E-GEOD-42619
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA182368PRJNA182369PRJNA178695
PROVIDER: E-GEOD-42619 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-42619-analysis-methods.tsv | Tabular | |||
| E-GEOD-42619-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-42619-configuration.xml | Xml | |||
| E-GEOD-42619-percentile-ranks.tsv | Tabular | |||
| E-GEOD-42619.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 140 |
Similar Datasets
Project description:Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERα agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).
| PRJNA182369 | ENA
Project description:Retinoic acid (RA) triggers growth-suppressive effects in tumor cells and therefore RA and its synthetic analogs have great potential as anti-carcinogenic agents. RA effects are mediated by retinoic acid receptors (RARs), which regulate gene expression in an RA-dependent manner. To define the genetic network regulated by RARs in breast cancer cells, we identified RAR genomic targets using chromatin immunoprecipitation and expression analysis in a model breast cancer cell line MCF-7. Furthermore, we identified genomic binding sites for two putative RAR coregulators FoxA1 and GATA3. Keywords: ChIP-Chip Analysis This series contains ChIP-Chip raw data for four transcription factors (RARA, RARG, FoxA1 and GATA3) in MCF-7 cells. All the experiments are done in triplicates. We mapped the binding sites of RARA, RARG and GATA3 in the bacterial artificial chromosome (BAC) transgenic MCF7 cells in which we tagged the transcription factors with a modified LAP (localization and affinity purification) tag containing green fluorescent protein (GFP). Goat anti-GFP (raised against His-tagged full-length eGFP and affinity-purified with GST-tagged full-length eGFP) was used to perform ChIP experiments in those transgenic lines. To map the binding sites of RARs, MCF7 Cells were hormone-deprived for 3 days and then were treated with 100 nM AM580 (RARA-selective agonist) or 100 nM CD437 (RARG-selective agonist) for 1 hour at 80% confluence. FoxA1 binding sites were mapped using goat anti-FoxA1 antibodies (Abcam: ab5089). Control data include Input from MCF-7 cells. ChIP-Chip experiments with eGFP antibody in wide type MCF-7 cells are used to control eGFP antibody non-specific binding.
2009-03-16 | E-GEOD-15244 | biostudies-arrayexpress
Project description:CUT&Tag technology were used for high-throughput profiling of RARG fusion genes or PML-RARA with core promoters of its target genes in hCD34+ cells with RARG fusion genes or PML-RARA overexpression. We first expressed HA-tagged X-RARG fusions or HA-tagged PML-RARA in hCD34+ cells and then performed CUT&Tag with antibody to RARG fusion genes or PML-RARA and analyzed the binding of RARG fusion genes or PML-RARA with core promoters of its target genes. Common peaks for the binding sites of RARG fusions and PML-RARA and unique peaks for specific targets of RARG fusions that are not targets of PML-RARA were identified.
2024-10-15 | GSE243414 | GEO
Project description:Currently, AML with RARG rearrangements (RARG AML), including NUP98-RARG, PML-RARG, CPSF6-RARG, NPM1-RARG, and HNRNPC-RARG, has been identified as a novel entity of AML. Overexpression of RARG fusions in human CD34+ cells promoted the expansion of immature myeloid cells, reduced the percentage of mature granulocytes, inhibited the differentiation of myeloid cells, and self-renewal abilities of hCD34+ cells. To understand how RARG fusion proteins regulate their target genes in the hematopoietic system, we first expressed HA-tagged X-RARG fusions or HA-tagged PML-RARA in hCD34+ cells. We then analyzed the differential genes expression in hCD34+ cells with or without RARG fusion genes or PML-RARA overexpression through RNA-seq.
2024-10-15 | GSE243437 | GEO
Project description:Steroid hormone receptors are simultaneously active in many tissues and capable of altering each other's function. Estrogen receptor ɑ (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors expressing high levels of ER, we surprisingly found that expression of GR is associated with poor prognosis. Dexamethasone reduced normal uterine growth in vivo; however, this growth inhibition was abolished in estrogen-induced endometrial hyperplasia. We observed low genomic binding site overlap when ER and GR are induced with their respective ligands; however, upon simultaneous induction they co-occupy more sites. GR binding is significantly altered by estradiol with GR recruited to ER bound loci that become more accessible upon estradiol induction. Gene expression responses to co-treatment were more similar to estradiol, but with novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.
2018-03-13 | GSE109892 | GEO
Project description:Steroid hormone receptors are simultaneously active in many tissues and capable of altering each other's function. Estrogen receptor ɑ (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors expressing high levels of ER, we surprisingly found that expression of GR is associated with poor prognosis. Dexamethasone reduced normal uterine growth in vivo; however, this growth inhibition was abolished in estrogen-induced endometrial hyperplasia. We observed low genomic binding site overlap when ER and GR are induced with their respective ligands; however, upon simultaneous induction they co-occupy more sites. GR binding is significantly altered by estradiol with GR recruited to ER bound loci that become more accessible upon estradiol induction. Gene expression responses to co-treatment were more similar to estradiol, but with novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.
