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accession-icon GSE17718
Expression data from CD4-positive HTLV-positive cell lines and from CD4-positive HTLV-negative primary cells.
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to compare the global programme of gene expression in HTLV-positive, ATL-derived and HTLV-positive in vitro-transformed cell lines with that of uninfected primary CD4 T cells.

Publication Title

Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1.

Sample Metadata Fields

Specimen part

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accession-icon SRP016623
De novo piRNA cluster formation in the Drosophila germline triggered by transgenes containing a transcribed transposon fragment
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

PIWI interacting RNAs (piRNAs) provide defense against transposable element (TE) expansion in the germline of metazoans. piRNAs are processed from the transcripts encoded by specialized heterochromatic clusters enriched in damaged copies of transposons. How these regions are recognized as a source of piRNAs is still elusive. The aim of this study is to determine how transgenes that contain a fragment of the LINE-like I transposon lead to an acquired TE resistance in Drosophila. We show that such transgenes, being inserted in unique euchromatic regions which normally do not produce small RNAs, become de novo bidirectional piRNA clusters that silence I-element activity in the germline. Strikingly, small RNAs of both polarities are generated from the entire transgene and flanking genomic sequences — not only from the transposon fragment. Chromatin immunoprecipitation analysis shows that in ovaries the trimethylated histone 3 lysine 9 (H3K9me3) mark associates with transgenes producing piRNAs. We show that transgene-derived hsp70 piRNAs stimulate in trans cleavage of cognate endogenous transcripts with subsequent processing of the non-homologous parts of these transcripts into piRNAs. Overall design: The fractions of small RNAs (19-29 nt) from ovaries of wild type and 11 transgenic lines of Drosophila melanogaster were sequenced using Illumina HiSeq 2000.

Publication Title

De novo piRNA cluster formation in the Drosophila germ line triggered by transgenes containing a transcribed transposon fragment.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE62993
Expression data of MYB36 mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

We have identified the causal genes, which is MYB36, of ionome mutants.

Publication Title

The MYB36 transcription factor orchestrates Casparian strip formation.

Sample Metadata Fields

Specimen part

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accession-icon GSE29060
Expression data from human HT-29 immortalized colorectal adenocarcinoma cell line
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling for identification of genes regulated by DNA methylation

Publication Title

Genome-wide screening of genes regulated by DNA methylation in colon cancer development.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE37364
Expression data from human colonic biopsy samples (adenoma-carcinoma)
  • organism-icon Homo sapiens
  • sample-icon 91 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Whole genomic microarray analysis was performed in order to identify gene expression profile alterations focusing on the dysplastic adenoma-carcinoma transition. Our aims were to determinate characteristic transcript sets for developing diagnostic mRNA expression patterns for objective classification of benign and malignant colorectal diseases and to test the classificatory power of these markers on an independent sample set.

Publication Title

Myofibroblast-derived SFRP1 as potential inhibitor of colorectal carcinoma field effect.

Sample Metadata Fields

Disease, Disease stage

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accession-icon GSE22541
Expression data from pulmonary metastases and primary tumors of clear-cell renal cell carcinoma (ccRCC) with different disease-free survivals
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The understanding of metastatic spread is limited and molecular mechanisms causing particular characteristics of metastasis are largely unknown. This comprises the extremely varying dormancy periods of tumor cells in the secondary organ after metastatic spread, represented by the disease-free survival (DFS) of the patients, or differing numbers of metastases in different patients. Knowing the molecular fundamentals of these phenomena would support the individual prediction of patients outcome and facilitate the decision for an appropriate monitoring and therapy regime.

Publication Title

CD31, EDNRB and TSPAN7 are promising prognostic markers in clear-cell renal cell carcinoma revealed by genome-wide expression analyses of primary tumors and metastases.

Sample Metadata Fields

Sex, Specimen part, Disease stage

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accession-icon GSE1124
Whole blood transcriptome of childhood malaria
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We aimed at finding differently expressed genes in whole blood cells of African children with asymptomatic Plasmodium falciparum infection (A), uncomplicated malaria (U), severe malarial anemia (A) and cerebral malaria (Ce) compared one to another and to healthy children (Co).

Publication Title

The blood transcriptome of childhood malaria.

Sample Metadata Fields

Specimen part

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accession-icon GSE27424
NOTCH3 knockdown in non-transformed human esophageal cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To determine the role of NOTCH3 in human esophageal epitheila homeostasis/squamous cell differentiation

Publication Title

A NOTCH3-mediated squamous cell differentiation program limits expansion of EMT-competent cells that express the ZEB transcription factors.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP070670
FOXF1 inhibits endothelial barrier function in the lung and transcriptionally activates the gene for the S1PR1 receptor
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Multiple signaling pathways, structural proteins and transcription factors are involved in regulation of endothelial barrier function. The Forkhead protein FOXF1 is a key transcriptional regulator of lung embryonic development, and we use a conditional knockout approach to examine the role of FOXF1 in adult lung homeostasis and lung injury and repair. Tamoxifen-regulated deletion of both Foxf1 alleles in endothelial cells of adult mice (Pdgfb-iCreER/Foxf1 caused lung inflammation and edema, leading to respiratory insuffency and uniform mortality. Deletion of a single foxf1 allele was sufficient to increase susceptibility of heterozygous mice to acute lung injury. FOXF1 abundance was decreased in pulmonary endothelial cells of human patients with acute lung injury. Gene expression analysis of pulmonary endothelial cells of FOXF1 deletion indicated reduced expression for genes critical for maintance and regulation of adherens junctions. FOXF1 knockdown in vitro and in vivo disrupted adherens junctions, increased lung endothelial permeability, and the abundance of mRNA and protein for sphingosine 1 phosphate receptor 1 (S1PR1), a key regulator of endothelial barrier function. Chromatin immunoprecipitation and luciferase reporter assay demonstrated that FOXF1 directly bound to and induced the tanscriptional activity of the S1pr1 promoter. Pharmacological administratiion of S1P to injured pdgfb-iCreER/Foxf1 mice restored endothelial barrier function, decreased lung edema and improved survival. Thus, FOXF1 promotes normal lung homeostasis and lung repair, at least in part, by enhancing endothelial barrier function through transcriptional activation of the S1P/S1PR1/ signaling pathway. Overall design: RNA was isolated and pooled from the lungs of multiple mice with either the Foxf1 floxed alleles alone or Pdgfb-iCreER Foxf1 floxed mice.

Publication Title

FOXF1 maintains endothelial barrier function and prevents edema after lung injury.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE48991
Myotonic dystrophy type 1 (DM1) leads to altered mRNA expression in heart tissue
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Myotonic dystrophy type 1 (DM1) is a dominantly inherited disease that affects multiple organ systems. Cardiac dysfunction is the second leading cause of death in DM1. We quantified gene expression in heart tissue from a heart-specific DM1 mouse model (EpA960/MCM) which inducibly expresses human DMPK exon 15 containing 960 CUG expanded repeats and that reproduced Celf1 up regulation. To assess if, in addition to splicing and miRNA defects, CUGexp RNA also perturbed the steady state mRNA levels of genes, we carried out a microarray study on wildtype E14, adult, MCM controls and DM1 mouse hearts. As anticipated we noted a large number of genes to be developmentally regulated in wildtype hearts, however, within 72h of induction of CUGexp RNA there appeared to be a coordinate adult-to-embryonic shift in steady state levels of many genes.

Publication Title

The Mef2 transcription network is disrupted in myotonic dystrophy heart tissue, dramatically altering miRNA and mRNA expression.

Sample Metadata Fields

Specimen part, Time

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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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