processed and hybridized on Affymetrix microarrays. In total 24 mice (6 vehicle-treated WT mice, 6 prednisolone-treated WT mice, 6 vehicle-treated GRdim mice and 6 prednisolone-treated GRdim mice) were included in the study.
2010-06-08 | E-GEOD-21048 | biostudies-arrayexpress
Project description:The liver of DNase II-deficient embryos contains numerous macrophages carrying undigested DNA, and the embryos die in feto. Here, we examined the gene expression in the wild-type (GSM32833) and DNase II-/- (GSM32834) fetal liver, and found that a set of interferon (IFN)-inducible genes is strongly activated in the DNase II-/- fetal liver. When the DNase II-/- mice were crossed to IFN type I receptor (IFN-IR)-null mice, the mice deficient in both DNase II and IFN-IR genes were born apparently normally, indicating that the type I IFN and its inducible genes had the lethal effect on the mouse development. To examine which genes induced by IFN is responsible to kill the embryos, the gene expression of the fetal liver of DNase II-/- IRF-IR-/- embryos (GSM32835) was also examined. Keywords: other
2004-12-01 | GSE1859 | GEO
Project description:Microglia (CD11b+ cells) were isolated from brain tissue of stress-naïve wild type and CB1-deficient (Cnr1-/-) mice using magnetic cell separation and gene expression analysed using 3' mRNA sequencing. Differential gene expression showed that Cnr1-/- microglial transcriptomes do not fundamentally differ from those of wild type controls. Only seven differentilly expressed genes remained significant after correcting for multiple testing. The top hit was Fkbp5 (encoding FK506 binding protein 5 (FKBP5), a regulator of glucocorticoid receptor activity.
2021-12-31 | GSE152266 | GEO
Project description:LEAFY COTYLEDON2 activity was induced via a LEC2-Glucocorticoid Receptor fusion protein in Arabidopsis seedlings. Experiment Overall Design: Transgenic plants carrying a 35S:LEC2-Glucocorticoid Receptor transgene were used for LEC2 induction. Activity was induced in 8 day old seedlings for 1 or 4 hours with Dexamethasone application. Controls include uninduced transgenic plants and non-transgenic plants treated with Dex. Experiment Overall Design: Two biological replicates per treatment.
2007-10-03 | E-GEOD-3959 | biostudies-arrayexpress
Project description:This study aimed to evaluate the change of liver status in the presence of hepatitis B viral proteins We evaluated the messenger RNA expression profiles of liver tissues of transgenic mices carrying wild type or mutant viral surface proteins We checked the differential RNA expressions in different transgenic mice, each with three biological replicates
2016-07-15 | E-GEOD-84429 | biostudies-arrayexpress
Project description:Cortisol, the central stress hormone in humans, activates the glucocorticoid receptor (GR). Anti-inflammatory effects are the most important pharmaceutical effects mediated by the GR. Inasmuch as electrophilic cyclopentenone prostaglandin 15-deoxy-M-NM-^T12,14-prostaglandin J2 (15d-PGJ2) has potent anti-inflammatory properties and activates the SUMOylation pathway, we have investigated the effect of 15d-PGJ2 on glucocorticoid signaling and receptor SUMOylation. To this end, we studied isogenic HEK293 cells expressing either wild-type GR or SUMOylation-defective GR. Interestingly, 15d-PGJ2 triggered SUMO-2/3 modification in the primary SUMOylation sites of the GR. Gene expression profiling and pathway analyses indicate that 15d-PGJ2 inhibits GR signaling in a genome-wide fashion that is significantly dependent on the GR SUMOylation sites. Chromatin immunoprecipitation assays showed that the repressive effect of 15d-PGJ2 on GR target gene expression occurs in parallel with the inhibition of receptor binding to the target gene chromatin. Furthermore, depletion of the sole SUMO E2 conjugase UBC9 from HEK293 cells confirmed the involvement of active SUMOylation in the regulatory process. Taken together, our data indicate that GR SUMOylation modulates the glucocorticoid signaling during acute cell stress. Our data also suggest that GR SUMOylation modulates crosstalk of the glucocorticoid signaling with other transcription factors that are responsive to cell stress. Total RNA isolated from isogenic HEK293 cell lines stably expressing either wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR) treated with 100 nM of dexamethasone (dex) in the presence or absence of 5 M-BM-5M 15d-PGJ2 for 6h. All conditions are performed in triplicate
2014-06-30 | E-GEOD-54087 | biostudies-arrayexpress
