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accession-icon GSE63325
The cohesin associated factor Wapal is required for proper polycomb-mediated gene silencing
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing.

Sample Metadata Fields

Specimen part

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accession-icon GSE63291
The cohesin offloading factor Wapal is required for proper polycomb-mediated gene silencing [array]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The cohesin offloading protein Wapal also acts as a polycomb factor in flies. We examined its role in transcriptional role in murine embryonic stem cells (ESCs)

Publication Title

The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing.

Sample Metadata Fields

Specimen part

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accession-icon SRP093382
Transcriptome profiling (RNA-seq) of CREBBP+/+ and CREBBP+/- clones of U2932 DLBCL cell line
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: Diffuse large B cell lymphomas (DLBCL) frequently harbor mutations in the histone acetyltransferase CREBBP, however their functional contribution to lymphomagenesis remains largely unknown. This study aims at elucidating and characterizing the molecular pathways affected by mutations in CREBBP. Methods: U2932, a DLBCL cell line that has wild type expression of CREBBP was manipulated by CRISPR-Cas9 strategy to mutate one allele of CREBBP and examine the pathways affected. RNA was isolated using the NucleoSping RNA Kit (Macherey-Nagel) from five wild type (CREBBP+/+) and five heterozygous clones (CREBBP+/-). RNA quality was assessed by Bioanalyzer 2100 followed by library preparation using the TruSeq RNA Sample Prep Kit v4 (Illumina). Sequencing was subsequently performed on the Illumina HiSeq 2500 instrument. RNA-seq reads were quality-checked with fastqc, which computes various quality metrics for the raw reads. RNA-seq reads were mapped to the GRCh38 reference human genome using STAR and reads were counted according to Ensembl gene annotation using the featureCounts function in the Rsubread Bioconductor package. Statistical analysis of differential expression was conducted with the DESeq2 package. Overall design: Trascriptomic profiles of CREBBP+/+ and CREBBP+/- clones were generated by deep sequencing.

Publication Title

Inactivation of CREBBP expands the germinal center B cell compartment, down-regulates MHCII expression and promotes DLBCL growth.

Sample Metadata Fields

Subject

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accession-icon GSE76320
Cohesin in AML
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Depletion of Rad21 in murine bone marrow leads to enhanced self-renewal in vitro

Publication Title

The cohesin subunit Rad21 is a negative regulator of hematopoietic self-renewal through epigenetic repression of Hoxa7 and Hoxa9.

Sample Metadata Fields

Specimen part

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accession-icon GSE147387
SMAD1 promoter hypermethylation and lack of SMAD1 expression in Hodgkin Lymphoma
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Global gene expression analysis was performed of several cell lines, mostly classical Hodgkin lymphoma, one DLBCL cell line and one NLPHL cell line.

Publication Title

SMAD1 promoter hypermethylation and lack of SMAD1 expression in Hodgkin lymphoma: a potential target for hypomethylating drug therapy.

Sample Metadata Fields

Cell line

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accession-icon SRP163173
Integrative epigenetic taxonomy of primary prostate cancer [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The Androgen Receptor (AR) is the key-driving transcription factor in prostate cancer, tightly controlled by epigenetic regulation. To date, most epigenetic profiling has been performed in cell lines or limited tissue samples. To comprehensively study the epigenetic landscape, we complemented RNA-seq with ChIP-seq for AR and histone modification marks (H3K27ac, H3K4me3, H3K27me3) in 100 primary prostate carcinomas. Integrative molecular subtyping of the five data streams revealed three major subtypes of which two were clearly TMPRSS2-ERG dictated. Importantly, a third novel subtype was identified, with low AR chromatin binding and activity, even though the receptor was clearly expressed. While positive for neuroendocrine-hallmark genes, these tumors were copy number-neutral with low mutation burden, significantly depleted for genes characteristic of poor-outcome associated luminal B-subtype. We present a rich novel resource on transcriptional and epigenetic control in prostate cancer, revealing a tight control of gene regulation differentially dictated by AR over the three subtypes. Overall design: RNA-seq data for primary prostate carcinomas

