Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-42619
PROVIDER: PRJNA182369 | ENA |
REPOSITORIES: ENA
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).
2015-08-25 | E-GEOD-42619 | ExpressionAtlas
Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. In order to understand the function of nuclear receptors in breast cancer, we treated MCF7 cells with 6 nuclear receptor agonist, and performed expression arrrays with three biological replicates each. MCF-7 cells were cultured for 48 hours in medium with 10% charcoal-stripped FBS, and then were treated with 6 diffferent NR ligand (E2, AM580, CD437, ATRA, R5020, DEX) separately for 24h before collection and processing for microarrays. Three biological replicates were collected and processed for both control and treatment. with the 100nM GW0742 (PPARD specific ligand) and 100nM ATRA (RARs ligand), then collected after 24h for microarray processing. Controls were non-treated MCF7 cells. Both treatments and controls have three biological replicates.
2013-01-01 | E-GEOD-42619 | biostudies-arrayexpress
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:Differentiating human dendritic cells were stimulated for 12 hours with RXR agonists (LG268, 9CRA, R- and S-9CDHRA) or agonists for RXR partners including GW3965 (LXRα/β panagonist), RSG (PPARγ agonist), and GW1516 (PPARδ agonist) and AM580 (RARa agonist). The gene expression changes were detected globally by Affymetrix Human Genome U133 Plus 2.0 Arrays.
2015-06-04 | GSE48573 | GEO
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:Nuclear hormone receptors (NRs) are ligand-binding transcription factors that are widely targeted therapeutically. Hormone binding triggers NR activation and their subsequent proteasomal degradation through unknown ligand-dependent ubiquitin ligase machinery. NR degradation is therapeutically relevant. Efficacy of all-trans-retinoic acid (ATRA) for the treatment of acute promyelocytic leukemia requires degradation of the oncogenic fusion between the Promyelocytic Leukemia Protein (PML) with the Retinoic Acid Receptor Alpha (RARA). Here we use CRISPR-based screens to identify the HECT E3 ubiquitin ligase UBR5 as a ligase for PML-RARA and RARA and observe an agonist-dependent association between RARA and UBR5, which occurs directly on chromatin to regulate transcription. We present the cryo-EM structure of full-length human UBR5 and identify a Leu-X-X-Leu-Leu (LxxLL) binding motif that associates with a conserved degron in RARA. A high-resolution crystal structure of the RARA ligand binding domain in complex with this LxxLL motif shows how UBR5 binding is mutually exclusive with nuclear co-activator engagement. We demonstrate that UBR5 utilizes this conserved degron to additionally regulate hormone dependent protein stability for the glucocorticoid, progesterone, and vitamin D receptors. Our work establishes UBR5-driven NR degradation as an integral regulator of transcriptional signaling by nuclear hormones.
2023-07-20 | PXD041749 | Pride
Project description:Nuclear hormone receptors (NRs) are ligand-binding transcription factors that are widely targeted therapeutically. Hormone binding triggers NR activation and their subsequent proteasomal degradation through unknown ligand-dependent ubiquitin ligase machinery. NR degradation is therapeutically relevant. Efficacy of all-trans-retinoic acid (ATRA) for the treatment of acute promyelocytic leukemia requires degradation of the oncogenic fusion between the Promyelocytic Leukemia Protein (PML) with the Retinoic Acid Receptor Alpha (RARA). Here we use CRISPR-based screens to identify the HECT E3 ubiquitin ligase UBR5 as a ligase for PML-RARA and RARA and observe an agonist-dependent association between RARA and UBR5, which occurs directly on chromatin to regulate transcription. We present the cryo-EM structure of full-length human UBR5 and identify a Leu-X-X-Leu-Leu (LxxLL) binding motif that associates with a conserved degron in RARA. A high-resolution crystal structure of the RARA ligand binding domain in complex with this LxxLL motif shows how UBR5 binding is mutually exclusive with nuclear co-activator engagement. We demonstrate that UBR5 utilizes this conserved degron to additionally regulate hormone dependent protein stability for the glucocorticoid, progesterone, and vitamin D receptors. Our work establishes UBR5-driven NR degradation as an integral regulator of transcriptional signaling by nuclear hormones.
2023-07-20 | PXD040953 | Pride
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:The aim of this study was to investigate the effect of T0901317 LXR agonist on Retinoic Acid Receptor (RAR) family gene expression. T0901317 alone increase RARalpha gene expression in monocytes and the effects of the co treatment of the cells with T0901317 and a specific RARalpha agonist (AM580) were further studied. For this monocytes were treated for 24h with DMSO or T0901317 to induce RARalpha expression and in a second step cells were treated or not with AM580 for another 24h period. Gene expression was analysed for all the treatments (T0901317, AM580 or T0901317+AM580) and we focussed on genes which expression was synergitically induced by the co treatment as compared to the cells treated either by T0901317 or AM580. Monocytes were obtained from 2 healthy donors with inform consent. Cells were treated in vitro with the vehicle (DMSO 0,1%) or 10µM of the LXR agonist T0901317 for 24 hours. Then after cells were treated for another 24 hour period with or without 100nM of the RARalpha specific agonist AM580.
2010-04-08 | E-GEOD-13407 | biostudies-arrayexpress
Project description:The aim of this study was to investigate the effect of T0901317 LXR agonist on Retinoic Acid Receptor (RAR) family gene expression. T0901317 alone increase RARalpha gene expression in monocytes and the effects of the co treatment of the cells with T0901317 and a specific RARalpha agonist (AM580) were further studied. For this monocytes were treated for 24h with DMSO or T0901317 to induce RARalpha expression and in a second step cells were treated or not with AM580 for another 24h period. Gene expression was analysed for all the treatments (T0901317, AM580 or T0901317+AM580) and we focussed on genes which expression was synergitically induced by the co treatment as compared to the cells treated either by T0901317 or AM580.
2009-10-01 | GSE13407 | GEO