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accession-icon SRP070184
RNA sequencing of diet-induced obese and lean mouse livers
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

No description.

Publication Title

Analysis of diet-induced differential methylation, expression, and interactions of lncRNA and protein-coding genes in mouse liver.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

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accession-icon SRP050591
A Saccharomyces cerevisiae strain with a minimal complement of glycolytic genes reveals strong redundancies in central metabolism
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

As a result of ancestral whole genome and small-scale duplication events, the genome of Saccharomyces cerevisiae's, and of many eukaryotes, still contain a substantial fraction of duplicated genes. In all investigated organisms, metabolic pathways, and more particularly glycolysis, are specifically enriched for functionally redundant paralogs. In ancestors of the Saccharomyces lineage, the duplication of glycolytic genes is purported to have played an important role leading to S. cerevisiae current lifestyle favoring fermentative metabolism even in the presence of oxygen and characterized by a high glycolytic capacity. In modern S. cerevisiae, the 12 glycolytic reactions leading to the biochemical conversion from glucose to ethanol are encoded by 27 paralogs. In order to experimentally explore the physiological role of this genetic redundancy, a yeast strain with a minimal set of 14 paralogs was constructed (MG strain). Remarkably, a combination of quantitative, systems approach and of semi-quantitative analysis in a wide array of growth environments revealed the absence of phenotypic response to the cumulative deletion of 13 glycolytic paralogs. This observation indicates that duplication of glycolytic genes is not a prerequisite for achieving the high glycolytic fluxes and fermentative capacities that are characteristic for S. cerevisiae and essential for many of its industrial applications and argues against gene dosage effects as a means for fixing minor glycolytic paralogs in the yeast genome. MG was carefully designed and constructed to provide a robust, prototrophic platform for quantitative studies, and is made available to the scientific community. Overall design: The goals of the present study are to experimentally explore genetic redundancy in yeast glycolysis by cumulative deletion of minor paralogs and to provide a new experimental platform for fundamental yeast research by constructing a yeast strain with a functional 'minimal glycolysis'. To this end, we deleted 13 minor paralogs, leaving only the 14 major paralogs for the S. cerevisiae glycolytic pathway. The cumulative impact of deleting all minor paralogs was investigated by two complementary approaches. A first, quantitative analysis focused on the impact on glycolytic flux under a number of controlled cultivation conditions that, in wild-type strains, result in different glycolytic fluxes. These quantitative growth studies were combined with transcriptome, enzyme-activity and intracellular metabolite assays to capture potential small phenotypic effects. A second, semi-quantitative characterization explored the phenotype of the 'minimal glycolysis' strain under a wide array of experimental conditions to identify potential context-dependent phenotypes

Publication Title

The Genetic Makeup and Expression of the Glycolytic and Fermentative Pathways Are Highly Conserved Within the <i>Saccharomyces</i> Genus.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE59312
Expression profiling of peripheral blood of chronic HCV infection
  • organism-icon Homo sapiens
  • sample-icon 76 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In the present study, we studied chronic HCV patients who responded to IFN-based therapy as evidenced by absence of HCV RNA at the end of treatment, and focused on two issues that have not received much attention. Firstly, we evaluated whether specific genes or gene expression patterns in blood were able to distinguish responder patients with a viral relapse from responder patients who remained virus-negative after cessation of treatment. We found that chronic HCV patients who were sustained responders and relapsers to IFN-based therapy showed comparable baseline clinical parameters and immune composition in blood. However, at baseline, the gene expression profiles of a set of 18 genes predicted treatment outcome with an accuracy of 94%. Secondly, we examined whether patients with successful therapy-induced clearance of HCV still exhibited gene expression patterns characteristic for HCV, or whether normalization of their transcriptome was observed. We observed that the relatively high expression of IFN-stimulated genes (ISG) in chronic HCV patients prior to therapy was reduced after successful IFN-based antiviral therapy (at 24 weeks follow-up). These ISG included CXCL10, OAS1, IFI6, DDX60, TRIM5 and STAT1. In addition, 1428 differentially expressed non-ISG genes were identified in paired pre- and post-treatment samples from sustained responders, which included genes involved in TGF- signaling, apoptosis, autophagy, and nucleic acid and protein metabolism. Interestingly, 1424 genes were identified with altered expression in responder patients after viral eradication in comparison to normal expression levels in healthy individuals. Additionally, aberrant expression of a subset of these genes, including IL-32, IL-16, CCND3 and RASSF1, was also observed at baseline. Our findings indicate that successful antiviral therapy of chronic HCV patients does not lead to normalization of their blood transcriptional signature. The altered transcriptional activity may reflect HCV-induced liver damage in previously infected individuals.

Publication Title

Gene expression profiling to predict and assess the consequences of therapy-induced virus eradication in chronic hepatitis C virus infection.

