CD14+ human monocytes differentiating into DCs in the presence of IL4 and GM-CSF were treated with agonists for RXR and its partners or vehicle 18 hours after plating (experiment with RXR and permissive partners, donor 1-3) or 14 hours after plating (experiment with nonpermissive partners, donor 4-6). Cells were harvested 12 hours thereafter. Experiments were performed in biological triplicates representing samples from three different donors.
Research resource: transcriptome profiling of genes regulated by RXR and its permissive and nonpermissive partners in differentiating monocyte-derived dendritic cells.
Specimen part, Subject
View SamplesIn this study transcriptome profiling of dendritic cell subtypes was performed using various human dendritic cells.
Research resource: transcriptome profiling of genes regulated by RXR and its permissive and nonpermissive partners in differentiating monocyte-derived dendritic cells.
Specimen part
View SamplesRationale: Chronic Obstructive Pulmonary Disease (COPD) is considered a chronic inflammatory disease characterized by progressive airflow limitation and also has significant extrapulmonary (systemic) effects that lead to comorbid conditions. Very little is known about the pathomechanism of the disease.
Chronic obstructive pulmonary disease-specific gene expression signatures of alveolar macrophages as well as peripheral blood monocytes overlap and correlate with lung function.
Specimen part, Disease
View SamplesCTCF is a master regulator that plays a role in genome architecture and gene expression. A key aspect of CTCF’s mechanism involves bringing together distant genetic elements for intra- and inter-chromosomal interactions. Evidence from epigenetic processes, such as X-chromosome inactivation (XCI), suggests that CTCF may carry out its functions through interacting RNAs. Using genome-wide approaches to investigate the relationship between CTCF’s RNA interactome and its epigenomic landscape, here we report that CTCF interacts with thousands of transcripts in mouse embryonic stem cells (mESC), many in close proximity to CTCF’s genomic binding sites. Biochemical analysis demonstrates that CTCF is a high-affinity RNA binding protein that contacts RNA directly and specifically. In the XCI model, CTCF binds the active and inactive X-chromosomes allele-specifically. At the X-inactivation center, Tsix RNA binds CTCF and targets CTCF to a region associated with X-chromosome pairing. Our work implicates CTCF-RNA interactions in long-range chromosomal interactions in trans and adds a new layer of complexity to CTCF regulation. The genome-wide datasets reported here will provide a useful resource for further study of CTCF-mediated epigenomic regulation. Overall design: CTCF RNA interactome was identified by UV-crosslinking and immunoprecipitation followed by high-throughput sequencing (CLIP-seq), and was compared to CTCF''s epigenomic landscape as obtained by chromatin immunoprecipitation (ChIP-seq).
Locus-specific targeting to the X chromosome revealed by the RNA interactome of CTCF.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.
Specimen part, Treatment, Subject, Time
View SamplesHuman CD14 positive monocytes were purified from healthy volunteers blood and cultured in vitro for 4, 12, 24, 72 hours. While culturing, macrophages were activated alternatively with interleukin-4 (IL-4 100 ng/ml) or classically with interferon-gamma (IFNg 100 ng/ml)+tumor necrosis factor (TNF 50 ng/ml) or left without activation. Simultaneously, macrophages were also treated with vehicle (DMSO:ethanol) or 1mM synthetic PPARg agonist, Rosiglitazone. We used Affymetrix microarrays (U133Plus 2.0) to analyze activation and PPARg-induced gene expression changes.
STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.
Specimen part, Treatment, Subject, Time
View SamplesC57Bl/6 wild-type and STAT6 KO mice were used to study PPARg and IL-4 signaling. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and frech media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix.
STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.
Specimen part, Treatment, Time
View SamplesConditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix.
STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.
Specimen part, Treatment, Time
View SamplesHuman CD14 positive monocytes were purified from healthy volunteers blood and cultured in vitro for 6 hours. While culturing, macrophages were activated alternatively with interleukin-4 (IL-4 100 ng/ml). Simultaneously, macrophages were also treated with vehicle (DMSO:ethanol) or 1uM synthetic PPARg agonist, Rosiglitazone. We used Affymetrix microarrays (U133Plus 2.0) to analyze activation and PPARg-induced gene expression changes.
STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.
Specimen part, Treatment, Subject, Time
View SamplesWe compared human female hiPSC lines (all derived from IMR-90 fibroblasts) that were XIST RNA-positive and XIST RNA-negative. We also examined the gene expression patterns for 2 female hIPSCs (derived from different disease model fibroblasts) that were also negative for XIST RNA. hiPS 12D-1 is derived from Huntington's Disease patient and 6C-1 is derived from a Type I Diabetes Mellitus patient (Park et al Nature 2008).
Molecular signatures of human induced pluripotent stem cells highlight sex differences and cancer genes.
Specimen part
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