VDR ChIP-seq in PMA-differentiated macrophages (human M2-type like macrophages)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51181 | GEO | 2016/07/13
SECONDARY ACCESSION(S): PRJNA221550
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of acute effects of ligand-treatment on vitamin D receptor binding genome-wide using ChIP-seq. THP-1 monocytic leucemia cells were treated with 1?,25(OH)2D3 (1,25D) or left unstimulated to investigate the acute effects of VDR chromatin occupancy. We identified in total 2340 VDR binding sites with and without the ligand. Without the ligand, there is a considerable presence of VDR already on the chromatin. However, upon a short (40 min) ligand treatment VDR shifts from sites that rarely contain a DR3 type element to sites that frequently contain one or more DR3-type element. Genome-wide identification of VDR binding in THP-1 cells at the unstimulated state and after 40 min ligand (10 nM 1?,25(OH)2D3 (1,25D, calcitriol)) treatment.
2011-08-17 | E-GEOD-27437 | biostudies-arrayexpress
Project description:The genome-wide analysis of the binding sites of the transcription factor vitamin D receptor (VDR) is essential for a global appreciation the physiological impact of the nuclear hormone 1M-NM-1,25-dihydroxyvitamin D3 (1,25(OH)2D3). Genome-wide analysis of lipopolysaccharide (LPS)-polarized THP-1 human monocytic leukemia cells via chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) resulted in 1,318 high-confidence VDR binding sites, of which 789 and 364 occurred uniquely with and without 1,25(OH)2D3 stimulation, while only 165 were common. We re-analyzed five public VDR ChIP-seq datasets with identical peak calling settings (MACS, version 2) and found in total 23,409 non-overlapping VDR binding sites, 75% of which are unique within the six analyzed cellular models. LPS-differentiated THP-1 cells have 22% more genomic VDR locations than undifferentiated cells and both cell types display more overlap in their VDR locations than the other investigated cell types. In general, the intersection of VDR binding profiles of ligand-stimulated cells is higher than those of unstimulated cells. De novo binding site searches and DR3-type binding site screening using HOMER of the six VDR ChIP-seq datasets suggest that DR3 sites are strongly associated with the ligand-responsiveness of VDR occupation. Importantly, all VDR ChIP-seq datasets display the same relationship between the VDR occupancy and the percentage of DR3-type sequences below the peak summits. The comparative analysis of six VDR ChIP-seq datasets demonstrated that the mechanistic basis for the action of the VDR is independent of the cell type. Only the minority of genome-wide VDR binding sites contains a DR3-type sequence. Moreover, the total number of identified VDR binding sites in each ligand-stimulated cell line inversely correlates with the percentage of peak summits with DR3 sites. Systematic reanalysis of 5 published VDR ChIP-seq datasets together with a new dataset from 24 h LPS-treated THP-1 cells at the unstimulated state and after 80 min ligand (10 nM 1M-NM-1,25(OH)2D3 (1,25D, calcitriol)) treatment. See GSM1280896 and GSM1280896 Sample records for data processing information. GSE53041_README.txt has additional details.
2014-11-14 | E-GEOD-53041 | biostudies-arrayexpress
Project description:Analysis of acute effects of ligand-treatment on vitamin D receptor binding genome-wide using ChIP-seq. THP-1 monocytic leucemia cells were treated with 1?,25(OH)2D3 (1,25D) or left unstimulated to investigate the acute effects of VDR chromatin occupancy. We identified in total 2340 VDR binding sites with and without the ligand. Without the ligand, there is a considerable presence of VDR already on the chromatin. However, upon a short (40 min) ligand treatment VDR shifts from sites that rarely contain a DR3 type element to sites that frequently contain one or more DR3-type element.
