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accession-icon SRP131393
Gata4-dependent differentiation of c-Kit+ derived endothelial cells underlies deceptive cardiomyocyte regeneration in the heart
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Overall goal: To elucidate the endothelial-specific role of Gata4 signaling in endothelial maturation and vascular maintenance. Purpose of analysis: To generate a transcriptional profile of Gata4-deficient endothelial cells in the adult myocardium under homeostatic conditions. Overall design: Experimental structure: Transcriptional profile generated using RNAseq and differential gene expression analyses of endothelial cells lacking Gata4 isolated from healthy hearts.

Publication Title

Gata4-Dependent Differentiation of c-Kit<sup>+</sup>-Derived Endothelial Cells Underlies Artefactual Cardiomyocyte Regeneration in the Heart.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP076540
Genetic lineage tracing defines myofibroblast origin and function in the injured heart
  • organism-icon Mus musculus
  • sample-icon 185 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Cardiac fibroblasts convert to myofibroblasts with injury to mediate healing after acute myocardial infarction and to mediate long-standing fibrosis with chronic disease. Myofibroblasts remain a poorly defined cell-type in terms of their origins and functional effects in vivo. Methods: Here we generate Postn (periostin) gene-targeted mice containing a tamoxifen inducible Cre for cellular lineage tracing analysis. This Postn allele identifies essentially all myofibroblasts within the heart and multiple other tissues. Results: Lineage tracing with 4 additional Cre-expressing mouse lines shows that periostin-expressing myofibroblasts in the heart derive from tissue-resident fibroblasts of the Tcf21 lineage, but not endothelial, immune/myeloid or smooth muscle cells. Deletion of periostin+ myofibroblasts reduces collagen production and scar formation after myocardial infarction. Periostin-traced myofibroblasts also revert back to a less activated state upon injury resolution. Conclusions: Our results define the myofibroblast as a periostin-expressing cell-type necessary for adaptive healing and fibrosis in the heart, which arises from Tcf21+ tissue-resident fibroblasts. Overall design: Fluidigm C1 whole genome transcriptome analysis of lineage mapped cardiac myofibroblasts

Publication Title

Genetic lineage tracing defines myofibroblast origin and function in the injured heart.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE21446
Identification of genes controlled by LMX1B in the developing limb, embryonic day (E) 13.5
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A control vs. genetic knockout experiment aimed at determining what RNAs are upregulated or downregulated in E13.5 mouse limb tissue lacking the Lmx1b gene. Because LMX1B is required for dorsal-ventral patterning of the limb, this screen gives insight into what putative downstream targets of Lmx1b contribute to dorsal-ventral patterning.

Publication Title

Identification of genes controlled by LMX1B in E13.5 mouse limbs.

Sample Metadata Fields

Specimen part

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accession-icon GSE10516
Identification of genes controlled by LMX1B in the developing mouse hindlimb bud
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

A control vs. genetic knockout experiment aimed at determining what RNAs are upregulated or downregulated in e11.5 mouse proximal limb tissue lacking the Lmx1b gene. Because Lmx1b is required for dorsal-ventral patterning of the limb, this screen gives insight into what putative downstream targets of Lmx1b contribute to dorsal-ventral patterning.

Publication Title

Identification of genes controlled by LMX1B in the developing mouse limb bud.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE33228
Expression profiling of wild-type and set3D fission yeast strains
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

In fission yeast the SET domain protein, Set3p is required for the reliable execution of cytokinesis.

Publication Title

The SET domain protein, Set3p, promotes the reliable execution of cytokinesis in Schizosaccharomyces pombe.

Sample Metadata Fields

Treatment

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accession-icon GSE21156
Expression data from rostral forebrains of wild-type and Fezf1-/- Fezf2-/- mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Zinc-finger genes Fezf1 and Fezf2 encode transcriptional repressors. Fezf1 and Fezf2 are expressed in the early neural stem/progenitor cells and control neuronal differentiation in mouse dorsal telencephalon.

Publication Title

Zinc finger genes Fezf1 and Fezf2 control neuronal differentiation by repressing Hes5 expression in the forebrain.

