RNA-seq was performed after MCF7 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine Overall design: Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples
Transcriptional Selectivity of Epigenetic Therapy in Cancer.
No sample metadata fields
View SamplesRNA-seq was performed after HL60 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine Overall design: Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples
Transcriptional Selectivity of Epigenetic Therapy in Cancer.
No sample metadata fields
View SamplesRNA-seq was performed after YB5 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine Overall design: Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples
Transcriptional Selectivity of Epigenetic Therapy in Cancer.
No sample metadata fields
View SamplesOur data represents the first analysis of histone methyltransferase Ezh2 regulated transcriptomes in mouse CD8 T cells. Overall design: Naïve and in vitro TCR stimulated CD8 T cell mRNA profiles of Pmel-1 wild type (WT) and Ezh2-/- mice were generated by deep sequencing, in triplicate, using Illumina.
Ezh2 phosphorylation state determines its capacity to maintain CD8<sup>+</sup> T memory precursors for antitumor immunity.
Specimen part, Subject
View SamplesExposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer.
Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.
No sample metadata fields
View SamplesHuman subjects were randomized for treatment with a GnRH-analogue, Goserelin, which suppresses endogenous testosterone or placebo for 12 weeks. Strength training was performed during the last 8 weeks. The suppression of testosterone resulted in an attenuation of the normal muscle adaptation to strength training (increased muscle mass and strength). To identify molecular signals involved in the response to testosterone levels, biopsies were obtained 4 hours after the last training session and gene expression compared with Affymetrix 3' microarrays. This timepoint should capture goserelin effect on both constitutive expression, training induced changes as well as acute exercise induced (4 hours) differences in mRNA levels.
The activity of satellite cells and myonuclei following 8 weeks of strength training in young men with suppressed testosterone levels.
Sex, Age, Specimen part, Treatment
View SamplesWe applied RNA sequencing (RNA-seq) to map the global changes in gene expression of interscapular brown adipose tissue (iBAT) of mice subjected to acute cold exposure for 3 days. Here we find extensive changes in the iBAT transcriptome in response to cold with a prominent induction of genes associated to lipid-related metabolic processes. Overall design: RNA-seq of poly-A enriched RNA isolated from brown adipose tissue of 5 mice housed at room temperature (22°C) and 5 mice exposed to cold (4°C) for 3 days.
RNA-Seq and Mass-Spectrometry-Based Lipidomics Reveal Extensive Changes of Glycerolipid Pathways in Brown Adipose Tissue in Response to Cold.
No sample metadata fields
View SamplesDespite over 3,000 articles published on dystrophin in the last 15 years, the reasons underlying the progression of the human disease, differential muscle involvement, and disparate phenotypes in different species are not understood. The present experiment employed a screen of 12,488 mRNAs in 16-wk-old mouse mdx muscle at a time when the skeletal muscle is avoiding severe dystrophic pathophysiology, despite the absence of a functional dystrophin protein. A number of transcripts whose levels differed between the mdx and human Duchenne muscular dystrophy were noted. A fourfold decrease in myostatin mRNA in the mdx muscle was noted. Differential upregulation of actin-related protein 2/3 (subunit 4), beta-thymosin, calponin, mast cell chymase, and guanidinoacetate methyltransferase mRNA in the more benign mdx was also observed. Transcripts for oxidative and glycolytic enzymes in mdx muscle were not downregulated. These discrepancies could provide candidates for salvage pathways that maintain skeletal muscle integrity in the absence of a functional dystrophin protein in mdx skeletal muscle.
Regenerated mdx mouse skeletal muscle shows differential mRNA expression.
No sample metadata fields
View SamplesCD34 positive hematopoietic stem cells were differentiated into erythroid lineage. Next generation sequencing (NGS) of 5hmC affinity pulldown and RNAseq were performed in four time point of different stages of erythroid differentiation. Overall design: 4 RNA-Seq Samples (d0, d3, d7 and d10); 4 affinity-pulldown (d0, d3, d7 and d10), and 4 input samples (d0, d3, d7 and d10).
Hydroxymethylation at gene regulatory regions directs stem/early progenitor cell commitment during erythropoiesis.
No sample metadata fields
View SamplesRecurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation.
Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation.
Specimen part
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