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Homo sapiens
34 Downloadable Samples
Illumina HiSeq 2500
Description
Introduction of brain tumor-relevant genetic aberrations initiates different subtypes of brain tumor-like neoplasms in cerebral organoids Overall design: Comparison of abundances (TPM) from different brain tumor organoid groups
Publication Title
Author Correction: Genetically engineered cerebral organoids model brain tumor formation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 26 Downloadable Samples
- Illumina HiSeq 2500
Description
Introduction of brain tumor-relevant genetic aberrations initiates different subtypes of brain tumor-like neoplasms in cerebral organoids Overall design: Comparison of transcriptomes from different brain tumor organoid groups
Publication Title
Author Correction: Genetically engineered cerebral organoids model brain tumor formation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2000
Description
The interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNFa, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ERa), the pioneer factor FoxA1 and the p65 subunit of the NF-?B transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between estrogen and TNFa signaling at the gene level is also evident in the patterns of ERa and NF-?B binding, which relocalize to new binding sites that are not occupied by either treatment alone. Interestingly, the chromatin accessibility of classical ERa binding sites is predetermined prior to estrogen treatment, whereas ERa binding sites gained upon co-treatment with TNFa require NF-?B and FoxA1 to promote chromatin accessibility de novo. Our data suggest that TNFa signaling recruits FoxA1 and NF-?B to latent ERa enhancer locations and directly impact ERa enhancer accessibility. Binding of ERa to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response. This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer. Overall design: Using GRO-seq and ChIP-seq (ER, FoxA1 and p65) to assay the molecular crosstalk of MCF-7 cells treated with E2, TNFa or both E2+TNFa.
Publication Title
TNFα signaling exposes latent estrogen receptor binding sites to alter the breast cancer cell transcriptome.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
The goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells.
Publication Title
Small RNA profiling of influenza A virus-infected cells identifies miR-449b as a regulator of histone deacetylase 1 and interferon beta.
Sample Metadata Fields
Cell line
View Samples- 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- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
The Wnt signaling pathway plays a fundamental role during the development of metazoans, where it functions in the regulation of diverse processes including cell fate specification, cell migration, and stem cell renewal. Activation of the beta-catenin dependent or canonical Wnt signaling pathway upregulates expression of Wnt target genes to mediate an appropriate cellular response. In the nematode C. elegans, a Wnt signaling pathway similar to the canonical pathway regulates several processes during larval development, however few target genes of this pathway have been identified. To address this deficit, we conditionally activated Wnt signaling in living animals during a defined stage of larval life by expressing a dominant, activated beta-catenin protein, then used microarray analysis to identify genes showing altered expression compared to control animals. In this way we identified 166 differentially expressed genes, of which 104 were upregulated. A subset of the upregulated genes were validated by qPCR and showed altered expression in Wnt pathway mutants with decreased or increased Wnt signaling; we consider these genes to be candidate Wnt pathway targets in the C. elegans hermaphrodite larva. Amongst these was a group of 6 genes, including the cuticular collagen genes, bli-1 col-38, col-49 and col-71, that show a peak of expression in the mid L4 stage during normal development. The L4 expression of these genes suggests they may be expressed for use in the adult cuticle, and consistent with this, reduction of function for several of the genes leads to phenotypes suggestive of defects in cuticle function or integrity. Therefore this work has identified a large number of putative Wnt pathway target genes during larval life, including a small subset of Wnt-regulated collagen genes that may function in synthesis of the adult cuticle.
Publication Title
Use of an activated beta-catenin to identify Wnt pathway target genes in caenorhabditis elegans, including a subset of collagen genes expressed in late larval development.
Sample Metadata Fields
No sample metadata fields
View Samples
GSE36057- Mus musculus
- 5 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Natural Helper cells constitute a unique lineage of Th2-cytokine producting innate lymphocytes, here we characterize the gene expression profile of non-stimulated or PMA/ionomycin-stimulated Natural Helper cells from naive C57Bl/6 mouse lungs.
