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accession-icon GSE25533
A chromatin-modifying function of JNK during embryonic stem cell differentiation
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A chromatin-modifying function of JNK during stem cell differentiation.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE25529
Expression data from DMSO and SP600125 treated neurons
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Expression profiling of from DMSO and SP600125 treated glutamatergic neurons reveals JNK target genes that are transcriptionally regulated by JNK signaling.

Publication Title

A chromatin-modifying function of JNK during stem cell differentiation.

Sample Metadata Fields

Specimen part

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accession-icon SRP007827
DNA binding factors shape the mouse methylome at distal regulatory regions [strand-specific-RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

To gain insights into the interplay between DNA methylation and gene regulation we generated a basepair resolution reference map of the mouse methylome in stem cells and neurons. High genome coverage allowed for a novel quantitative analysis of local methylation states, which identified Low Methylated Regions (LMR) with an average methylation of 30%. These regions are evolutionary conserved, reside outside of CpG islands and distal to promoters. They represent regulatory regions evidenced by their DNaseI hypersensitivity and chromatin marks of enhancer elements. LMRs are occupied by transcription factors (TF) and their reduced methylation requires TF binding while introduction of TF binding sites creates LMRs de novo. This dependency on TF activity is further evident when comparing the methylomes of embryonic stem cells and derived neuronal cells. LMRs present in both cell types are occupied by broadly expressed factors, while LMRs present at only one state are occupied by cell-type specific TFs. Methylome data can thus enhance the prediction of occupied TF binding sites and identification of active regulatory regions genome-wide. Our study provides reference methylomes for the mouse at two cell states, identifies a novel and highly dynamic feature of the epigenome that defines distal regulatory elements and shows that transcription factor binding dynamically shapes mammalian methylomes. Overall design: Strand specific expression profiling by high throughput sequencing.

Publication Title

DNA-binding factors shape the mouse methylome at distal regulatory regions.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE27247
Topoisomerase IIbeta occupies H3K4 methylated sites and regulates neuronal survival via repression of the neurotrophin receptor p75
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Target genes of Topoisomerase IIβ regulate neuronal survival and are defined by their chromatin state.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE27245
Expression data from Top2 KO cells as well ICRF-193 treatment of in vitro derived neurons and cortical glutamatergic neurons
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Expression profiling of from Top2 knokout and ICRF-193 treated neurons reveals a significant number of genes that are transcriptionally deregulated

Publication Title

Target genes of Topoisomerase IIβ regulate neuronal survival and are defined by their chromatin state.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE89409
HOXA5 is a survival locus associated with chromosome 7 gain in IDH-wildtype glioblastoma
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Glioblastomas (GBMs) are divided into CpG Island Methylator Phenotype (CIMP) and non-CIMP tumors. Non-CIMP GBMs derive from cells with non-disjunction of chromosome (chr7) and chromosome 10 (chr10), resulting in chr7 gain and chr10 loss, while CIMP GBMs have mutations in isocitrate dehydrogenase 1 or 2 (IDH1/2). Gain of chr7 is largely driven by PDGFA, but other genes on chr7 are likely to contribute to fitness gains and aggressiveness of these GBMs. We computationally investigated genes on chr7 whose gene expression correlated with survival, identifying HOXA5 as a potential driver of proneural gliomagenesis. Using a combination of human GBM cells and mouse PDGF-driven gliomas, we showed that HOXA5 drives increased proliferation and radiation resistance in culture and in vivo. These phenotypes appear to be in part due to effects on p53 and other apoptosis-related genes.

Publication Title

Increased <i>HOXA5</i> expression provides a selective advantage for gain of whole chromosome 7 in IDH wild-type glioblastoma.

Sample Metadata Fields

Disease

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accession-icon GSE86068
Increasing of antitumor effect of decitabine against classical Hodgkin lymphoma (cHL) by targeting decitabine-activated pro-survival pathways
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We found that 5-Aza-dC/decitabine induces various prosurvival pathways (JAK-STAT-, NFkB-, MEK/ERK- and PI3K/AKTpathway) in cHL cell lines. Inhibition of these pathways with specific small molecular weight inhibitors potentiates the antitumor effect of 5-Aza-dC.

Publication Title

Activation of oncogenic pathways in classical Hodgkin lymphoma by decitabine: A rationale for combination with small molecular weight inhibitors.

Sample Metadata Fields

Cell line

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accession-icon GSE52794
Gene expression in aortic roots of wild type versus klotho-deficient mice at 6 weeks of age
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Klotho-deficient mice develop aortic valve annulus calcification by 6 weeks of age. Understanding the molecular basis by which aortic valve calcification is initiated will help define potential molecular targets which may be inhibited to reduce or prevent aortic valve calcification.

Publication Title

COX2 inhibition reduces aortic valve calcification in vivo.

Sample Metadata Fields

Specimen part

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accession-icon GSE17129
The IKK2/NF-kB-pathway suppresses MYC-induced lymphomagenesis
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Abstract.

Publication Title

The IKK2/NF-{kappa}B pathway suppresses MYC-induced lymphomagenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE50019
Study of expression changes during RPS4-mediated resistance in Arabidopsis using a temperature-inducible system
  • organism-icon Arabidopsis thaliana
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Innate immune responses of plant cells confer the first line of defence against pathogens. Signals generated by activated receptors are integrated inside the cell and converge on transcriptional programmes in the nucleus. The Arabidopsis Toll-related intracellular receptor RPS4 operates inside nuclei to trigger resistance to Pseudomonas bacteria expressing AvrRps4 and defence gene reprogramming through the stress response regulator, EDS1.

Publication Title

Arabidopsis TNL-WRKY domain receptor RRS1 contributes to temperature-conditioned RPS4 auto-immunity.

Sample Metadata Fields

Specimen part

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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