2011-08-17 | GSE27437 | GEO
Project description:The genome-wide analysis of the binding sites of the transcription factor vitamin D receptor (VDR) is essential for a global appreciation the physiological impact of the nuclear hormone 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3). Genome-wide analysis of lipopolysaccharide (LPS)-polarized THP-1 human monocytic leukemia cells via chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq) resulted in 1,318 high-confidence VDR binding sites, of which 789 and 364 occurred uniquely with and without 1,25(OH)2D3 stimulation, while only 165 were common. We re-analyzed five public VDR ChIP-seq datasets with identical peak calling settings (MACS, version 2) and found in total 23,409 non-overlapping VDR binding sites, 75% of which are unique within the six analyzed cellular models. LPS-differentiated THP-1 cells have 22% more genomic VDR locations than undifferentiated cells and both cell types display more overlap in their VDR locations than the other investigated cell types. In general, the intersection of VDR binding profiles of ligand-stimulated cells is higher than those of unstimulated cells. De novo binding site searches and DR3-type binding site screening using HOMER of the six VDR ChIP-seq datasets suggest that DR3 sites are strongly associated with the ligand-responsiveness of VDR occupation. Importantly, all VDR ChIP-seq datasets display the same relationship between the VDR occupancy and the percentage of DR3-type sequences below the peak summits. The comparative analysis of six VDR ChIP-seq datasets demonstrated that the mechanistic basis for the action of the VDR is independent of the cell type. Only the minority of genome-wide VDR binding sites contains a DR3-type sequence. Moreover, the total number of identified VDR binding sites in each ligand-stimulated cell line inversely correlates with the percentage of peak summits with DR3 sites.
2014-11-14 | GSE53041 | GEO
Project description:Identification of primary target genes of vitamin D receptor (VDR) in an immune-related cellular model (THP-1 cells) to study, in conjunction with VDR binding data from ChIP-seq, the genome-wide mechanisms of transcriptional regulation by VDR. THP-1 cells were treated 4 h either with 0.1% ethanol (vehicle, control) or 1?,25(OH)2D3 (1,25D)
2011-08-16 | E-GEOD-27270 | biostudies-arrayexpress
Project description:ChIP-seq for VDR in THP-1 cells after stimulation with the the natural VDR ligand 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)
2017-07-18 | GSE89431 | GEO
Project description:The vitamin D receptor (VDR) has been knocked out in monocytic THP-1 cells after stimulation of ko and control cells with the the natural VDR ligand 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), quadruplicate mRNA-seq has been performed
2021-09-06 | GSE157514 | GEO
Project description:Analysis of mouse placenta retrieved at day 18.5pc from vitamin D (1,25-dihydroxyvitamin D3) receptor (Vdr) knockout, heterozygous and wild-type mice. Results provide insight into the molecular mechanisms underlying the effect of vitamin D on placental function. Vdr heterozygous males and females were mated to generate Vdr knockout, heterozygous and wild-type offspring. At day 18.5pc, mouse placentae were collected and RNA was extracted and assayed on Affymetrix MoGene 2.1 ST arrays to measure the effect of Vdr on global gene expression.
2015-08-04 | E-GEOD-61583 | biostudies-arrayexpress
Project description:The biologically active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), is a direct regulator of gene transcription, since it is the only high affinity natural ligand of the transcription factor vitamin D receptor (VDR). Transcriptome-wide analysis of THP-1 human monocyte-like cells had indicated more than 600 genes to be significantly (p < 0.05) regulated after a 4 h stimulation with 1,25(OH)2D3. In this study, we screened of the list of primary vitamin D targets for genes encoding for transcriptional regulators and selected those of the activating transcription factor NFE2 and the transcriptional repressor BCL6. Both genes are under the control of two VDR loci and are the only 1,25(OH)2D3 targets within their respective chromosomal domain. However, NFE2 mRNA was rapidly up-regulated, while the increase of BCL6 expression showed a slower rise. After 24 h incubation of THP-1 cells with 1,25(OH)2D3 more than 1,500 genes responded significantly (p < 0.001), of which 132 where more than 2-fold induced. Public chromatin immunoprecipitation-sequencing datasets suggested that the majority of these genes could be targets of NFE2 or BCL6. In time course experiments we displayed for representative gene examples the specific delayed response of secondary 1,25(OH)2D3 targets and confirmed for the respective chromosomal domains the genomic binding of NFE2, BCL6 and VDR. In conclusion, our study indicated that the physiological response of monocytes to 1,25(OH)2D3 involves the action of NFE2 and BCL6. THP-1 cells were treated 24 h either with 0.1% ethanol (vehicle, control) or 1?,25(OH)2D3 (1,25D)
2015-04-26 | E-GEOD-60102 | biostudies-arrayexpress
Project description:Signaling through the vitamin D receptor (VDR) has been proposed to suppress the development of epithelial cancers, including prostate cancer. We conducted ChIP-seq to identify the VDR binding sites in the genome of the prostate epithelial cell line, RWPE1. This analysis reveals a large number of VDR binding sites in both control cells and in cells treated with 10 nM 1,25 dihydroxyvitamin D3 for 3 hours. These peaks are associated with genes controlling a wide variety of cellular functions.
2019-04-10 | GSE116843 | GEO