Sample Metadata Fields

Specimen part

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accession-icon GSE19935
Identifying genetic loci and spleen gene coexpression networks driving immunophenotypes in the BXD panel
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

The immune system plays a pivotal role in susceptibility to and progression of a variety of diseases. Due to its strong genetic basis, heritable differences in immune function may contribute to differential disease susceptibility between individuals. Genetic reference populations, such as the BXD (C57BL/6J X DBA/2J) panel of recombinant inbred (RI) mouse strains, provide a unique model through which to integrate baseline phenotypes in healthy individuals with heritable risk for disease because of the ability to combine data collected from these populations across multiple studies and time. We performed basic immunophenotyping (e.g. percentage of circulating B and T lymphocytes and CD4+ and CD8+ T cell subpopulations) in peripheral blood of healthy mice from 41 BXD RI strains to define the phenotypic variation in this model system and to characterize the genetic architecture that unlerlies these traits. Significant QTL models that explained the majority (50-77%) of phenotypic variance were derived for each trait and for the T:B cell and CD4+:CD8+ ratios. Combining QTL mapping with spleen gene expression data uncovered two quantitative trait transcripts (QTTs), Ptprk and Acp1, that which are candidates for heritable differences in the relative abundance of helper and cytotoxic T cells. These data will be valuable in extracting genetic correlates of the immune system in the BXD panel. In addition, they will be a useful resource in prospective, phenotype-driven model selection to test hypotheses about differential disease or environmental susceptibility between individuals with baseline differences in the composition of the immune system.

Publication Title

Identifying genetic loci and spleen gene coexpression networks underlying immunophenotypes in BXD recombinant inbred mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP116217
EZH2 is required for gene repression in Plasmablasts
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To understand the role of EZH2 in Plasmablast function EZH2 was inducibly deleted using tamoxifen and B cells stimulated to differentiate with LPS in vivo. After 3 days, CD138+ cells were enriched from the spleens and RNA-seq was performed to identify the genes targeted by EZH2 for repression. Overall design: RNAseq on control or EZH2-deficient murine plasmablasts.

Publication Title

EZH2 Represses the B Cell Transcriptional Program and Regulates Antibody-Secreting Cell Metabolism and Antibody Production.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE17666
Regulatory Role for PC-TP/StarD2 in the Metabolic Response to Peroxisome Proliferator Activated Receptor Alpha (PPAR)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Phosphatidylcholine transfer protein (PC-TP, a.k.a StarD2) is abundantly expressed in liver and is regulated by PPAR. When fed the synthetic PPAR ligand fenofibrate, Pctp-/- mice exhibited altered lipid and glucose homeostasis. Microarray profiling of liver from fenofibrate fed wild type and Pctp-/- mice revealed differential expression of a broad array of metabolic genes, as well as their regulatory transcription factors. Because its expression controlled the transcriptional activities of both PPAR and HNF4 in cell culture, the broader impact of PC-TP on nutrient metabolism is most likely secondary to its role in fatty acid metabolism.

Publication Title

Regulatory role for phosphatidylcholine transfer protein/StarD2 in the metabolic response to peroxisome proliferator activated receptor alpha (PPARalpha).

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP100953
JUN-Mediated downregulation of EGFR signaling is associated with resistance to gefitinib in EGFR-mutant NSCLC cell lines [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Epidermal Growth Factor Receptor (EGFR) regulates a diverse set of biological processes including cell growth, proliferation, and differentiation. Deregulation of the EGFR pathway has been implicated in a variety of human diseases including cancer. Gefitinib and erlotinib are tyrosine kinase inhibitors (TKIs) that have demonstrated clinical benefit for patients with Non-small cell lung cancer (NSCLC) and EGFR activating mutations. However, patients invariably acquire resistance to TKI treatment through a number of mechanisms. We utilized in vitro models of NSCLC with EGFR activating mutations and derived three isogenic cell lines with acquired resistance to gefitinib. We next studied genomewide mRNA expression in resistance and wild type cells and their effect in the reprogramming of pathways in lung cancer cell line models.. Overall design: Differntial expresssion profile of transcripts of parental (HCC827) and EGFR-TKI (HCC827 ZDR3) resistance cells

Publication Title

JUN-Mediated Downregulation of EGFR Signaling Is Associated with Resistance to Gefitinib in EGFR-mutant NSCLC Cell Lines.

Sample Metadata Fields

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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