Each total RNA sample is hybridized to two different arrays: Affymetrix U133A (GPL96) and U133B (GPL97).
Previously unidentified changes in renal cell carcinoma gene expression identified by parametric analysis of microarray data.
No sample metadata fields
View SamplesPharmacogenomic identification of targets for adjuvant therapy with the topoisomerase poison camptothecin.
Pharmacogenomic identification of targets for adjuvant therapy with the topoisomerase poison camptothecin.
No sample metadata fields
View SamplesIt is unclear how epigenetic changes regulate the induction of erythroid-specific genes during terminal erythropoiesis. Here we use global mRNA sequencing (mRNA-seq) and chromatin immunoprecipitation coupled to high-throughput sequencing (CHIP-seq) to investigate the changes that occur in mRNA levels, RNA Polymerase II (Pol II) occupancy and multiple post-translational histone modifications when erythroid progenitors differentiate into late erythroblasts. Among genes induced during this developmental transition, there was an increase in the occupancy of Pol II, the activation marks H3K4me2, H3K4me3, H3K9Ac and H4K16Ac, and the elongation methylation mark H3K79me2. In contrast, genes that were repressed during differentiation showed relative decreases in H3K79me2 levels yet had levels of Pol II binding and active histone marks similar to those in erythroid progenitors. We also found that relative changes in histone modification levels-in particular, H3K79me2 and H4K16ac-were most predictive of gene expression patterns. Our results suggest that in terminal erythropoiesis both promoter and elongation-associated marks contribute to the induction of erythroid genes, while gene repression is marked by changes in histone modifications mediating Pol II elongation. Our data maps the epigenetic landscape of terminal erythropoiesis and suggests that control of transcription elongation regulates gene expression during terminal erythroid differentiation. Overall design: Mouse fetal liver cells are double-labeled for erythroid-specific TER119 and non erythroid-specific transferrin receptor (CD71) and then sorted by flow-cytometry. E14.5 fetal livers contain at least five distinct populations of cells (R1 through R5); as they progressively differentiate they gain TER119 and then gain and subsequently lose CD71. CFU-E cells and proerythroblasts make up the R1 population; R2 consists of proerythroblasts and early basophilic erythroblasts; R3 includes early and late basophilic erythroblasts; R4 is mostly polychromatophilic and orthochromatophilic erythroblasts; and R5 is comprised of late orthochromatophilic erythroblasts and reticulocytes. We have sorted for R2-R5 cells for RNA-seq experiment.
Gene induction and repression during terminal erythropoiesis are mediated by distinct epigenetic changes.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Chromatin structure and gene expression programs of human embryonic and induced pluripotent stem cells.
Cell line
View SamplesKnowledge of both the global chromatin structure and the gene expression programs of human embryonic stem (ES) cells and induced pluripotent stem (iPS) cells should provide a robust means to assess whether the genomes of these cells have similar pluripotent states. Recent studies have suggested that ES and iPS cells represent different pluripotent states with substantially different gene expression profiles. We describe here a comparison of global chromatin structure and gene expression data for a panel of human ES and iPS cells. Genome-wide maps of nucleosomes with histone H3K4me3 and H3K27me3 modifications indicate that there is little difference between ES and iPS cells with respect to these marks. Gene expression profiles confirm that the transcriptional programs of ES and iPS cells show very few consistent differences. Although some variation in chromatin structure and gene expression was observed in these cell lines, these variations did not serve to distinguish ES from iPS cells.
Chromatin structure and gene expression programs of human embryonic and induced pluripotent stem cells.
Cell line
View SamplesPeripheral blood samples were collected before (0 hour) and at 24 hours after exposure from healthy subjects who participated in previous controlled exposures to ultrafine carbon particles (UFP, 50 microg/m3) or filtered air (FA)(n = 3 each). The exposure time was 2 hours. RNA from mononuclear cell fraction (>85% lymphocytes) was extracted, amplified and hybridized to Affymetrix HU133 plus 2 microarrays.
Gene expression profile in circulating mononuclear cells after exposure to ultrafine carbon particles.
Specimen part, Time
View SamplesWe describe a function of focal adhesion kinase (FAK) in driving anti-tumor immune evasion. The kinase activity of nuclear-targeted FAK in squamous cancer cells drives exhaustion of CD8+ T-cells and recruitment of regulatory T-cells by transcriptionally regulating chemokine/cytokine and ligand-receptor networks, including transcription of Ccl5 that is crucial. These changes inhibit antigen-primed cytotoxic CD8+ T-cell activity, permitting growth of FAK-expressing tumors.
Nuclear FAK controls chemokine transcription, Tregs, and evasion of anti-tumor immunity.
Specimen part
View SamplesRNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-26a in both MCF-7 and MDA-MB-231 breast cancer cell lines. Overall design: To evaluate the entire set of genes modulated by miR-26a in breast cancer, we performed RNA-seq after ectopic manipulation of this miRNA. We over-expressed miR-26a in MCF-7 epithelial cancer cell lines and also reduced its activity by stably transfecting MDA-MB-231 mesenchymal-like cancer cell lines with a specific sponge vector. GO terms and pathway enriched analysis of the transcripts that significantly change upon miR-26 ectopic manipulation implicates miR-26ab in cell cycle, apoptosis, cell spreading and cell adhesion in breast cancer
Sustained expression of miR-26a promotes chromosomal instability and tumorigenesis through regulation of CHFR.
Specimen part, Cell line, Subject
View SamplesLow levels of MYB promote the development of myeloproliferative neoplasm (MPN). The cell type identified that can transplant the MPN phenotype has been identified as expressing KIT, CD11b and low levels of lineage markers (K11bL).
Transcriptional regulation of SPROUTY2 by MYB influences myeloid cell proliferation and stem cell properties by enhancing responsiveness to IL-3.
Sex, Age, Specimen part
View SamplesAnalysis of the transcriptome of mononuclear side population (SP) and main population (MP) cells of human fetal skeletal muscle from 12 human subjects of gestational age 14-18 weeks.
Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.
Specimen part
View Samples