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accession-icon GSE51257
Functional heterogeneity of cancer-associated fibroblasts from human colon tumors shows specific prognostic gene expression signature
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Tumor growth and metastasis is controlled by paracrine signaling between cells of the tumor microenvironment and malignant cells. Cancer-associated fibroblasts (CAFs), are functionally important components of the tumor microenvironment. Although some steps involved in the cross-talk between these cells are known, there is still a lot that is not clear. Thus, the addition of, the consideration of microenvironment in the development of the disease, to the clinical and pathological procedures (currently admitted as the consistent value cancer treatments) could lay the foundations for the development of new treatment strategies to control the disease.

Publication Title

Functional heterogeneity of cancer-associated fibroblasts from human colon tumors shows specific prognostic gene expression signature.

Sample Metadata Fields

Specimen part

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accession-icon GSE74057
Snail1 controls fibroblast action on tumor cell invasion and metastasis [MSC]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Snail1 transcriptional factor is essential for triggering epithelial-to-mesenchymal transition (EMT) and inducing tumor cell invasion. We report here that Snail1 plays also a key role in tumor associated fibroblasts since is necessary for enhancement by these cells on epithelial cells tumor invasion. Snail1 expression in fibroblast requires signals derived from tumor cells such as TGF-b; reciprocally, in fibroblasts Snail1 organizes a complex program that favors collective invasion of epithelial cells at least in part by the secretion of diffusible signaling molecules, such as prostaglandin E2. The capability of human or murine tumor-derived cancer associated fibroblasts to promote tumor invasion is associated to Snail1 expression and obliterated by Snail1 depletion. In vivo experiments show that tumor cells co-transplanted with Snail1 depleted fibroblasts show lower invasion than those xenografted with control fibroblasts. Finally Snail1 depletion in mice prevents the formation of breast tumors and decreased their invasion. Therefore, these results demonstrate that the role of Snail1 in tumor invasion is not limited to its effect in EMT but dependent on its expression in stromal fibroblasts where it orchestrates its activation and the crosstalk with epithelial cells.

Publication Title

Snail1-Dependent Activation of Cancer-Associated Fibroblast Controls Epithelial Tumor Cell Invasion and Metastasis.

Sample Metadata Fields

Specimen part

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accession-icon SRP040137
Core promoter factor TAF9B controls neuronal gene expression
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon

Description

Purpose: Characterize the role of the coactivator subunit TAF9b during differentiation of embryonic stem cells into motor neurons as well in mouse newborn spinal column tissues. Overall design: RNA-seq comparing WT and TAF9B KO mouse ES cells differentiated into motor neurons. RNA-seq comparing WT and TAF9B KO mouse newborn spinal column tissues. ChIP-seq mapping TAF9b and RNA Pol II binding sites in in vitro differentiated motor neurons.

Publication Title

Core promoter factor TAF9B regulates neuronal gene expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49073
Gene expression from NMuMG cells overexpressing major satellite treated with TGFbeta
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Although heterochromatin is enriched with repressive traits, it is also actively transcribed, giving rise to large amounts of non-coding RNAs. Although these RNAs are responsible for the formation and maintenance of heterochromatin, little is known about how their transcription is regulated. Here we show that the Snail1 transcription factor represses pericentromeric transcription, acting through the H3K4 deaminase LOXL2. Since Snail1 plays a key role in the epithelial to mesenchymal transition (EMT), we analyzed the regulation of mouse heterochromatin transcription in this process. At the onset of EMT, one of the major structural heterochromatin proteins, HP1a, is transiently released from heterochromatin foci in a Snail1/LOXL2dependent manner during EMT, concomitantly with a down-regulation of major satellite transcription. Global transcriptome analysis indicated that ectopic expression of heterochromatin transcripts affects the transcription profile of EMT-related genes. Additionally, preventing the down-regulation of major satellite transcripts compromised the migratory and invasive behavior of mesenchymal cells. We propose that Snail1 regulates heterochromatin transcription through the histone-modifying enzyme, LOXL2, thus creating the favorable transcriptional state necessary for completing EMT.