2018-03-13 | GSE109891 | GEO
Project description:Steroid hormone receptors are simultaneously active in many tissues and capable of altering each other's function. Estrogen receptor ɑ (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors expressing high levels of ER, we surprisingly found that expression of GR is associated with poor prognosis. Dexamethasone reduced normal uterine growth in vivo; however, this growth inhibition was abolished in estrogen-induced endometrial hyperplasia. We observed low genomic binding site overlap when ER and GR are induced with their respective ligands; however, upon simultaneous induction they co-occupy more sites. GR binding is significantly altered by estradiol with GR recruited to ER bound loci that become more accessible upon estradiol induction. Gene expression responses to co-treatment were more similar to estradiol, but with novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.
2018-03-13 | GSE109890 | GEO
Project description:In zebrafish, ovulated oocytes contain both cortisol deposited from the maternal circulation and maternal mRNA for the glucocorticoid receptor (gr mRNA), which is spread as granular structures throughout the central ooplasm. At the 1-cell stage (0.2 hpf), this transcript is relocated by streamers in the blastodisc area and equally partitioned among blastomeres. At 15 hpf, it is replaced by the zygotic transcript. Morpholino knockdown was applied to block translation (grATG1MO or MO2-nr3c1 and grATG2MO or MO3-nr3c1) of both maternal and zygotic gr transcripts, while a missplicing morpholino (grmismMO or MO4-nr3c1) was used to block post-transcriptionally the zygotic transcript alone. MO2-nr3c1 and MO3-nr3c1 (but not MO4-nr3c1) treatment produced craniofacial and caudal malformations in 1-dpf embryos and 5-dpf larvae, which were also affected by pericardial oedema, persistent yolk sac, reduced subintestinal veins, altered neurogenesis and uninflated swim bladder. Such effects were rescued with trout gr2 mRNA. Pangenomic microarray analysis revealed that 114 and 37 highly expressed transcripts were up- and down-regulated, respectively, by maternal GR protein deficiency in 5-hpf embryos. Similar alterations were found at 10 hpf. These effects were confirmed by real-time PCR of 2 up- (casp8, grp1 and igf2a) and 1 down-regulated transcripts (mcm6) evaluated at 4, 8 and 12 hpf. As the contents of transcripts were modified already at 4 hpf, it seems that the lack of GR affects both ways the molecular machinery for the degradation of maternal mRNAs. These results indicate that the maternal gr transcript participates in the maternal programming of zebrafish development. MO2-nr3c1 morphants were compared with MO2-nr3c1-5m morphants at 5 hpf and 10 hpf. MO2-nr3c1 morphants were compared with wild type (WT) at 5 hpf and 10 hpf. MO2-nr3c1 is a morpholino selected to knockdown translation of gr mRNA. MO2-nr3c1-5m is a specific control morpholino.
2011-11-16 | E-GEOD-25517 | biostudies-arrayexpress
Project description:To understand how RARG fusion proteins regulate their target genes in the hematopoietic system, we overexpressed fusions or PML-RARA in hCD34+ cells and identified target genes that are regulated by RARG fusions. We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we dected the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) associated with RARG fusions binding in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.
2024-10-16 | GSE275303 | GEO
Project description:Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors comprising retinoic acid (RARa,b,g) and retinoid X (RXRa,b,g) receptors. How a single signal induces highly complex temporally controlled networks that ultimately orchestrate physiological processes is unclear. Using an RA-inducible differentiation model we defined the temporal changes in the genome-wide binding patterns of RARg and RXRa and correlated them with transcription regulation. Unexpectedly, both receptors displayed a highly dynamic binding, with different RXRa heterodimers targeting identical loci. Comparison of RARg and RXRa co-binding at RA-regulated genes identified putative RXRa-RARg target genes that were validated with subtype-selective agonists. Gene regulatory decisions during differentiation were inferred from transcription factor target gene information and temporal gene expression. This analysis revealed 6 distinct co-expression paths of which RXRa-RARg is associated with transcription activation, while Sox2 and Egr1 were predicted to regulate repression. Finally, RXRa-RARg regulatory networks were reconstructed through integration of functional co-citations. Our analysis provides a dynamic view of RA signalling during cell differentiation, reveals RA heterodimer dynamics and promiscuity, and predicts decisions that diversify the RA signal into distinct gene-regulatory programs. Transcriptional activity in F9 cells treated with different retinoic acid receptor (RAR) agonists; like all-trans retinoic acid (ATRA), BMS961 (RARg-specific), BMS753 (RARa-specific) or BMS641(RARb-specific); has been evaluated at different time-points (2, 6, 24, 48h) and compared with that found under Ethanol-vehicle treatment conditions (48h treatment).
2011-10-10 | E-GEOD-30537 | biostudies-arrayexpress