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accession-icon GSE62039
Defining a mesenchymal progenitor niche at single cell resolution
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Most vertebrate organs are composed of epithelium surrounded by support and stromal tissues formed from mesenchyme cells, which are not generally thought to form organized progenitor pools. Here we use clonal cell labeling with multicolor reporters to characterize individual mesenchymal progenitors in the developing mouse lung. We observe a diversity of mesenchymal progenitor populations with different locations, movements, and lineage boundaries. Airway smooth muscle (ASM) progenitors map exclusively to mesenchyme ahead of budding airways. Progenitors recruited from these tip pools differentiate into ASM around airway stalks; flanking stalk mesenchyme can be induced to form an ASM niche by a lateral bud or by an airway tip plus focal Wnt signal. Thus, mesenchymal progenitors can be organized into localized and carefully controlled domains that rival epithelial progenitor niches in regulatory sophistication.

Publication Title

Mesenchymal cells. Defining a mesenchymal progenitor niche at single-cell resolution.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon E-MEXP-1344
Transcription profiling of Arabidopsis plants grown under diurnal conditions and transferred to cold conditions at different times of day to identify factors influencing cold-responsive genes
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Arabidopsis plants growing under diurnal conditions were transferred to cold of approximately one day duration, starting at different times of the day. All comparisons are of unreplicated pairs and are thus not designed to identify cold-responsive gens in isolation but are rather to supplement existing publicly available data. The overall aim was to use a diverse set of experiments to see which factors have the greatest influence on the identity of cold-responsive genes.

Publication Title

Disruption of the Arabidopsis circadian clock is responsible for extensive variation in the cold-responsive transcriptome.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon E-MEXP-1345
Transcription profiling of Arabdiposis plants before and after cold treatment using spike-in controls to allow measurement of absolute mRNA expression at the global level
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

To address the neglected possibility for global mRNA changes in microarray experiments we developed a simple method to generate external controls for Affymetrix microarrays to allow these platforms to measure absolute mRNA expression at the global level. We used publicly available data to select probesets that never detect endogenous transcripts, and used PCR and IVT to generate synthetic mRNAs corresponding to them. After quality control and testing, these control transcripts were spiked into total RNA samples from plants before and after 24 h of cold treatment. Due to changes in the proportion of mRNA, these data reveal intensity-dependent bias in expression estimates based on standard all-gene normalizations. When not accounted for, this leads to false classification of the differential expression for thousands of genes.

Publication Title

Disruption of the Arabidopsis circadian clock is responsible for extensive variation in the cold-responsive transcriptome.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE19199
Expression data from serum-starved control and CDK8 depleted cells following serum stimulation
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The Mediator complex allows communication between transcription factors and RNA polymerase II (RNAPII). CDK8, the kinase found in some variants of Mediator, has been characterized mostly as a transcriptional repressor. Recently, CDK8 was demonstrated to be a potent oncoprotein. Here we show that CDK8 is predominantly a positive regulator of gene expression within the serum response network, as it is required for expression of several members of the AP-1 and EGR family of oncogenic transcription factors (e.g. FOS, JUN, EGR1-3). Mechanistic studies demonstrate that CDK8 is not required for recruitment of RNAPII and promoter escape at these loci. Instead, CDK8 depletion leads to the appearance of slower elongation complexes carrying hypophosphorylated RNAPII. We show that CDK8-Mediator regulates precise steps in the assembly of a functional elongation complex, including the recruitment of P-TEFb and BRD4, but is dispensable for recruitment of SPT5 and FACT. Furthermore, CDK8-Mediator specifically interacts with P-TEFb. Thus, we uncovered a novel role for CDK8 in transcriptional regulation that may contribute to its oncogenic effects.

Publication Title

CDK8 is a positive regulator of transcriptional elongation within the serum response network.

Sample Metadata Fields

Cell line

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accession-icon GSE53474
A novel class of alternative 3-terminal exons is involved in cell-cycle regulation by topoisomerase inhibitors
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Alternative 3-terminal exons, which use intronic polyadenylation sites, are generally unconserved and lowly expressed, while the main gene products end in the last exon of genes. In this study, we discover a class of human genes, where the last exon appeared recently during evolution, and the major gene product uses an alternative 3-terminal exon corresponding to the ancestral last exon of the gene. This novel class of alternative 3-terminal exons are down-regulated on a large scale by doxorubicin, a cytostatic drug targeting topoisomerase II, and play a role in cell cycle regulation, including centromere-kinetochore assembly. The RNA-binding protein, HuR/ELAVL1 is a major regulator of this specific set of alternative 3-terminal exons. HuR binding to the alternative 3-terminal exon in the pre-messenger RNA promotes its splicing, and is reduced by topoisomerase inhibitors. These findings provide new insights into the evolution, function and molecular regulation of alternative 3-terminal exons.

