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accession-icon SRP149997
Saccharomyces cerevisiae W303 Raw sequence reads
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptome study of 2 Saccharomyces cerevisiae W303 derivatives, one carrying GFP (control) and one carrying aSyn-GFP

Publication Title

Different 8-hydroxyquinolines protect models of TDP-43 protein, α-synuclein, and polyglutamine proteotoxicity through distinct mechanisms.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon GSE19672
Effects of MaxiK silencing in corporal smooth muscle cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The MaxiK potassium channel is a key modulator of smooth muscle tone. Due to its calcium and voltage sensitivity, MaxiK is activated following depolarization and Ca2+ mobilization, therefore relaxing the muscle. We investigate the effects of silencing MaxiK for 48h in corpus cavernosuml smooth muscle (CCSM) cells to identify possible mechanisms of compensation through molecular crosstalk between pathways regulating smooth muscle tone.

Publication Title

Silencing MaxiK activity in corporal smooth muscle cells initiates compensatory mechanisms to maintain calcium homeostasis.

Sample Metadata Fields

Specimen part

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accession-icon SRP047290
Molecular signatures of heterogeneous stem cell populations are resolved by linking single cell functional assays to single cell gene expression
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The discovery of significant heterogeneity in the self-renewal durability of adult haematopoietic stem cells (HSCs) has challenged our understanding of the molecules involved in population maintenance throughout life. Gene expression studies in bulk populations are difficult to interpret since multiple HSC subtypes are present and HSC purity is typically less than 50% of the input cell population. Numerous groups have therefore turned to studying gene expression profiles of single HSCs, but again these studies are limited by the purity of the input fraction and an inability to directly ascribe a molecular program to a durable self-renewing HSC. Here we combine single cell functional assays with flow cytometric index sorting and single cell gene expression assays to gain the first insight into the gene expression program of HSCs that possess durable self-renewal. This approach can be used in other stem cell systems and sets the stage for linking key molecules with defined cellular functions. Overall design: single-cell RNA-Seq of haematopoietic stem cells

Publication Title

Combined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP052568
NeuroD1 reprograms chromatin and transcription factor landscapes to induce the neuronal program
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Cell fate specification relies on the action of critical transcription factors that become available at distinct stages of embryonic development. One such factor is NeuroD1, which is essential for eliciting the neuronal development program and possesses the ability to reprogram other cell types into neurons. Given this capacity, it is important to understand its targets and the mechanism underlying neuronal specification. Here, we show that NeuroD1 directly binds regulatory elements of neuronal genes that are developmentally silenced by epigenetic mechanisms. This targeting is sufficient to initiate events that confer transcriptional competence, including reprogramming of transcription factor landscape, conversion of heterochromatin to euchromatin and increased chromatin accessibility, indicating potential pioneer factor ability of NeuroD1. The transcriptional induction of neuronal fate genes is maintained via epigenetic memory despite a transient NeuroD1 induction during neurogenesis. Our study not only reveals the NeuroD1-dependent gene regulatory program driving neurogenesis but also increases our understanding of how cell-fate specification during development involves a concerted action of transcription factors and epigenetic mechanisms. Overall design: 1. Ectopic NeuroD1 was induced for 48 hours (+Dox) in ES cells for checking initiation of neuronal transcriptional program in comparison to uninduced condition (-Dox) 2. ChIP-seq was performed after 24 hours of NeuroD1 induction in ES cells.

Publication Title

NeuroD1 reprograms chromatin and transcription factor landscapes to induce the neuronal program.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12134
The transcription factor AP2 regulates the number of basal progenitors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Understanding the mechanisms that specify neuronal subtypes is important to unravel the complex mechanisms of neuronal circuit assembly. Here we have identified a novel role for the transcription factor AP2 in progenitor and neuronal subtype specification in the cerebral cortex. Conditional deletion of AP2 causes misspecification of basal progenitors starting at

