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accession-icon GSE75214
Mucosal gene expression profiling in patients with inflammatory bowel disease study
  • organism-icon Homo sapiens
  • sample-icon 193 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Microarrays were used to analyze the gene expression in endoscopic-derived intestinal mucosal biopsies from patients with inflammatory bowel diseas (IBD) and controls

Publication Title

Genetic and Transcriptomic Bases of Intestinal Epithelial Barrier Dysfunction in Inflammatory Bowel Disease.

Sample Metadata Fields

Specimen part, Disease

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accession-icon SRP113472
ZBTB2 as a novel reader for unmethylated DNA [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

DNA methylation is a dynamic epigenetic modification that plays a key role in various cellular processes. Proteins that bind to DNA depending on its methylation status are thought to play an important role in DNA methylation-mediated gene expression. Using a variety of genomics and proteomics approaches, we identified ZBTB2 as a novel reader of unmethylated DNA. ZBTB2, which forms a complex with ZBTB25 and ZNF639, preferentially binds at CpG island promoters in mouse embryonic stem cells, from where it regulates genes that are involved in the exit from pluripotency. Binding of ZBTB2 to target genes is mostly associated with gene activation. Furthermore, ZBTB2 is intricately interwoven with DNA methylation, as we found not only that its binding to DNA is methylation-sensitive, but also that ZBTB2 regulates the turnover of methylated DNA. Summarising, we propose that ZBTB2 is a DNA methylation-sensitive transcription factor that is involved in cellular differentiation. Overall design: RNA-seq samples of wildtype ESCs and Zbtb2 KO ESCs

Publication Title

ZBTB2 reads unmethylated CpG island promoters and regulates embryonic stem cell differentiation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP151306
Transition between fermentation and respiration determines history-dependent behavior in fluctuating carbon sources
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 50 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptome of S. cerevisiae in shifts between glucose and maltose media with different re-growth conditions Overall design: Cells are pregrown in maltose, then grown for different durations in glucose and then washed back to maltose

Publication Title

A new protocol for single-cell RNA-seq reveals stochastic gene expression during lag phase in budding yeast.

Sample Metadata Fields

Subject

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accession-icon GSE29331
Expression data from diclofenac-treated yeast cells
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Diclofenac is a widely used analgesic drug that can cause serious adverse drug reactions. We used Saccharomyces cerevisiae as model eukaryote to elucidate the molecular mechanisms of diclofenac toxicity and resistance. Although most yeast cells died during initial diclofenac treatment, some survived and started growing again. Microarray analysis of the adapted cells identified three major processes involved in diclofenac detoxification and tolerance. Especially pleiotropic drug resistance genes and genes under control of Rlm1p, a transcription factor in the protein kinase C (PKC) pathway, were upregulated in diclofenac-adapted cells. Genes involved in ribosome biogenesis and rRNA processing were downregulated, as well as zinc-responsive genes.

Publication Title

Involvement of the pleiotropic drug resistance response, protein kinase C signaling, and altered zinc homeostasis in resistance of Saccharomyces cerevisiae to diclofenac.

Sample Metadata Fields

Treatment

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accession-icon SRP123625
Translatome analysis of the ribosomal protein L10 R98S mutation reveals altered serine metabolism in acute lymphoblastic leukemia [supplementaryRNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Somatic ribosomal protein defects have recently been described in cancer, yet their impact on cellular transcription and translation remain poorly understood. Here we integrated mRNA sequencing, ribosome footprinting, polysomal RNA seq and quantitative mass spectrometry datasets obtained from an isogenic mouse lymphoid cell model in order to study the T-cell acute lymphoblastic leukemia (T-ALL) associated R98S mutation in ribosomal protein L10 (RPL10 R98S). RPL10 R98S induced changes in protein levels were to a much larger extent caused by transcriptional then translational changes and RPL10 R98S cells showed a gene signature corresponding to deregulation of hematopoietic transcription factors. Phosphoserine phosphatase (PSPH), a key enzyme in serine biosynthesis, displayed elevated transcription and translation and was one of the proteins showing the strongest upregulation in RPL10 R98S cells. Increased Psph protein levels were confirmed in RPL10 R98S engineered JURKAT cells and in hematopoietic cell cultures derived from Rpl10 R98S knock-in mice. Moreover, elevated serine and glycine biosynthesis in RPL10 R98S cells was supported by metabolic flux analyses. Analysis of PSPH expression levels in T-ALL patient samples revealed that PSPH upregulation is a generalized phenomenon in this disease, associated with elevated circulating serine and glycine levels. Addition of serine and glycine enhanced survival of stromal and myeloid cells, suggesting supportive effects on the hematopoietic niche. Finally, reduction of PSPH expression levels in T-ALL cell lines suppressed their in vitro proliferation and their capacity to expand in T-ALL xenograft models. In conclusion, transcriptome, translatome and proteome analysis of the RPL10 R98S mutation identified RPL10 R98S driven induction of cellular serine biosynthesis. Whereas serine metabolism has been implicated in cancer via PHGDH amplification, this is the first report supporting dependence of ALL cells on the serine biosynthesis enzyme PSPH. Overall design: 3 biological replicates for each condition (RPL10 R98S, RPL10 WT)

