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SRP049713
Homo sapiens
25 Downloadable Samples
IlluminaHiSeq2000
Description
In this study, we have integrated RNA-seq data from subcellular fractionated RNA (i.e., cytoplasm, nucleoplasm, and chromatin-associated) with GRO-seq data using a novel bioinformatics pipeline. This has yielded a comprehensive catalog of polyadenylated lncRNAs in MCF-7 cells, about half of which have not been annotated previously and about a quarter of which are estrogen-regulated. Knockdown of selected lncRNAs, such as lncRNA152 and lncRNA67 followed by RNA-seq suggest that these lncRNAs regulate the expression of cell cycle genes. Overall design: characterization of long noncoding RNAs
Publication Title
Discovery, Annotation, and Functional Analysis of Long Noncoding RNAs Controlling Cell-Cycle Gene Expression and Proliferation in Breast Cancer Cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 53 Downloadable Samples
- Illumina HiSeq 2500
Description
The meningeal space is occupied by a diverse repertoire of innate and adaptive immune cells. CNS injury elicits a rapid immune response that affects neuronal survival and recovery, but the role of meningeal inflammation in CNS injury remains poorly understood. Here we describe group 2 innate lymphoid cells (ILC2s) as a novel cell type resident in the healthy meninges that is activated following CNS injury. ILC2s are present throughout the naïve mouse meninges, though are concentrated around the dural sinuses, and have a unique transcriptional profile relative to lung ILC2s. After spinal cord injury, meningeal ILC2s are activated in an IL-33 dependent manner, producing type 2 cytokines. Using RNAseq, we characterized the gene programs that underlie the ILC2 activation state. Finally, addition of wild type lung-derived ILC2s into the meningeal space of IL-33R-/- animals improves recovery following spinal cord injury. These data characterize ILC2s as a novel meningeal cell type that responds to and functionally affects outcome after spinal cord injury, and could lead to new therapeutic insights for CNS injury or other neuroinflammatory conditions. Overall design: ILC2s were isolated from 10 week C57/Bl6 mice with and without spinal cord injury (1 day post injury). 5 mice were pooled per group, with meninges dissected, digested, and FACs sorted (CD45+/DAPI-/Lin–/St2+/Thy1+) directly into RNA lysis buffer.
Publication Title
Characterization of meningeal type 2 innate lymphocytes and their response to CNS injury.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Bone-marrow mesenchymal stem cells (MSCs) are plastic adherent cells that can differentiate into various tissue lineages, including osteoblasts, adipocytes and chondrocytes. However, this progenitor property is not shared by all cells within the MSC population. In addition, MSCs vary in their proliferation capacities and expression of markers. Because of heterogeneity of CD146 expression in the MSC population, we compared CD146-/Low and CD146High cells under clonal and non-clonal (sorted MSCs) conditions to determine whether this expression is associated with specific functions. CD146-/Low and CD146High MSCs did not differ in colony-forming unit-fibroblast number, osteogenic and adipogenic differentiation or in vitro hematopoietic supportive activity. However, CD146-/Low clones proliferated slightly but significantly faster than did CD146High clones. In addition, a strong expression of CD146 molecule was associated with a commitment towards a vascular smooth muscle cell lineage with upregulation of calponin-1 expression. Thus, within a bone-marrow MSC population, certain subpopulations characterized by high expression of CD146, are committed toward a vascular smooth muscle cell lineage.
Publication Title
CD146 expression on mesenchymal stem cells is associated with their vascular smooth muscle commitment.
Sample Metadata Fields
Specimen part, Subject
View Samples- Rattus norvegicus
- 6 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Maternal obesity during the pre-implantation period leads to a pro-inflammatory milieu in the ovaries. We conducted a global transcriptomic profiling in ovaries from TEN fed rats during the pre-implantation period. Microarray analysis revealed that obesity lead to increased expression of genes related to inflammation, decreased glucose transporters, and dysregulation of ovarian function-related genes in the ovaries. Our results suggest maternal obesity led to an up-regulation of inflammatory genes and Egr-1 protien expression in peri-implantation ovarian tissue, and a concurrent down-regulation of glucose transporters mRNA and AKT and PI3K protein levels.