Sample Metadata Fields

Sex, Specimen part, Disease, Race

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accession-icon GSE41410
Co-expression of genes with ERG in prostate cancers and cell lines
  • organism-icon Homo sapiens
  • sample-icon 65 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of TDRD1 as a direct target gene of ERG in primary prostate cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE41408
Co-expression of genes with ERG in prostate cancers
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

ERG overexpression is the most frequent molecular alteration in prostate cancer. We analyzed different stages of prostate cancer to identify genes that were coexpressed with ERG overexpression. In primary prostate tumors, it was shown that TDRD1 expression was the strongest correlated gene with ERG overexpression and we suggest TDRD1 as a direct ERG target gene.

Publication Title

Identification of TDRD1 as a direct target gene of ERG in primary prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41407
Co-expression of genes with ERG in prostate cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

ERG overexpression is the most frequent molecular alteration in prostate cancer. We analyzed different stages of prostate cancer to identify genes that were coexpressed with ERG overexpression. In primary prostate tumors, it was shown that TDRD1 expression was the strongest correlated gene with ERG overexpression and we suggest TDRD1 as a direct ERG target gene.

Publication Title

Identification of TDRD1 as a direct target gene of ERG in primary prostate cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE4717
5`aza-dC demethylation of three short term cultured glioblastomas
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Glioblastoma, the most aggressive and least treatable form of malignant glioma, is the most common human brain tumor. Although many regions of allelic loss occur in glioblastomas, relatively few tumor suppressor genes have been found mutated at such loci. To address the possibility that epigenetic alterations are an alternative means of glioblastoma gene inactivation, we coupled pharmacological manipulation of methylation with gene profiling to identify potential methylation-regulated, tumor-related genes. Triplicates of three short-term cultured glioblastomas were exposed to 5M 5-aza-dC for 96 hours followed by cRNA hybridization to an oligonucleotide microarray (Affymetrix U133A). We based candidate gene selection on bioinformatics, RT-PCR, bisulfite sequencing, methylation-specific PCR and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Two genes identified in this manner, RUNX3 and Testin (TES), were subsequently shown to harbor frequent tumor-specific epigenetic alterations in primary glioblastomas. This overall approach therefore provides a powerful means to identify candidate tumor suppressor genes for subsequent evaluation and may lead to the identification of genes whose epigenetic dysregulation is integral to glioblastoma tumorigenesis.

Publication Title

Downregulation of RUNX3 and TES by hypermethylation in glioblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14330
Comparison of stable human Treg and Th clones by transcriptional profiling - experiment I
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The aim of this work was to identify functional features that are specific of human Treg cells, through the identification of genes that are differentially expressed: 1/ in activated Treg clones versus activated Thelper clones; 2/ in Th clones activated in the presence versus the absence of TGFb; 3/ in suppressed Th clones, i.e. Th clones activated in the presence of Treg clones, versus controls.

Publication Title

Comparison of stable human Treg and Th clones by transcriptional profiling.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE146110
The role of lncRNA Lassie in endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

The vascular endothelium forms a physical barrier between blood and the surrounding tissue. Its constant exposure to haemodynamic shear stress controls endothelial barrier function which is of major importance for vascular homeostasis. The role of long non-coding RNAs (lncRNAs) in this process remains elusive. Here we identify the shear stress-induced lncRNA LASSIE (linc00520) as a stabilizer of adherens junctions (AJs) in endothelial cells (ECs), that is indispensable for normal endothelial barrier function and shear stress sensing. Silencing of LASSIE in ECs resulted in impaired cell survival, loss of cell-cell contacts and failure to align in the direction of flow. RNA affinity purification followed by mass spectrometry identified several junction proteins associated with LASSIE, including the endothelial adhesion protein PECAM-1 and intermediate filament (IF) protein nestin. Proteomic analysis of VE-cadherin-associated proteins showed that LASSIE silencing reduces VE-cadherin interaction with nestin and microtubule (MT)-associated cytoskeletal proteins. We confirmed that LASSIE silencing results in a decreased connection between VE-Cadherin and the cytoskeleton, resulting in loss of barrier function and shear stress sensing. Together, this study identifies the shear stress-induced lncRNA LASSIE as a critical link between AJs and the IF cytoskeleton, which is indispensable for normal EC junction stabilization and shear stress sensing.

Publication Title

Long non-coding RNA LASSIE regulates shear stress sensing and endothelial barrier function.

Sample Metadata Fields

Specimen part

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accession-icon GSE32937
MicroRNA-29 in Aortic Dilation: Implications for Aneurysm Formation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We compared the aorta of 6-weeks-old mice (young) with 18-months-old mice (old). Using the publicly available tools Sylamer and DIANA-mirExTra, we identified an enrichment for miR-29 binding sites in the 3'UTR of genes downregulated in the aged aortas. We subsequently showed that inhibition of miR-29 in aged mice prevented dilation of the aorta.

Publication Title

MicroRNA-29 in aortic dilation: implications for aneurysm formation.

Sample Metadata Fields

Age, Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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