Publication Title

Translatome analysis reveals altered serine and glycine metabolism in T-cell acute lymphoblastic leukemia cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP156476
Identification of the genes under the control of the transcription factor Prdm12 in somatosensory neurons
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Prdm12, a novel key regulator of the Nerve Growth Factor-TrkA signaling pathway, is required for nociceptive sensory neuron development Overall design: RNA-seq analysis in triplcate of the transcriptome of thoracic dorsal root ganglia with associated spinal cord of E11.5 Prdm12 KO and WT embryos.

Publication Title

Prdm12 Directs Nociceptive Sensory Neuron Development by Regulating the Expression of the NGF Receptor TrkA.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP031459
MicroRNA profiling of primary cutaneous large B-cell lymphomas
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

High-throughput sequencing of primary cutaneous follicle center lymphoma (PCFCL), primary cutaneous diffuse large B-cell lymphoma, leg type (PCLBCL-LT) and in vitro activated peripheral blood B-cells. We performed high-throughput sequencing analysis on frozen tumor biopsies from 19 cases of PCFCL and PCLBCL-LT to establish microRNA profiles. Cluster analysis of the complete microRNome could not distinguish between the two subtypes, but 16 single microRNAs were found to be differentially expressed. Overall design: Lymphoma miRNA profiles of were generated by deep sequencing, using Illumina Genome Analyzer II.

Publication Title

MicroRNA profiling of primary cutaneous large B-cell lymphomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP091793
Mechanism of Induction of Mouse Breast Cancer by Non-coding Heterochromatic RNAs
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Heterochromatic non-coding RNAs induce breast tumor formation in mice by interacting with BRCA1-associated proteins functioning in the DNA damage response. Overall design: mouse tumor mRNA profiles using ribosomal mRNA depletion

Publication Title

Heterochromatin-Encoded Satellite RNAs Induce Breast Cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE33115
Molecular changes induced by melanoma cell conditioned medium (MCM) in HUVEC cells.
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Malignant melanoma is a complex genetic disease and the most aggressive form of skin cancer. Melanoma progression and metastatic dissemination fundamentally relies on the process of angiogenesis. Melanomas produce an array of angiogenic modulators that mediate pathological angiogenesis. Such tumor-associated modulators arbitrate the enhanced proliferative, survival and migratory responses exhibited by endothelial cells, in the hypoxic tumor environment. The current study focuses on melanoma-induced survival of endothelial cells under hypoxic conditions. Melanoma conditioned media were capable of enabling prolonged endothelial cell survival under hypoxia, in contrast with the conditioned media derived from melanocytes, breast and pancreatic tumors. To identify the global changes in gene expression and further characterize the pro-survival pathway induced in endothelial cells, we performed microarray analysis on endothelial cells treated with melanoma conditioned medium under normoxic and hypoxic conditions.

Publication Title

Melanomas prevent endothelial cell death under restrictive culture conditions by signaling through AKT and p38 MAPK/ ERK-1/2 cascades.

Sample Metadata Fields

Specimen part

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accession-icon GSE73661
The effect of vedolizumab (anti-47-integrin) therapy on colonic mucosal gene expression in patients with ulcerative colitis (UC)
  • organism-icon Homo sapiens
  • sample-icon 175 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Microarrays were used to investigate the the effect of vedolizumab (VDZ) therapy on colonic mucosal gene expression in UC patients and compared the changes to those observed with infliximab (IFX) therapy.

Publication Title

Effect of vedolizumab (anti-α4β7-integrin) therapy on histological healing and mucosal gene expression in patients with UC.

Sample Metadata Fields

Specimen part

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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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