1,25(OH)2D3 time course in THP-1 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Carsten Carlberg
PROVIDER: E-GEOD-69303 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:ChIP-seq for the insulator protein CTCF in THP-1 cells after stimulation with the the natural VDR ligand 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) THP-1 cells were treated for 24 h with 100 nM 1,25(OH)2D3 before ChIP assay
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Project description:gene expression profiling by RNA-seq in THP-1 cells treated with 1,25(OH)2D3 for 2.5-24 h three independent experiments of 1,25(OH)2D3 time course in THP-1 cells
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Project description:Assessment of regions of open chromatin by FAIRE-seq in THP-1 cells treated with 1,25(OH)2D3 for 0-48 h Three independent experiments of 1,25(OH)2D3 time course in THP-1 cells
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Project description:Open chromatin regions have been shown to associate with the location of transcriptiotal enhancers, i.e., the binding locations of DNA-binding transcription factors. To investigate the effects of short-term treatment by the nuclear hormone 1α,25-dihydroxyvitamin D3 (VD), a specific ligand of the transcription factor vitamin D receptor, on chromatin accessibility, FAIRE-seq was utilized on the chromatin samples from THP-1 monocytic leukemia cells that were treated with 100 nM 1α,25-dihydroxyvitamin D3 for 20, 40, 60, 80, 100 and 120 min, or with vehicle (0.1% (v/v) ethanol) for 20 and 100 min. THP-1 monocytic leukemia cells were treated with 100 nM 1α,25-dihydroxyvitamin D3 for 20, 40, 60, 80, 100 and 120 min or with vehicle (0.1% (v/v) ethanol) for 20 and 100 min. Chromatin sample from one biological replicate for each time point was subjected to the FAIRE-seq protocol and subsequent data analysis using an Input chromatin sample as control.
2012-10-25 | E-GEOD-40075 | 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.
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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.
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Project description:This study characterizes the genetic basis of variation in the immunomodulatory effects of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25D). This was done by mapping quantitative traits of 1,25D response both at the cellular and transcriptional level in peripheral blood mononuclear cells (PBMCs). Total RNA extraced from peripheral blood mononuclear cells from 85 healthy individuals of African-African ancestry treated with 1,25D or the vehicle control, ethanol, for 6 hours.
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Project description:This study examines patterns of genome-wide transcriptional response to the active form of vitamin D, 1,25-dihyroxyvitamin D3 (1,25D), and the bacterial lipopolysaccharide (LPS) in primary human monocytes, to better understand pathways underlying the immunomodulatory role of 1,25D. Total RNA extraced from monocytes from 20 healthy individuals of African-African and European-American ancestry treated with 1,25D alone or in the presence of LPS for 24 hours.
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Project description:Androgen receptor (AR) plays an important regulatory role during prostate cancer development. ARM-bM-^@M-^Ys transcriptional activity is regulated by androgenic ligands, but also by post-translational modifications. To study the role of the AR SUMOylation in genuine chromatin environment, we compared androgen-regulated gene expression and AR chromatin occupancy in PC-3 prostate cancer and HEK293 cell lines stably expressing wild-type (wt) or SUMOylation site-mutated AR (AR-K386R,K520R). Our genome-wide gene expression analyses reveal that the SUMOylation modulates the AR function in a target gene and pathway selective manner. The transcripts that are differentially regulated by androgen and SUMOylation are linked to cellular movement, cell death, cellular proliferation, cellular development and cell cycle. In line with these data, SUMOylation mutant AR cells proliferate faster and are more sensitive to apoptosis. Moreover, ChIP-seq analyses show that the SUMOylation modulates the chromatin occupancy of AR on many loci in a fashion that parallels with their differential androgen-regulated expression. De novo motif analyses show that other transcription factor-binding motifs are differentially enriched at the wtAR- and the AR-K386R,K520R-preferred genomic binding positions. Taken together, our data indicate that SUMOylation does not simply repress the AR activity, but it regulates ARM-bM-^@M-^Ys interaction with the chromatin and the receptorM-bM-^@M-^Ys target gene selection. Androgen receptor (AR) genomic binding was studied in wild-type AR (wtAR) or SUMOylation-deficient AR (AR-K2R) stably expressing cells PC-3 cells, in biological dublicates. Cells were treated 1h either with 10 nM R1881 or vehicle and inputs were used as controls.
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