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accession-icon SRP057156
RNA sequencing of cells treated with DMSO or Retinoic acid during cardiac differentiation
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Analysis of transcriptional differences between control and RA-treated cells during cardiac differentiation. The hypothesis tested in these samples is that addition of RA during differentiation towards atrial-like cardiomyocytes while control cells treated with DMSO result in ventricular-like cardiomyocytes. Overall design: NKX2.5 (eGFP/w)-hESCs were differentiated to cardiomyocytes with spin EB protocol, with the addition of RA or DMSO. Cells were sorted at day-31 based on GFP resulting in CTplus, CTminus, RAplus or RAminus goups. RNA was isolated from each of these fractions for sequencing.

Publication Title

KeyGenes, a Tool to Probe Tissue Differentiation Using a Human Fetal Transcriptional Atlas.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10581
Nrf2-related oxidative stress response and impaired dopamine biosynthesis in a PC12 cell model of Huntingtons disease
  • organism-icon Rattus norvegicus
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Huntingtons disease (HD) is a devastating disease for which currently no therapy is available. It is a progressive autosomal dominant neurodegenerative disorder that is caused by a CAG repeat expansion in the HD gene, resulting in an expansion of polyglutamines at the N-terminal end of the encoded protein, designated huntingtin, and the accumulation of cytoplasmic and nuclear aggregates. Not only is there a loss of normal huntingtin function, upon expansion of the CAG repeat there is also a gain of toxic function of the huntingtin protein and this affects a wide range of cellular processes. To identify groups of genes that could play a role in the pathology of Huntingtons disease, we studied mRNA changes in an inducible PC12 model of Huntingtons disease before and after aggregates became visible. This is the first study to show the involvement Nrf2-responsive genes in the oxidative stress response in HD. Oxidative stress related transcripts were altered in expression suggesting a protective response in cells expressing mutant huntingtin at an early stage of cellular pathology. Furthermore, there was a down-regulation of catecholamine biosynthesis resulting in lower dopamine levels in culture. Our results further demonstrate an early impairment of transcription, the cytoskeleton, ion channels and receptors. Given the pathogenic impact of oxidative stress and neuroinflammation, the Nrf2-ARE signaling pathway is an attractive therapeutic target for neurodegenerative diseases.

Publication Title

Mutant huntingtin activates Nrf2-responsive genes and impairs dopamine synthesis in a PC12 model of Huntington's disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE73599
Celiac disease T cell clone response to CD3/CD28 stimulation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To identify the CD4+ T cell cytokines responsible for the proliferation of the Lin-IEL lines CD4+ T cell clone L10, which recognises DQ2-glia-1, one of the immunodominant T cell epitopes in celiac disease, was stimulated for 3 hours in IMDM with plate-bound CD3/CD28-specific (2.5 g/ml each) or control antibodies coated onto 6-well non-tissue culture treated plates. Three independent biological replicates were performed, each time including 6 million Ficoll-purified live cells per condition. RNA was purified from these cells using the RNAeasy mini kit (Qiagen, Venlo, the Netherlands). cDNA was amplified using the Applause WT-Amp system (NuGEN technologies, Bemmel, the Netherlands) and biotin-labelled with the Encore Biotin Module (NuGEN). Human Gene 1.0 ST arrays (Affymetrix, High Wycombe, UK) were employed to quantify global gene expression.

Publication Title

CD4 T-cell cytokines synergize to induce proliferation of malignant and nonmalignant innate intraepithelial lymphocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP128458
Expansion of adult human pancreatic tissue yields organoids harbouring progenitor cells with endocrine differentiation potential
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Gene expression profiles from ALDH high cells sorted from expanded adult human pancreatic organoids are more similar to fetal pancreatic tissue and ALDH high cells sorted from expanded fetal human pancreatic organoids than to adult human islets or adult islet-depleted exocrine tissue. Overall design: RNA was isolated from ALDHhi cells sorted from organoids after 7 days expansion derived from human adult pancreatic tissue, ALDHhi cells sorted from organoids after 7 days expansion derived from human fetal pancreatic tissue, primary fetal pancreatic tissue, adult human islets from different donors and adult exocrine (islet-depleted) pancreatic tissue from different donors.