Publication Title
Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 1000
Description
Purpose: determine RNA expression differences in an unbiased fashion between UPS tumors derived from LSL-KrasG12D;Trp53-/- (KP) mice, and UPS tumors derived from LSL-KrasG12D;Trp53-/-;Epas1-/- (KPH2) mice. Epas1 encodes HIF-2alpha protein. Overall design: RNA-seq was performed on KP (n = 4) and KPH2 (n = 4) derived UPS tumors using Illumina HiSeq 2000.
Publication Title
Epigenetic re-expression of HIF-2α suppresses soft tissue sarcoma growth.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 60 Downloadable Samples
- Affymetrix Clariom S Human array (clariomshuman)
Description
Actinic keratosis is a common skin disease that may progress to invasive squamous cell carcinoma. Ingenol mebutate has demonstrated efficacy in field treatment of actinic keratosis. However, molecular mechanisms on ingenol mebutate response are not yet fully understood.
Publication Title
Identification of differentially expressed genes in actinic keratosis samples treated with ingenol mebutate gel.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 3 Downloadable Samples
Description
The TCF7L2 transcription factor is linked to a variety of human diseases, including type 2 diabetes and cancer. One mechanism by which TCF7L2 could influence expression of genes involved in diverse diseases is by binding to distinct regulatory regions in different tissues. To test this hypothesis, we performed ChIP-seq for TCF7L2 in 6 human cell lines. We identified 116,000 non-redundant TCF7L2 binding sites, with only 1,864 sites common to the 6 cell lines. Using ChIP-seq, we showed that many genomic regions that are marked by both H3K4me1 and H3K27Ac are also bound by TCF7L2, suggesting that TCF7L2 plays a critical role in enhancer activity. Bioinformatic analysis of the cell type-specific TCF7L2 binding sites revealed enrichment for multiple transcription factors, including HNF4alpha and FOXA2 motifs in HepG2 cells and the GATA3 motif in MCF7 cells. ChIP-seq analysis revealed that TCF7L2 co-localizes with HNF4alpha and FOXA2 in HepG2 cells and with GATA3 in MCF7 cells. Interestingly, in MCF7 cells the TCF7L2 motif is enriched in most TCF7L2 sites but is not enriched in the sites bound by both GATA3 and TCF7L2. This analysis suggested that GATA3 might tether TCF7L2 to the genome at these sites. To test this hypothesis, we depleted GATA3 in MCF7 cells and showed that TCF7L2 binding was lost at a subset of sites. RNA-seq analysis suggested that TCF7L2 represses transcription when tethered to the genome via GATA3. Our studies demonstrate a novel relationship between GATA3 and TCF7L2, and reveal important insights into TCF7L2-mediated gene regulation. Overall design: RNAseq analysis of MCF7 cells transfected with siCONTROL, siTCF7L2 or siGATA3. ChIP-seq analysis of H3K27ac, H3K4me1, H3K27me3, H3K9me3 in MCF7 cells; H3K4me1 and H3K27ac in HCT116 cells.
Publication Title
Cell type-specific binding patterns reveal that TCF7L2 can be tethered to the genome by association with GATA3.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Glucocorticoids are first-line agents for the treatment of many eosinophil-associated disorders. However, their mechanism of action in this group of disorders remains poorly understood, including the well-known clinical observation that glucocorticoids at therapeutic doses lead to profound, transient eosinopenia within hours of administration. To gain an unbiased, genome-wide view of the early transcriptional effects of glucocorticoids on human eosinophils in vivo, and torelate them to the kinetics of glucocorticoid-induced eosinopenia, RNA sequencing was performed on purified blood eosinophils obtained before and 30, 60, and 120 minutes after administration of a single dose of oral prednisone (1 mg/kg) to healthy subjects with hypereosinophilia (hypereosinophilia of unknown significance). Overall design: Three subjects with hypereosinophilia of unknown significance were each given a single dose of oral prednisone, 1 mg/kg. Whole blood was collected before and 30 minutes, 1 hour, and 2 hours after prednisone administration. Eosinophils were purified from each peripheral blood sample. Total RNA was obtained from purified eosinophils and subject to library preparation and high-throughput sequencing.
