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accession-icon GSE60179
Role of Ror2 in primordial germ cell migration
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Primordial germ cells (PGCs), the embryonic precursors of eggs and sperm, are a unique model for identifying and studying regulatory mechanisms in singly migrating cells. From their time of specification to eventual colonization of the gonad, mouse PGCs traverse through and interact with many different cell types, including epithelial cells and mesenchymal tissues. Work in drosophila and zebrafish have identified many genes and signaling pathways involved in PGC migration, but little is known about this process in mammals.

Publication Title

Discrete somatic niches coordinate proliferation and migration of primordial germ cells via Wnt signaling.

Sample Metadata Fields

Specimen part

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accession-icon GSE16590
Ascorbate effect on serum free cultured hESC
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Ascorbate activates CD30 expression and causes widespread specific demethylation of the epigenome of serum free cultured hESC.

Publication Title

Vitamin C promotes widespread yet specific DNA demethylation of the epigenome in human embryonic stem cells.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE38571
Integrated transcriptomic and epigenomic analysis of primary human lung cell differentiation
  • organism-icon Homo sapiens, Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina ratRef-12 v1.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrated transcriptomic and epigenomic analysis of primary human lung epithelial cell differentiation.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE38570
Integrated transcriptomic and epigenomic analysis of primary human lung cell differentiation (Rat)
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Analysis of gene expression during differentiation of alveolar epithelial type 2 (AT2) cells into AT1 cells. Timepoints taken at Day 0 (AT2 cell), Days 2, 4, and 6 in culture (differentiating) and Day 8 in culture (AT1-like cells).

Publication Title

Integrated transcriptomic and epigenomic analysis of primary human lung epithelial cell differentiation.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE46403
Vitamin C induces Tet-dependent DNA demethylation in ES cells to promote a blastocyst-like methylome
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE46319
Vitamin C induces Tet-dependent DNA demethylation in ES cells to promote a blastocyst-like methylome [Affymetrix]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

DNA methylation is a heritable epigenetic modification involved in gene silencing, imprinting, and the suppression of retrotransposons. Global DNA demethylation occurs in the early embryo and the germline and may be mediated by Tet (ten-eleven-translocation) enzymes, which convert 5-methylcytosine (mC) to 5-hydroxymethylcytosine (hmC). Tet enzymes have been extensively studied in mouse embryonic stem (ES) cells, which are generally cultured in the absence of Vitamin C, a potential co-factor for Fe(II) 2-oxoglutarate dioxygenase enzymes like Tets. Here we report that addition of Vitamin C to ES cells promotes Tet activity leading to a rapid and global increase in hmC. This is followed by DNA demethylation of numerous gene promoters and up-regulation of demethylated germline genes. Tet1 binding is enriched near the transcription start site (TSS) of genes affected by Vitamin C treatment. Importantly, Vitamin C, but not other antioxidants, enhances the activity of recombinant human Tet1 in a biochemical assay and the Vitamin C-induced changes in hmC and mC are entirely suppressed in Tet1/2 double knockout (Tet DKO) ES cells. Vitamin C has the strongest effects on regions that gain methylation in cultured ES cells compared to blastocysts and in vivo are methylated only after implantation. In contrast, imprinted regions and intracisternal A-particle (IAP) elements, which are resistant to demethylation in the early embryo, are resistant to Vitamin C-induced DNA demethylation. Collectively, this study establishes that Vitamin C is a direct regulator of Tet activity and DNA methylation fidelity in ES cells.

Publication Title

Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE32867
DNA methylation and gene expression in lung adenocarcinoma
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-scale analysis of DNA methylation in lung adenocarcinoma and integration with mRNA expression.

Sample Metadata Fields

Sex, Age, Specimen part, Race, Subject

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accession-icon GSE32863
Gene expression analysis of lung adenocarcinoma and matched adjacent non-tumor lung tissue
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Gene expression profiling of 60 lung adenocarcinoma tumors and their matched histologically normal adjacent lung tissue samples were analyzed using Illumina HumanWG-6 v3.0 expression beadchip. We integrated these data with DNA methylation profiles of the same samples to identify potential DNA methylation regulated genes.

Publication Title

Genome-scale analysis of DNA methylation in lung adenocarcinoma and integration with mRNA expression.

Sample Metadata Fields

Sex, Age, Specimen part, Race, Subject

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accession-icon SRP055932
Cross-species transcriptome profiling identifies new alveolar epithelial type I cell-specific genes
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Diseases involving the distal lung alveolar epithelium include chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung adenocarcinoma. Accurate labeling of specific cell types is critical for determining the contribution of each to pathogenesis of these diseases. The distal lung alveolar epithelium is comprised of two cell types, alveolar epithelial type 1 (AT1) and type 2 (AT2) cells. While cell type-specific markers, most prominently surfactant protein C (SFTPC), have allowed detailed studies of AT2 cell differentiation and their roles in disease, studies of AT1 cells have been hampered by lack of genes with expression unique to AT1 cells. To address this, we performed genome-wide expression profiling of multiple rat organs alongside purified rat AT2, AT1 and in vitro differentiated AT1-like cells, resulting in identification of 54 candidate AT1 cell markers. Cross-referencing with genes upregulated in human in vitro differentiated AT1-like cells narrowed the potential list to 18 candidate genes. Testing the top four candidate genes at RNA and protein levels revealed GRAM domain 2 (GRAMD2), a protein of unknown function, as unique to AT1 cells, while SCNN1G within lung is restricted to AT1 cells. RNAseq confirmed that GRAMD2 is transcriptionally silent in human AT2 cells. Immunofluorescence of mouse alveoli verified that GRAMD2 expression is restricted to the plasma membrane of AT1 cells. These new AT1 cell-specific genes, with GRAMD2 as a leading candidate, will enhance AT1 cell isolation, investigation of alveolar epithelial cell differentiation potential, and contribution of AT1 cells to distal lung diseases. Overall design: RNAseq of purified primary human alveolar epithelial type 2 (AT2) and in vitro differentiated type 1 (AT1-like) cells.

Publication Title

Cross-Species Transcriptome Profiling Identifies New Alveolar Epithelial Type I Cell-Specific Genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE25070
Gene expression analysis of colorectal tumors and matched adjacent non-tumor colorectal tissues.
  • organism-icon Homo sapiens
  • sample-icon 52 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

We performed gene expression profiling of 26 colorectal tumors and matched histologically normal adjacent colonic tissue samples using the Illumina Ref-8 whole-genome expression BeadChip. We performed an integrated analysis of promoter DNA methylation and gene expression data to investigate the effects of DNA hypermethylation on gene expression.

Publication Title

Genome-scale analysis of aberrant DNA methylation in colorectal cancer.

Sample Metadata Fields

Sex, Disease, 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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