The primary goal of this study was to assess differences in gene expression between prostate cancer cell lines and normal prostate epithelial and stromal cells in primary culture.
DNA hypomethylation arises later in prostate cancer progression than CpG island hypermethylation and contributes to metastatic tumor heterogeneity.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Oncogene activation induces metabolic transformation resulting in insulin-independence in human breast cancer cells.
Specimen part, Cell line, Treatment, Time
View SamplesResults of blocking the HER-2 oncogene kinase function in SUM-225 cells by treatment with CP724,714 and measuring gene expression as a function of time provides information as to what genes are regulated by HER-2 in this breast cancer cell line.
Oncogene activation induces metabolic transformation resulting in insulin-independence in human breast cancer cells.
Specimen part, Cell line, Treatment, Time
View SamplesPurpose: The objective of this study was to determine cardiac transcriptional pathways regulated in response to 1.) hypothyroidism and re-establishment of a euthyroid state and 2.) Med13-dependent cardiac transcriptional pathways regulated in response to hypothyroidism and re-establishment of a euthyroid state Overall design: Methods: WT and Med13 cardiac-specific knockout mice (Med13cKO) were put on a normal chow or PTU diet at 8 weeks of age for a duration of 4 weeks. A third group was put on a PTU diet for 4 weeks followed by 3 daily injections of T3.
Regulation of cardiac transcription by thyroid hormone and Med13.
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View SamplesThe transcriptomic profiling of psoriasis has led to an increased understanding of disease pathogenesis. Although microarray technologies have been instrumental in this regard, it is clear that these tools detect an incomplete set of DEGs. RNA-seq can be used to supplement these prior technologies. Here, the use of RNAseq methods substantially increased the number of psoriasis-related DEGs. Furthermore, DEGs that were uniquely identified by RNA-seq, but not in other published microarray studies, further supported the role of IL-17 and tumor necrosis factor-a synergy in psoriasis. Examination of one of these factors at the protein level confirmed that RNA-seq is a powerful tool that can be used to identify molecular factors present in psoriasis lesions, and may be useful in the identification of therapeutic targets that to our knowledge have not been reported previously. Further studies are in progress to determine the biological significance of DEGs uniquely discovered by RNA-seq. Overall design: To define the transcriptomic profile of psoriatic skin, three pairs of lesional and nonlesional skin biopsy specimens were taken from patients with untreated moderate-to-severe plaque psoriasis.
Transcriptional profiling of psoriasis using RNA-seq reveals previously unidentified differentially expressed genes.
Specimen part, Subject
View SamplesSnt2 is a yeast chromatin-interacting protein whose function has not been well characterized, that was recently shown to associate with Ecm5 and the Rpd3 deacetylase. Using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq), we show that in response to H2O2, Snt2 and Ecm5 colocalize to promoters of genes involved in various aspects of the environmental stress response. By integrating these ChIP-seq results with expression analysis, we identify a key set of target genes that require Snt2 for proper expression after H2O2 stress. Finally, by mapping Snt2 and Ecm5 localization before and after rapamycin treatment, we identify a subset of H2O2-specific Snt2 and Ecm5 target promoters that are also targeted in response to rapamycin. Our results establish a function for Snt2 in regulating transcriptional changes in response to oxidative stress, and suggest Snt2 may have a role in additional stress pathways. Overall design: RNA-seq analysis to look at gene expression levels in wild-type, snt2 deletion, or ecm5 deletion strains before or 0.5 hours after treatment with H2O2 (final concentration 0.4 mM). This sequencing was done on biological triplicate samples.
The yeast Snt2 protein coordinates the transcriptional response to hydrogen peroxide-mediated oxidative stress.
Subject
View SamplesRNA-seq transcriptome analysis identified an early requirement for zic2 in periocular neural crest as an activator of alx1, a transcription factor with essential roles in craniofacial and ocular morphogenesis in human and zebrafish Overall design: Embryos derived from a zic2aGBT133/+; zic2bUW1127/+ incross were sorted by presence or absence of coloboma. RNA was prepared from each individual embryo at ~ 25 hpf
Zebrafish zic2 controls formation of periocular neural crest and choroid fissure morphogenesis.
No sample metadata fields
View SamplesAlas2 gene encodes the rate-limiting enzyme in heme biosynthesis. CRISPR/Cas9-mediated ablation of two Alas2 intronic cis-elements strongly reduced GATA-1-induced Alas2 transcription, heme biosynthesis, and GATA-1 regulation of other vital constituents of the erythroid cell transcriptome. Bypassing Alas2 function in Alas2 cis-element-mutant (double mutant) cells by providing its catalytic product 5-aminolevulinic acid (5-ALA) rescued heme biosynthesis and the GATA-1-dependent genetic network. We discovered a GATA factor- and heme-dependent circuit that establishes the erythroid cell transcriptome. Overall design: G1E-ER-GATA-1 WT and double mutant cells were examined. Untreated WT, beta-estradiol-treated WT, beta-estradiol-treated double-mutant, and beta-estradiol/5-ALA-treated double-mutant cells were subjected to RNA-seq.
Mechanism governing heme synthesis reveals a GATA factor/heme circuit that controls differentiation.
Treatment, Subject
View SamplesIn this analysis we have compared the gene expression profiles of lymphatic endothelial cells (LECs) isolated from human intestine (iLECs) versus LECs from human skin (dLECs).
Liprin (beta)1 is highly expressed in lymphatic vasculature and is important for lymphatic vessel integrity.
Specimen part
View SamplesHistone modifications and DNA methylation represent two distinct modes of varying epigenetic landscapes, but whose exact interrelationship remains unclear. Previous studies have shown that histone H3 lysine 4 trimethylation (H3K4me3) inhibits the binding of de novo DNA methyltransferases (Dnmt) through the ATRX-DNMT3-DNMTL (ADD) domain, thus protecting H3K4me3 marked CpG islands (CGI) from DNA methylation. In addition to H3K4me3, we identified antagonistic relationship between H3T3 phosphorylation and the binding of the ADD domain to the unmodified H3 N-terminus. To assess the physiological relevance of these restrictions, we engineered the wild-type ADD domain of Dnmt3a (WT) to permit additional binding to either H3K4me3 (WWD) or H3T3ph (R) and stably introduced FLAG-tagged, full-length normal or mutant Dnmt3a2 into ESCs lacking all Dnmts (TKO; triple knock-out of Dnmt1, Dnmt3a, and Dnmt3b) using the PiggyBac transposon system. For each WT-, WWD-, and R-Dnmt3a2, we generated bulk and clonally-derived ESC lines. We then employed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) to identify the genomic distribution of full-length WT-, WWD-, R-Dnmt3a2, and the H3K4me3 distribution. In parallel, we quantitatively measured genome-wide CpG (cytosine) methylation at base-pair resolution using an enhanced form of reduced representation bisulfite sequencing (RRBS), and performed RNA-seq to assess transcription in matched ESC lines. Overall design: Examination of mRNA profiles in Dnmt TKO-ESCs expressing wild-type/mutant Dnmt3a2.
Engineering of a Histone-Recognition Domain in Dnmt3a Alters the Epigenetic Landscape and Phenotypic Features of Mouse ESCs.
No sample metadata fields
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