Publication Title
Transcript- and protein-level analyses of the response of human eosinophils to glucocorticoids.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment, Subject, Time
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose: To determine early changes in gene expression that drive gastric cancer development in the landscape of CLDN18 loss using RNAseq. Results: Although claudin-18 is a tight junction protein and should regulate paracellular permeabiity and/or ion flux across the mucosa, we showed this protein is rather a potent tumor suppressor that regulates cellular signaling and differentiation pathways in gastric epithelial cells. Methods: Stomach neck region mRNA profiles of 7-day-old wild-type (WT) and claudin-18 knockout (CLDN18-/-) mice were generated by deep sequencing, in triplicate, using the Illumina HiSeq2000 sequencing system. The resulting sequences were mapped to the Mouse genome (mm10) using STAR aliger and P-values were adjusted using the Benjamini-Hochberg procedure (J R Statist Soc B 1995;57:289-300). Conclusions: Loss of claudin-18 promotes gastric cancer development by modulating the expression program of gastric epithelial cells, including cellular signaling and differentiation pathways that are required for mucosal homeostasis. Overall design: Stomach (neck region only) mRNA profiles of 7-day old wild-type (WT) and CLDN18-/- mice were generated by deep sequencing, in triplicate, using an Illumina HiSeq2000 sequencing system.
Publication Title
Loss of Tight Junction Protein Claudin 18 Promotes Progressive Neoplasia Development in Mouse Stomach.
Sample Metadata Fields
Age, Cell line, Subject
View Samples- Homo sapiens
- 53 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Rhabdoid tumors (RT) are aggressive tumors characterized by genetic loss of SMARCB1 (SNF5, INI-1), a component of the SWI/SNF chromatin remodeling complex. No effective treatment is currently available. This study seeks to shed light on the SMARCB1-mediated pathogenesis of RT and to discover potential therapeutic targets. Global gene expression of 10 RT was compared with 12 cellular mesoblastic nephromas, 16 clear cell sarcomas of the kidney, and 15 Wilms tumors. 114 top genes were differentially expressed in RT (p<0.001, fold change >2 or <0.5). Among these were down-regulation of SMARCB1 and genes previously associated with SMARCB1 (ATP1B1, PTN, DOCK4, NQO1, PLOD1, PTP4A2, PTPRK). 28/114 top differentially expressed genes were involved with neural or neural crest development and were all sharply down-regulated. This was confirmed by Gene Set Enrichment Analysis (GSEA). Neural and neural crest stem cell marker proteins SOX10, ID3, CD133 and Musashi were negative by immunohistochemistry, whereas Nestin was positive. Decreased expression of CDKN1A, CDKN1B, CDKN1C, CDKN2A, and CCND1 was identified, while MYC-C was upregulated. GSEA of independent gene sets associated with bivalent histone modification and polycomb group targets in embryonic stem cells demonstrated significant negative enrichment in RT. Several differentially expressed genes were associated with tumor suppression, invasion and metastasis, including SPP1 (osteopontin), COL18A1 (endostatin), PTPRK, and DOCK4. We conclude that RTs arise within early progenitor cells during a critical developmental window in which loss of SMARCB1 directly results in repression of neural development, loss of cyclin dependent kinase inhibition, and trithorax/polycomb dysregulation.
Publication Title
Rhabdoid tumor: gene expression clues to pathogenesis and potential therapeutic targets.
Sample Metadata Fields
No sample metadata fields
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