Publication Title

Regulation of heterochromatin transcription by Snail1/LOXL2 during epithelial-to-mesenchymal transition.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE54340
Expression data from Saccharomyces cerevisiae strains carrying the spt16-11 or the pob3-7 allele
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The conserved FACT (FAcilitates Chromatin Transcription) complex is a chromatin-reorganizing complex that promotes RNAPII transcription through chromatin templates by interacting with histones. It facilitates promoter activation by nucleosome eviction, and transcription elongation by nucleosome disruption and reassembly ahead and behind the RNAP. It also has a role in replication not fully understood yet. Genome-wide microarray analyses in spt16-11 and pob3-7 strains revealed a set of genes whose mRNA levels were altered with respect to the WT levels. These include 48 up-regulated and 80 down-regulated genes that are common to both strains. The up-regulated genes were longer and expressed at lower levels than the genome average whereas the down-regulated genes were more similar to the average of the genome.

Publication Title

The yeast and human FACT chromatin-reorganizing complexes solve R-loop-mediated transcription-replication conflicts.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP187597
Intrinsic Resistance to MEK Inhibition Through BET Protein Mediated Kinome
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Mutation or deletion of Neurofibromin (NF1), an inhibitor of RAS signaling, frequently occurs in epithelial ovarian cancer (EOC), supporting therapies that target downstream RAS effectors, such as the RAF-MEK-ERK pathway. However, no comprehensive studies have been carried out testing the efficacy of MEK inhibition in NF1-deficient EOC. Here, we performed a detailed characterization of MEK inhibition in NF1-deficient EOC cell lines using kinome profiling and RNA sequencing. Our studies showed MEK inhibitors were ineffective at providing durable growth inhibition in NF1-deficient cells due to kinome reprogramming. MEKi-mediated destabilization of FOSL1 resulted in induced expression of RTKs and their downstream RAF and PI3K signaling overcoming MEKi therapy. MEKi synthetic enhancement screens identified BRD2 and BRD4 as integral mediators of the MEKi-induced RTK signatures. Inhibition of BET proteins using BET bromodomain inhibitors (BETi) blocked MEKi-induced RTK reprogramming, indicating BRD2 and BRD4 represent promising therapeutic targets in combination with MEKi to block resistance due to kinome reprogramming in NF1-deficient EOC. Overall design: Examination of the global effects on transcription in response to trametinib (GSK212) in A1847 cells.

Publication Title

Intrinsic Resistance to MEK Inhibition through BET Protein-Mediated Kinome Reprogramming in NF1-Deficient Ovarian Cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE61062
Whole-genome expression profile in zebrafish embryos after chronic exposure to morphine
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

A great number of studies have investigated changes induced by morphine exposure in gene expression using several experimental models. In this study, we examined gene expression changes during chronic exposure to morphine during maturation and differentiation of zebrafish CNS.

Publication Title

Whole-genome expression profile in zebrafish embryos after chronic exposure to morphine: identification of new genes associated with neuronal function and mu opioid receptor expression.

Sample Metadata Fields

Treatment

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accession-icon GSE35600
Gene expression from MDA-MB-231
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Gene expression from MDA-MB-231 cells shControl and shLOXL2.

Publication Title

Lysyl oxidase-like 2 (LOXL2) oxidizes trimethylated lysine 4 in histone H3.

Sample Metadata Fields

Cell line

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accession-icon GSE17170
A systems genetics approach implicates USF1, FADS3 and other causal candidate genes for familial combined hyperlipidemia
  • organism-icon Homo sapiens
  • sample-icon 68 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Assessment of mRNA expression levels in fat biopsies from subcutaneous adipose tissue from unrelated individuals.

Publication Title

A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE17300
Overexpression of USF1 in HEK293T cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Overexpression of USF1 in HEK293T cells in vitro to ascertain the genes downstream of USF1. Will identify direct targets as well as indirect targets of USF1.

Publication Title

A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.

Sample Metadata Fields

Cell line

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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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