Project description:In addition to the glucocorticoids, the glucocorticoid receptor (GR) is regulated by post-translational modifications, including SUMOylation. We have analyzed how SUMOylation influences the activity of endogenous GR target genes and the receptor chromatin binding by using isogenic HEK293 cells expressing wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR). Gene expression profiling revealed that both dexamethasone up- and down-regulated genes are affected by the GR sumoylation and that the affected genes are significantly associated with pathways of cellular proliferation and survival. The GR3KR-expressing cells proliferated more rapidly and their anti-proliferative response to dexamethasone was less pronounced than in the wtGR-expressing cells. ChIP-seq analyses indicated that the SUMOylation modulates the chromatin occupancy of GR on several loci associated with cellular growth in a fashion which parallels with their differential dexamethasone-regulated expression between the two cell lines. Moreover, genome-wide SUMO-2/3 marks, which were generally associated with active chromatin, showed markedly higher overlap with the wtGR cistrome than with the GR3KR cistrome. In sum, our results indicate that the SUMOylation does not simply repress the GR activity, but regulates the activity of the receptor in a target locus selective fashion, playing an important role in controlling the GR activity on genes influencing cell growth. Total RNA isolated from U2Os cell lines stably expressing either wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR) treated with either vehicle (EtOH) or 100 nM of dexamethasone (dex) for 6h.
2013-11-05 | E-GEOD-48330 | biostudies-arrayexpress
Project description:In addition to the glucocorticoids, the glucocorticoid receptor (GR) is regulated by post-translational modifications, including SUMOylation. We have analyzed how SUMOylation influences the activity of endogenous GR target genes and the receptor chromatin binding by using isogenic HEK293 cells expressing wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR). Gene expression profiling revealed that both dexamethasone up- and down-regulated genes are affected by the GR sumoylation and that the affected genes are significantly associated with pathways of cellular proliferation and survival. The GR3KR-expressing cells proliferated more rapidly and their anti-proliferative response to dexamethasone was less pronounced than in the wtGR-expressing cells. ChIP-seq analyses indicated that the SUMOylation modulates the chromatin occupancy of GR on several loci associated with cellular growth in a fashion which parallels with their differential dexamethasone-regulated expression between the two cell lines. Moreover, genome-wide SUMO-2/3 marks, which were generally associated with active chromatin, showed markedly higher overlap with the wtGR cistrome than with the GR3KR cistrome. In sum, our results indicate that the SUMOylation does not simply repress the GR activity, but regulates the activity of the receptor in a target locus selective fashion, playing an important role in controlling the GR activity on genes influencing cell growth. Total RNA isolated from isogenic HEK293 cell lines stably expressing either wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR) treated with either vehicle (EtOH) or 100 nM of dexamethasone (dex) for 6h. All conditions are performed in triplicate
2013-11-05 | E-GEOD-48328 | biostudies-arrayexpress
Project description:A single nucleotide polymorphism (SNP) in the human glucocorticoid receptor (GR), N363S, has been the focus of several clinical studies, and some epidemiological data link this SNP to increased glucocorticoid sensitivity, coronary artery disease and increased body mass index (BMI). However, molecular studies in vitro using reporter gene expression systems have failed to define a link between this polymorphism and altered glucocorticoid receptor function. To address the biological relevancy of N363S in glucocorticoid receptor mechanisms and function, we established stable U-2 OS (human osteosarcoma) cell lines expressing wild type hGR or N363S using a tetracycline-regulated expression system. Functional assays with reporter gene systems revealed only minor differences between the wild type hGR and N363S receptors under a variety of conditions that probe for GR function. However, examination of this polymorphism by human gene microarray analysis showed, for the first time, that there are significant differences between wild type hGR and the N363S SNP in their ability to selectively regulate gene expression. Several of these genes may define the link between the N363S SNP and human disease. Keywords: human glucocorticoid receptor, N363S single nucleotide polymorphism, microarray gene analysis
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