Publication Title

Expansion of Adult Human Pancreatic Tissue Yields Organoids Harboring Progenitor Cells with Endocrine Differentiation Potential.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE39881
Lgr5+ve stem cells in nephrogenesis
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Multipotent stem cells and their lineage-restricted progeny drive nephron formation within the developing kidney. Validated markers of these early stem/progenitor populations are essential for deciphering their in vivo function and for evaluating their clinical potential for treating adult kidney disease. Here, we document expression of the adult stem cell marker Lgr5 in the developing kidney and assess the stem/progenitor identity of Lgr5+ve cells via in vivo lineage tracing. The appearance and localization of Lgr5+ve cells coincided with that of the S-shaped body around E14. Lgr5 expression remained restricted to cell clusters within developing nephrons in the cortex until P7, when expression was permanently silenced. In vivo lineage tracing identified Lgr5 as a marker of a novel progenitor population within nascent nephrons dedicated to generating the thick ascending limb of Henle's loop and distal convoluted tubule. The Lgr5 surface marker and experimental models described here will be invaluable for deciphering the contribution of early nephron stem cells to developmental defects and for isolating human nephron progenitors as a prerequisite to evaluating their therapeutic potential.

Publication Title

Lgr5(+ve) stem/progenitor cells contribute to nephron formation during kidney development.

Sample Metadata Fields

Specimen part

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accession-icon GSE75676
Identification of Circulating Fibrocytes and Dendritic Derivatives in Corneal Endothelium of Patients with Fuchs' Dystrophy
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of Circulating Fibrocytes and Dendritic Derivatives in Corneal Endothelium of Patients With Fuchs' Dystrophy.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE74123
Identification of Circulating Fibrocytes and Dendritic Derivatives in Corneal Endothelium of Patients with Fuchs' Dystrophy [microarray expression analysis]
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

PURPOSE: Fuchs endothelial corneal dystrophy (FECD) is a degenerative eye disorder affecting 4% of Americans older than 40. It is the leading indication for corneal endothelial (CE) transplantation for which there is a global donor shortage. This study aimed to gain further insight into the pathophysiology of FECD and identify targets for nonsurgical therapy.

Publication Title

Identification of Circulating Fibrocytes and Dendritic Derivatives in Corneal Endothelium of Patients With Fuchs' Dystrophy.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP114373
Profiling proliferative cells and their progeny in damaged murine hearts
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The significance of cardiac stem cell (CSC) populations for cardiac regeneration remains disputed. Here, we apply the most direct definition of stem cell function (the ability to replace lost tissue through cell division) to interrogate the existence of CSCs. By single-cell mRNA sequencing and genetic lineage tracing using two Ki67 knockin mouse models, we map all proliferating cells and their progeny in homoeostatic and regenerating murine hearts. Cycling cardiomyocytes were only robustly observed in the early postnatal growth phase, while cycling cells in homoeostatic and damaged adult myocardium represented various noncardiomyocyte cell types. Proliferative postdamage fibroblasts expressing follistatin-like protein 1 (FSTL1) closely resemble neonatal cardiac fibroblasts and form the fibrotic scar. Genetic deletion of Fstl1 in cardiac fibroblasts results in postdamage cardiac rupture. We find no evidence for the existence of a quiescent CSC population, for transdifferentiation of other cell types toward cardiomyocytes, or for proliferation of significant numbers of cardiomyocytes in response to cardiac injury. Overall design: We generated transciptome data from proliferative cardiac cells collected from 3, 7 or 14 days following myocardial infarction (MI) or sham surgery. This series includes single-cell transcriptome data from (Ki67-RFP+) cardiac cells collected from neonatal murine hearts, adult homeostatic murine hearts or adult murine hearts collected 14 days following myocardial infarction (MI), ischemic/perfusion (I/R) or sham surgery.

Publication Title

Profiling proliferative cells and their progeny in damaged murine hearts.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE6540
Expression data from olfactory epithelium of Lip-C-treated mice compared to Lip-O-treated control mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Microarray analysis of gene expression in the olfactory epithelium of macrophage depleted mice to study the role of macrophages in regulating neurodegeneration, neuroprotection, and neurogenesis of olfactory sensory neurons

Publication Title

Macrophage-mediated neuroprotection and neurogenesis in the olfactory epithelium.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE30472
Gene expression profiles of gliomas in formalin-fixed paraffin-embedded material
  • organism-icon Homo sapiens
  • sample-icon 54 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

In this study we have performed expression analysis using paired FF-FFPE glioma samples. We show that expression data from FFPE glioma material is concordant with expression data from matched FF tissue, and can be used for molecular profiling in gliomas.

Publication Title

Gene expression profiles of gliomas in formalin-fixed paraffin-embedded material.

Sample Metadata Fields

Specimen part, Disease stage

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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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