Publication Title
Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Canonical Wnt signaling controls proliferation and differentiation of osteogenic progenitor cells, and tumor-derived secretion of the Wnt antagonist Dickkopf-1 (Dkk1) is correlated with osteolyses and metastasis in many bone malignancies. However, the role of Dkk1 in the oncogenesis of primary osteosarcoma (OS) remains unexplored. Here, we over-expressed Dkk1 in the OS cell line MOS-J. Contrary to expectations, Dkk1 had autocrine effects on MOSJ cells in that it increased proliferation and resistance to metabolic stress in vitro. In vivo, Dkk1 expressing MOS-J cells formed larger and more destructive tumors than controls. These effects were attributed in part to up-regulation of the stress response enzyme and cancer stem cell marker aldehyde-dehydrogenase-1 (ALDH1) through Jun-N-terminal kinase signaling. This is the first report linking Dkk1 to tumor stress resistance, further supporting the targeting of Dkk1 not only to prevent and treat osteolytic bone lesions but also to reduce numbers of stress-resistant tumor cells.
Publication Title
An unexpected role for a Wnt-inhibitor: Dickkopf-1 triggers a novel cancer survival mechanism through modulation of aldehyde-dehydrogenase-1 activity.
Sample Metadata Fields
Specimen part, Cell line
View Samples GSE1295- Homo sapiens
- 32 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
STRRIDE is an exercise intervention study of different doses and intensities in overweight women and men with the metabolic syndrome. We profiled biopsies from 3 female and 3 male STRRIDE subjects in the high exercise group (2,200 kCal/wk). Muscle biopsies were profiled at entry (0h), and after 9 months of aerobic training (24 hrs post-last bout, 96 hrs post last bout, and 336h (14 days) de-training). Included also are pilot expression data from 3 male subjects.
Publication Title
Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 20 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Dysfunction of the cystic fibrosis transmembrane regulator (CFTR) in cystic fibrosis (CF) results in exaggerated and chronic inflammation as well as increased susceptibility to chronic pulmonary infections, in particular with Pseudomonas aeruginosa. Based on the concept that host immune responses do not seem to be adequate to eradicate P.aeruginosa from the lungs of CF patients and that dendritic cells (DC) play an important role in initiating and shaping adaptive immune responses, this study analyzed the role of CFTR in bone marrow-derived murine DC from CFTR knockout (CF) mice with and without exposure to P.aeruginosa. DC expressed CFTR mRNA and protein, although at much lower levels compared to whole lung. Microarray analysis of gene expression levels in DC generated from CF and wild type (WT) mice revealed significantly different expression of 16 genes in CF DC compared to WT DC. Among the genes with lower expression in CF DC was Caveolin-1, a membrane lipid raft protein. Messenger RNA and protein levels of Caveolin-1 were decreased in the CF DC compared to WT DC. Consistently, the active form of sterol-responsive element binding protein (SREBP), a negative regulator of Caveolin-1 expression, was increased in CF DC. Following exposure to P.aeruginosa, gene expression levels in CF and WT DC changed for 912 genes involved in inflammation, chemotaxis, signaling, cell cycling and apoptosis more than 1.5-fold. Among the genes that showed a different response between WT and CF DC infected with P.aeruginosa, were 3-hydroxysterol-7 reductase (Dhcr7) and stearoyl-CoA desaturase 2 (Scd2), two enzymes involved in the lipid metabolism that are also regulated by SREBP. These results suggest that CFTR dysfunction in non-epithelial cells results in changes in the expression of genes encoding factors involved in membrane structure and lipid-metabolism. These membrane alterations in immune cells may contribute to the abnormal inflammatory and immune response characteristic of CF.
Publication Title
Influence of the cystic fibrosis transmembrane conductance regulator on expression of lipid metabolism-related genes in dendritic cells.
Sample Metadata Fields
No sample metadata fields
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