Publication Title

AP2gamma regulates basal progenitor fate in a region- and layer-specific manner in the developing cortex.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP126788
Single-cell RNA-sequencing reveals distinct populations of glucagon-like peptide-1 producing cells in the mouse upper small intestine
  • organism-icon Mus musculus
  • sample-icon 288 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Enteroendocrine L-cells release hormones that control metabolism and appetite and are targets under investigation for the treatment of diabetes and obesity. Understanding L-cell diversity and expression profiles is critical for identifying target receptors that will translate into altered hormone secretion. We performed single cell RNA sequencing of mouse L-cells from the upper small intestine to distinguish cellular populations, revealing that L-cells form 3 major clusters: a group with typical characteristics of classical L-cells, including high expression of Gcg and Pyy; a cell type overlapping with Gip-expressing K-cells; and a unique cluster expressing Tph1 and Pzp that was predominantly located in duodenal villi and co-produced 5HT. Expression of G-protein coupled receptors differed between clusters, suggesting the cell types are differentially regulated, and would be differentially targetable. Our findings support the emerging concept that many enteroendocrine cell populations are highly overlapping, with individual cells producing a range of peptides previously assigned to distinct cell types. Overall design: Single cell RNA sequencing of mouse duodenal L-cells cells

Publication Title

Single-cell RNA-sequencing reveals a distinct population of proglucagon-expressing cells specific to the mouse upper small intestine.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE68529
Functionally distinct subsets of lineage-biased multipotent progenitors control blood production in normal and regenerative conditions
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To identify the molecular characterisitics of parallel lineage-biased MPP populations arising from hematopoietic stem cells (HSC) we conducted genome-wide analyses of hematopoietic stem, progenitor and mature myeloid cell populations using Affymetrix Gene ST1.0 arrays.

Publication Title

Functionally Distinct Subsets of Lineage-Biased Multipotent Progenitors Control Blood Production in Normal and Regenerative Conditions.

Sample Metadata Fields

Specimen part

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accession-icon GSE8646
The Hay Wells Syndrome-Derived TAp63alphaQ540L Mutant Has Impaired Transcriptional and Cell Growth Regulatory Activity
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

p63 mutations have been associated with several human hereditary disorders characterized by ectodermal dysplasia such as EEC syndrome, ADULT syndrome and AEC syndrome . The location and functional effects of the mutations that underlie these syndromes reveal a striking genotype-phenotype correlation. Unlike EEC and ADULT that result from missense mutations in the DNA-binding domain of p63, AEC is solely caused by missense mutations in the SAM domain of p63. We report a study on the TAp63a isoform, the first to be expressed during development of the embryonic epithelia, and on its naturally occurring Q540L mutant derived from an AEC patient. To assess the effects of the Q540L mutation, we generated stable cell lines expressing TAp63a wt, DeltaNp63 alpha or the TAp63 alpha-Q540L mutant protein and used them to systematically compare the cell growth regulatory activity of the mutant and wt p63 proteins and to generate, by microarray analysis, a comprehensive profile of differential gene expression. We found that the Q540L substitution impairs the transcriptional activity of TAp63a and causes misregulation of genes involved in the control of cell growth and epidermal differentiation.

Publication Title

The Hay Wells syndrome-derived TAp63alphaQ540L mutant has impaired transcriptional and cell growth regulatory activity.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP108902
Dihydropyrimidine-thiones and clioquinol synergize to target b-amyloid cellular pathologies through a metal-dependent mechanism
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

DHPM-thiones rescue Ab-mediated toxicity in a metal-dependent manner that strongly synergizes with clioquinol, a known metal-binding and cytoprotective compound. RNA-seq experiments reveal a modest, yet specific effect on metal-responsive genes that do not change with the inactive control compound. Overall design: Treatment of biological replicates with DMSO, 0.8 uM clioquinol, or 20 uM 10{3,3,1} (DHPM-thione) for ~6 hours prior to harvesting of cells and isolation of total RNA.

Publication Title

Dihydropyrimidine-Thiones and Clioquinol Synergize To Target β-Amyloid Cellular Pathologies through a Metal-Dependent Mechanism.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE62232
Large-scale gene expression profiling of 81 hepatocellular carcinomas
  • organism-icon Homo sapiens
  • sample-icon 90 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hepatocellular carcinoma (HCC) is ranked second in cancer-associated deaths worldwide. Most cases of HCC are secondary to either a viral hepatitis infection (hepatitis B or C) or cirrhosis (alcoholism being the most common cause of hepatic cirrhosis). It is a complex and heterogeneous tumor due to activation of multiple cellular pathways and molecular alterations.

Publication Title

Exome sequencing of hepatocellular carcinomas identifies new mutational signatures and potential therapeutic targets.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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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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