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accession-icon GSE141296
Gene expression analysis in Tibialis anterior (TA) muscle upon titration of myonuclear numbers
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

Skeletal muscle myofibers accrue hundreds of nuclei during post-natal development via fusion with activated satellite cells (myoblasts), which is absolutely reliant on expression of the muscle fusogen myomaker (Mymk) in the myoblasts. Using an inducible genetic approach to render myoblasts non-fusogenic (by tamoxifen-inducible Pax7-CreER mediated recombination of the Mymk gene exclusively in satellite cells), we blocked myonuclear accrual at different time-points of post-natal development and thereby titrated the number of nuclei in resultant mutant myofibers. These Microarray assays were carried out on age day 28 (P28) using total RNA isolated from control and mutant muscle to determine changes in transcriptional profiles of these muscles to (a) assess effects of myonuclear titration, and (b) identify adaptive mechanisms elicited in mutant muscles in response to myonuclear deficiency.

Publication Title

Nuclear numbers in syncytial muscle fibers promote size but limit the development of larger myonuclear domains.

Sample Metadata Fields

Specimen part

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accession-icon SRP117692
TMPRSS2-ERG suppresses PTEN/TP53 alteration-induced cancer lineage plasticity
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Lineage plasticity is a major mechanism driving prostate cancer progression and antiandrogen therapy resistance. Deletions or mutations in phosphatase and tensin homolog (PTEN) and TP53 tumor suppressor genes have been linked to lineage plasticity in prostate cancer. Fusion-driven overexpression of the E-twenty-six transformation specific (ETS)-related gene (ERG), encoding an oncogenic transcription factor, is observed in approximately 50% of all prostate cancers, yet its role in prostate cell lineage determination remains elusive. Here we demonstrate that transgenic expression of prostate cancer-associated ERG blocks Pten and Trp53 mutation-induced decreased expression of Ar and its downstream target genes and loss of luminal epithelial cell identity in the mouse prostate. Integrative analyses of ERG chromatin-immunoprecipitation sequencing (ChIP-seq) and transcriptome data show that ERG suppresses expression of a subset of cell cycle-promoting genes and RB phosphorylation, which in turn causes repression of E2F1-mediated expression of non-epithelial lineage genes. Xenograft studies show that PTEN/TP53 double mutated prostate tumors are responsive to the cyclin-dependent kinase 4 or 6 (CDK4/6) inhibitor palbociclib, but resistant to the AR inhibitor enzalutamide, while ERG/PTEN/TP53 triple-mutated prostate tumors behave completely opposite. Our studies identify ERG and the repressed cell cycle gene signature as intrinsic inhibitors of PTEN/TP53 double mutation-elicited lineage plasticity in prostate cancer. Our findings also suggest that ERG fusion can be utilized as a biomarker to guide the treatment of PTEN/TP53-mutated, RB1-intact prostate cancer with either antiandrogen or anti-CDK4/6 therapies. Overall design: Prostate tissue from mice with 1) prostate specific PTEN deletion, p53 R172H mutation with loss of heterozygosity, or 2) prostate specific PTEN deletion, p53 R172H mutation with loss of heterozygosity and transgenic ERG expression were harvested at 4-5 months. RNA was isolated from tissue and RNA-seq experiments were then performed for both genotype samples in triplicates. Differentially expressed genes were identified by comparing genotype #1 and genotype #2.

Publication Title

<i>TMPRSS2-ERG</i> Controls Luminal Epithelial Lineage and Antiandrogen Sensitivity in <i>PTEN</i> and <i>TP53</i>-Mutated Prostate Cancer.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE4235
Whole genome gene expression profiles of migratory cells in the Drosophila ovary
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Cell migration contributes to normal development and homeostasis as well as to pathological processes such as inflammation and tumor metastasis. Previous genetic screens have revealed a few major signaling pathways that govern follicle cell migrations in the Drosophila ovary, several of which elicit transcriptional responses. However few downstream targets of the critical transcriptional regulators, such as the C/EBP homolog SLBO, have been identified. To characterize the gene expression profile of two migratory cell populations and identify SLBO targets, we employed a magnetic bead based cell separation approach to purify border cells and centripetal cells expressing the mouse CD8 antigen, and carried out whole genome microarray analysis.