Publication Title

A recently evolved class of alternative 3'-terminal exons involved in cell cycle regulation by topoisomerase inhibitors.

Sample Metadata Fields

Cell line

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accession-icon GSE6766
C2C12 Myotubes in response to Palmitate
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify mediators of obesity-linked reductions in PGC-1, we tested the effects of cellular nutrients in C2C12 myotubes. While overnight exposure to high insulin, glucose, glucosamine, or amino acids had no effect, saturated fatty acids (FA) potently reduced PGC-1a and b mRNA expression.

Publication Title

Peroxisome proliferator activator receptor gamma coactivator-1 expression is reduced in obesity: potential pathogenic role of saturated fatty acids and p38 mitogen-activated protein kinase activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP058619
RNA-Sequencing experiment for effects of PKF115-584 treatment on four T-ALL cell lines (RPMI8402, HPB-ALL, Jurkat, CCRF-CEM).
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Notch activation is instrumental in the development of most T-cell acute lymphoblastic leukemia (T-ALL) cases, yet Notch mutations alone are not sufficient to recapitulate the full human disease in animal models. We here found that Notch1 activation at the fetal liver (FL) stage expanded the hematopoietic progenitor population and conferred it transplantable leukemic-initiating capacity. However, leukemogenesis and leukemic-initiating cell capacity induced by Notch1 was critically dependent on the levels of ß-Catenin in both FL and adult bone marrow contexts. In addition, inhibition of ß-Catenin compromised survival and proliferation of human T-ALL cell lines carrying activated Notch1. By transcriptome analyses, we identified the MYC pathway as a crucial element downstream of ß-Catenin in these T-ALL cells and demonstrate that the MYC 3'' enhancer required ß-Catenin and Notch1 recruitment to induce transcription. Finally, PKF115-584 treatment prevented and partially reverted leukemogenesis induced by active Notch1. Overall design: Four T-ALL cell lines (RPMI8402, HPB-ALL, Jurkat, CCRF-CEM) were treated with DMSO (control) or PKF115-584 (310nM) for 3hrs. Gene expression changes were measured with Cufflinks comparing the 4 control with the 4 treated samples.

Publication Title

β-Catenin is required for T-cell leukemia initiation and MYC transcription downstream of Notch1.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP111864
Intestinal IKKa is required for tumor initiation in APC mutant mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We have generated a mouse model for tumor initiation carrying a mutation in APC and lacking IKKa in intestinal epithelial cells. IKKa-deficient intestinal cells primarily failed to generate adenomas, and the few adenomas arising in this background displayed a significant reduction in cell proliferation. Using an in vitro model for intestinal tumoroids (derived from adenoma initiating cells), we have performed RNA sequencing of wild type and IKKa-deficient intestinal tumoroids. This has demonstrated that epithelial IKKa controls transcription of stem cell-related genes and genes associated with proliferation and apoptosis. Overall design: RNA sequencing of IKKa WT and KO tumoroids, done in triplicates

Publication Title

IKKα is required in the intestinal epithelial cells for tumour stemness.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE35395
Expression from early pre-hematopoietic progenitors from mouse embryo
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hematopoietic Stem Cells (HSC) are originated during embryonic development from endothelial-like cells located in the ventral side of the dorsal aorta around day E10-12 of murine development. This region is called AGM for Aorta/Gonad/Mesonephros and refers to the tissues around the hemogenic aorta. Cells that emerge from the endothelium and show hematopoietic traits can be distinguished by the expression of the c-kit receptor and finally acquire the CD45 marker.

Publication Title

Hematopoietic stem cell development requires transient Wnt/β-catenin activity.

Sample Metadata Fields

Specimen part

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accession-icon GSE48378
PBMCs from patients with Sjgren's syndrome and healthy controls
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Sjgren's syndrome is an autoimmune disease manifesting primarily as dryness of eyes and mouth. In this study, we compared gene expression in PBMCs between age- and gender-matched patients with Sjgren's syndrome (diagnosed by ACR criteria) and healthy controls. Cells were collected in heparinized tubes and PBMCs were prepared using Ficoll.

Publication Title

Expression of the immune regulator tripartite-motif 21 is controlled by IFN regulatory factors.

Sample Metadata Fields

Specimen part, Disease

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)

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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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