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accession-icon SRP073245
RNA-seq analysis reveals profound changes in transcript profiles between siCon- and siH19-transfected EVT cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We used high throughput sequencing to analyze the transcriptional profiling of EVT. By comparing the transcriptional profiling of EVT with or without H19 knockdown, numerous genes showed significantly altered expression as a result of H19 repression. Overall design: HTR cells were transfected with either control siRNA or siH19. 48h later after transfection, total RNA was extracted for library preparation and RNA-seq analysis to compare trancript profiles between siCon and siH19 cells.

Publication Title

H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.

Sample Metadata Fields

Cell line, Subject, Time

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accession-icon GSE22132
Expression data from purified human platelets
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Patients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.

Publication Title

Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE22295
Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. The aim of this study was to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF

Publication Title

Lack of chemokine signaling through CXCR5 causes increased mortality, ventricular dilatation and deranged matrix during cardiac pressure overload.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE38043
Dysregulated expression of genes in regulatory T cells from metastatic castration-resistant prostate cancer patients
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We analyzed the global gene expression pattern of Tregs between healthy donors and prostate cancer patients. We found that genes related to cell cycle, cellular proliferation, immune responses, hematological system development and function were differentially expressed in Tregs from prostate cancer patients.

Publication Title

Up-regulation of proliferative and migratory genes in regulatory T cells from patients with metastatic castration-resistant prostate cancer.

Sample Metadata Fields

Specimen part, Disease stage

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accession-icon GSE6613
Parkinson's disease vs. controls, whole blood
  • organism-icon Homo sapiens
  • sample-icon 105 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Parkinsons disease (PD) progresses relentlessly and affects five million people worldwide. Laboratory tests for PD are critically needed for developing treatments designed to slow or prevent progression of the disease. We performed a transcriptome-wide scan in 105 individuals to interrogate the molecular processes perturbed in cellular blood of patients with early-stage PD. The molecular marker here identified is strongly associated with risk of PD in 66 samples of the training set (third tertile cross-validated odds ratio of 5.7 {P for trend 0.005}). It is further validated in 39 independent test samples (third tertile odds ratio of 5.1 {P for trend 0.04}). The genes differentially expressed in patients with PD, or Alzheimers or progressive supranuclear palsy offer unique insights into disease-linked processes detectable in peripheral blood. Combining gene expression scans in blood and linked clinical data will facilitate the rapid characterization of candidate biomarkers as demonstrated here with respect to PD.

Publication Title

Molecular markers of early Parkinson's disease based on gene expression in blood.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE59533
Expression data from Zea mays cultivars Tietar and DKC 6575
  • organism-icon Zea mays
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Maize transgenic event MON810, grown and commercialised worldwide, is the only cultivated GM event in EU. Maize MON810, variety DKC6575, and the corresponding near-isogenic Tietar were studied in different growing conditions, to assess their behaviour in response to drought. Profiling gene expression in water deficit regimes and in generalised water stress showed an up-regulation of different stress- responsive genes. A greater number of differentially expressed genes was observed in Tietar rather than in DKC6575, with genes belonging to transcription factor families and genes encoding HSPs, LEAs and detoxification enzymes. Since these genes have been from literature, indicated as typical of stress responses, their activation in Tietar rather than in DKC6575 may be reminiscent of a more efficient water stress response. DKC6575 was also analysed for the expression of the transgene CryIAb (encoding for the delta-endotoxin insecticidal protein) in water limiting conditions. In all the experiments the CryIAb transcript was not influenced by water stress, but expressed at a constant level. This suggests that though a different pattern of sensitivity to stress, the transgenic variety maintains the same expression level for the transgene.

Publication Title

Comparison of drought stress response and gene expression between a GM maize variety and a near-isogenic non-GM variety.

Sample Metadata Fields

Specimen part

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accession-icon SRP095021
Requirements for different Tcf1 isoforms in T cell development
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Comparison of transcriptome between control, Tcf1 long isoform (p45)-deficient, complete Tcf1-deficient DN3 thymoctyes Overall design: lineage-negative, CD4-, CD8-, CD44 low and CD25 high (DN3) thymocytes were sorted from control mice or those are deficient for either Tcf1 long isoforms (p45) or all Tcf1 proteins. Lck-Cre was used to ablate all Tcf1 proteins

Publication Title

Cutting Edge: β-Catenin-Interacting Tcf1 Isoforms Are Essential for Thymocyte Survival but Dispensable for Thymic Maturation Transitions.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE42682
Repression of genes for stimulators of glycolysis
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The overall aim of the present work was to identify MTG16 functions in leukemia cells. Alterations in quantity of the MTG16 co-repressor might affect gene regulation and cell metabolism in malignant cells. Differentiated cells secure energy for cellular homeostasis largely by mitochondrial oxidation. Whereas, mature cells, proliferating tumour cells including leukemia cells depend on glycolysis and mitochondrial respiration may be low even in oxygenrich environments.The same signal transduction pathways that govern cell proliferation give instructions for nutrient uptake and co-regulate metabolic processes. In this manner, the metabolism of tumor cells, and other highly proliferating cells, is adapted to stimulate anabolic glycolysisdriven processes for incorporation of nutrients into nucleotides, amino acids and lipids to synthesize macromolecules required for growth and proliferation.

Publication Title

The transcriptional co-repressor myeloid translocation gene 16 inhibits glycolysis and stimulates mitochondrial respiration.

Sample Metadata Fields

Specimen part

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accession-icon SRP105428
Differential requirements for Tcf1 long isoforms in CD8+ and CD4+ T cell responses to acute viral infection
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Comparison of the transcriptome between control Tfh and Tcf1 long isoform-deficient Tfh cells Overall design: SMARTA CD4+ T cells (control or Tcf1 long isoform deficient) were adoptively transferred into B6.SJL recipient mice and then infected with LCMV-Arm. On day 8 after infection, the splenocytes were isolated, and CD45.2+CD4+CXCR5+PD-1 negative cells were sorted as Tfh cells and used in RNAseq analysis.

Publication Title

Differential Requirements for Tcf1 Long Isoforms in CD8<sup>+</sup> and CD4<sup>+</sup> T Cell Responses to Acute Viral Infection.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP076550
Genome-wide analysis of gene expression in infarcted and non-infarcted left ventricle from NEIL3-deficient mice subjected to myocardial infarction
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Myocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme endonuclease VIII-like 3 (NEIL3) was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 following MI in mice, especially in a fibroblast-enriched cell fraction. Neil3-/- mice showed increased mortality after MI compared to WT, caused by myocardial rupture. Neil3-/- hearts displayed enrichment of mutations in genes involved in mitogenesis of fibroblasts and transcriptome analysis revealed dysregulated fibrosis. Correspondingly, proliferation of vimentin+ and aSMA+ (myo)fibroblasts was increased in Neil3-/- hearts following MI. We propose that NEIL3 operates in genomic regions crucial for regulation of cardiac fibroblast proliferation and thereby controls extracellular matrix modulation after MI. Overall design: RNA from infarcted and non-infarcted LV of WT and Neil3-/- C57BL/6 mice obtained three days after induced myocardial infarction were subjected to RNA sequencing using Illumina Hiseq 2000

Publication Title

NEIL3-Dependent Regulation of Cardiac Fibroblast Proliferation Prevents Myocardial Rupture.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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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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