Publication Title

Analysis of cell migration using whole-genome expression profiling of migratory cells in the Drosophila ovary.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE2144
Gene induction by low pH in oesophageal cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Differential gene expression analysis of oesophageal cells stimulated with a low pH environment. Study designed to identify pathways involved in progression of gastro-oesophageal reflux disease through Barrett's oesophagus to adenocarcinoma. Identified many subsets of genes with involvement in pathogenesis.

Publication Title

Low pH induces co-ordinate regulation of gene expression in oesophageal cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE49975
Integrative analysis of histone ChIP-seq and gene expression microarray data using Bayesian mixture models
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Histone modifications are a key epigenetic mechanism to activate or repress the expression of genes. Data sets of matched microarray expression data and histone modification data measured by ChIP-seq exist, but methods for integrative analysis of both data types are still rare. Here, we present a novel bioinformatic approach to detect genes that are differentially expressed between two conditions putatively caused by alterations in histone modification. We introduce a correlation measure for integrative analysis of ChIP-seq and gene expression data and demonstrate that a proper normalization of the ChIP-seq data is crucial. We suggest applying Bayesian mixture models of different distributions to further study the distribution of the correlation measure. The implicit classification of the mixture models is used to detect genes with differences between two conditions in both gene expression and histone modification. The method is applied to different data sets and its superiority to a naive separate analysis of both data types is demonstrated. This GEO series contains the expression data of the Cebpa example data set.

Publication Title

Integrative analysis of histone ChIP-seq and transcription data using Bayesian mixture models.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15434
Gene expression profiling in AML with normal karyotype: A multicenter study investigating molecular markers in 251 cases
  • organism-icon Homo sapiens
  • sample-icon 251 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Acute myeloid leukemia (AML) is a heterogeneous disease and AML with normal karyotype (AML-NK) is categorized as an intermediate-risk group. Over the past years molecular analyses successfully identified biomarkers that will further allow to dissecting clinically meaningful subgroups in this disease. Thus far, somatic mutations were identified which elucidate the disturbance of cellular growth, proliferation, and differentiation processes in hematopoietic progenitor cells. In AML-NK, acquired gene mutations with prognostic relevance were identified for FLT3, CEBPA, and NPM1. FLT3-ITD mutations were associated with short relapse-free and overall survival, while mutations in CEBPA or NPM1 (without concomitant FLT3-ITD) had a more favorable outcome.

Publication Title

Quantitative comparison of microarray experiments with published leukemia related gene expression signatures.

Sample Metadata Fields

Sex, Age, Disease, Disease stage

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accession-icon GSE13400
Exposure of SKGT4 and HET-1A cell lines to deoxycholic acid (DCA)
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE2120
Growth Hormone (GH) Treatment of 3T3-F442A Adipocytes
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Expression profiling of 3T3-F442A adipocytes treated with growth hormone (GH, 500 nM) or vehicle (DMEM + 1% BSA) control for 30 min., 4 hr., or 48 hr in three independent experiments. Chronic GH treatment induces metabolic changes consistent with insulin resistance in 3T3-F442A adipocytes.

Publication Title

Profiles of growth hormone (GH)-regulated genes reveal time-dependent responses and identify a mechanism for regulation of activating transcription factor 3 by GH.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13376
Exposure of Barrett's associated adenocarcinoma cell lines SKGT4 to deoxycholic acid (DCA)
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barretts metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisons with data derived from gene expression studies of Barretts esophagus and associated adenocarcinoma.

Publication Title

An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13378
Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA)
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barretts metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barretts esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line.

Publication Title

An integrative genomic approach in oesophageal cells identifies TRB3 as a bile acid responsive gene, downregulated in Barrett's oesophagus, which regulates NF-kappaB activation and cytokine levels.

Sample Metadata Fields

No sample metadata fields

View Samples
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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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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