Publication Title

Integrative epigenetic taxonomy of primary prostate cancer.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP079189
Dysregulated synaptic gene expression and axonal neuropathology in a human iPSC-based model of familial Parkinson''s disease
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We generated de novo induced pluripotent stem cells (iPSCs) from two Parkinson’s Disease patients (PD) harboring the p.A53T mutation. iPSC-derived mutant neurons displayed disease-relevant phenotypes at basal conditions, including protein aggregation, compromised neuritic outgrowth and contorted axons with swollen varicosities containing aSyn and tau. We have performed RNA Sequencing (RNA-Seq) of neurons from PD patient and control samples. RNA sequencing has also been performed to neurons derived from HUES samples subjected to the same differentiation protocol as reference. Overall design: We have performed RNA Sequencing (RNA-Seq) in neurons PD and control samples (two clones from each individual), along with HUES-derived neurons.

Publication Title

Defective synaptic connectivity and axonal neuropathology in a human iPSC-based model of familial Parkinson's disease.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP045355
Adenosine-to-inosine RNA editing controls cathepsin S expression in atherosclerosis by enabling HuR-mediated post-transcriptional regulation
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Adenosine-to-inosine (A-to-I) RNA editing, which is catalyzed by a family of adenosine deaminase acting on RNA (ADAR) enzymes, is important in the epitranscriptomic regulation of RNA metabolism. However, the role of A-to-I RNA editing in vascular disease is unknown. Here we show that cathepsin S mRNA (CTSS), which encodes a cysteine protease associated with angiogenesis and atherosclerosis, is highly edited in human endothelial cells. The 3' untranslated region (3' UTR) of the CTSS transcript contains two inverted repeats, the AluJo and AluSx+ regions, which form a long stem–loop structure that is recognized by ADAR1 as a substrate for editing. RNA editing enables the recruitment of the stabilizing RNA-binding protein human antigen R (HuR; encoded by ELAVL1) to the 3' UTR of the CTSS transcript, thereby controlling CTSS mRNA stability and expression. In endothelial cells, ADAR1 overexpression or treatment of cells with hypoxia or with the inflammatory cytokines interferon-? and tumor-necrosis-factor-a induces CTSS RNA editing and consequently increases cathepsin S expression. ADAR1 levels and the extent of CTSS RNA editing are associated with changes in cathepsin S levels in patients with atherosclerotic vascular diseases, including subclinical atherosclerosis, coronary artery disease, aortic aneurysms and advanced carotid atherosclerotic disease. These results reveal a previously unrecognized role of RNA editing in gene expression in human atherosclerotic vascular diseases. Overall design: 1) Evaluation of transcriptome expression and RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in poly(A) RNA-seq data derived from endothelial cell transcriptome after ADAR1 or ADAR2 knockdown (n=2 biological replicates per condition, total n=8 biological samples). 2) Evaluation of transcriptome expression and RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in total-RNA-seq data derived from peripheral blood mononuclear cells (n=12 total biological samples; n=4 replicates per condition). 3) Evaluation of transcriptome expression and RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in total-RNA-seq data derived from endothelial cell transcriptome under basal and hypoxic conditions (n=2 biological replicates per condition, total n=4 biological samples). 4) Evaluation of RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in total RNA-seq data derived from endothelial cell transcriptome under basal and hypoxic conditions after ADAR1 knockdown (n=3 replicates per condition, total n=12 biological samples). 5) HuR iCLIP RNA-sequencing data derived from HUVEC HuR iCLIP after ADAR1 knockdown (scrambled control and siADAR1, n=1 per condition, total n=2 biological samples).

Publication Title

Adenosine-to-inosine RNA editing controls cathepsin S expression in atherosclerosis by enabling HuR-mediated post-transcriptional regulation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54852
Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome.

Sample Metadata Fields

Treatment

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accession-icon GSE54850
Dynamic mRNA gene expression during a nutritional downshift from glutamine to proline
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Dynamic mRNA gene expression from the wildtype YSBN6 during a nutritional downshift from glutamine to proline. Glutamine and proline were initially together in the media, with cells consuming exlusively glutamine (proline utilization inhibited due to nitrogen catabolite repression). The concentration of glutamine was frequently evaluated at-line, and the moment at which glutamine was not detected anymore is referred to as the time of the shift.

Publication Title

Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome.

Sample Metadata Fields

Treatment

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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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