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accession-icon GSE64395
Genome-wide mapping of DNA hydroxymethylation in osteoarthritic chondrocytes
  • 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

Genome-wide mapping of DNA hydroxymethylation in osteoarthritic chondrocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP041599
Detained introns are novel, widespread class of posttranscriptionally-spliced introns
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer II

Description

Removal of introns by pre-mRNA splicing is a critical and in some cases rate-limiting step in mammalian gene expression. Deep sequencing of mouse embryonic stem cell RNA revealed many specific internal introns that are significantly more abundant than the other introns within poly(A) selected transcripts; we classify these as “detained” introns (DIs). We identified thousands of DIs flanking both constitutive and alternatively spliced exons in human and mouse cell lines. Drug inhibition of Clk SR-protein kinase activity triggered rapid splicing changes in a specific set of DIs, about half of which showed increased splicing and half increased intron detention, altering the transcript pool of over 300 genes. These data suggest a widespread mechanism by which a nuclear detained pool of mostly processed pre-mRNAs can be rapidly mobilized in response to stress or homeostatic autoregulation. Overall design: v6.5 mouse embryonic stem cells were untreated, treated with the Clk kinase inhibitor KH-CB19, or treated with DMSO as a negative control. Untreated cells were harvested and a single replicate was sequenced using a custom, ligation-based, stranded library preparation protocol. Treated cells were harvested at time 0 and at 2 hours post-treatment, and poly(A)-selected RNA-seq libraries were made from biological duplicates for each treatment/time, barcoded, and sequenced by strand-specific, paired-end sequencing using the Illumina TruSeq kit.

Publication Title

Detained introns are a novel, widespread class of post-transcriptionally spliced introns.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE64394
Genome-wide mapping of DNA hydroxymethylation in osteoarthritic chondrocytes [expression]
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Examination of the genome-wide distribution of 5hmC in osteoarthritic chondrocytes compared to normal chondrocytes in order to elucidate the effect on OA-specific gene expression.

Publication Title

Genome-wide mapping of DNA hydroxymethylation in osteoarthritic chondrocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP077998
Next Generation Sequencing Facilitates Quantitative Analysis of Human Primary and Pluripotent Stem Cell-Derived Epicardial Cell Transcriptomes
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Next-generation sequencing (NGS) has significantly advanced the elucidation of developmental signaling mechanisms that are important for different cell lineage formation from human pluripotent stem cells (hPSCs). We report here the application of RNA-sequencing technology for transcriptome profile of human primary and hPSC-derived epicardial cell, and compare to those of other cell lineages including hPSCs, mesoderm, cardiomcyotyes. Eight epicaridal cell samples from four different hPSC lines and four different donors were performed in IIIumina HiSeq2500. The resulting sequence reads (about 20 million reads per sample) were mapped to human genome (hg19) using HISAT, and the RefSeq transcript levels (RPKMs) were quantified using the python script rpkmforgenes.py. Our RNA-seq data confirmed the stable expression of key epicardial cell markers including WT1, TBX18, TCF21, ALDH1A2 and ZO1, and the gene set enrichment analysis (GSEA) showed enrichment in extracellular matrix related pathways and keratinocyte (epithelial) differentiation. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to epicardial function. This study represents the first detailed analysis of epicardial transcriptomes generated by RNA-seq technology, providing insight into the mechanisms underlying the differentiation of hPSCs into epicardial cells. Overall design: Epicardial transcriptome profiles of 8 different samples from 4 hPSC lines and donors were generated by RNA-seq technology using IIIumina HiSeq2500

Publication Title

Long-term self-renewing human epicardial cells generated from pluripotent stem cells under defined xeno-free conditions.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP062223
The Polycomb protein BMI1 induces an invasive gene expression signature in melanoma that promotes metastasis and chemoresistance.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The epigenetic regulator BMI1 is upregulated in many human malignancies and has been implicated in cell migration, but the impact on autochthonous tumor progression is unexplored. Our analyses of human expression data show that BMI1 levels increase with progression in melanoma. We find that BMI1 expression in melanoma cells does not influence cell proliferation or primary tumor growth. In contrast, BMI1 levels are a key determinant of melanoma metastasis, whereby deletion impairs and overexpression enhances dissemination. Remarkably, BMI1’s pro-metastatic effect reflects enhancement of all stages of the metastatic cascade including invasion, migration, extravasation, adhesion and survival. Additionally, downregulation or upregulation of BMI1 induces sensitivity or resistance to BRAF inhibitor. Consistent with these pleiotropic effects, we find that BMI1 promotes widespread gene expression changes that encompass key hallmarks of the melanoma invasive signature, including activation of TGFß, non-canonical Wnt, EMT and EGF/PDGF pathways. Importantly, for both primary and metastatic melanoma samples, this BMI1-induced signature identifies invasive subclasses of human melanoma and predicts poor patient outcome. Our data yield key insights into melanoma biology and establish BMI1 as a compelling drug target whose inhibition would suppress both metastasis and chemoresistance. Overall design: Three replicates of A375 BMI1 or GFP overexpressing cells.

Publication Title

BMI1 induces an invasive signature in melanoma that promotes metastasis and chemoresistance.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE64200
Stable 5-Hydroxymethylcytosine (5hmC) Acquisition Marks Gene Activation During Chondrogenic Differentiation.
  • organism-icon Mus musculus
  • sample-icon 4 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

Stable 5-Hydroxymethylcytosine (5hmC) Acquisition Marks Gene Activation During Chondrogenic Differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE64141
Stable 5-Hydroxymethylcytosine (5hmC) Acquisition Marks Gene Activation During Chondrogenic Differentiation [array]
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Regulation of chondrogenic differentiation by DNA demethylation is little understood. The ten-eleven-translocation (TET) proteins oxidize methylated cytosines (5mC) to 5hmC, 5fC and 5caC eventually leading to DNA demethylation. However, 5hmC is stable and can potentially act as an epigenetic mark as well. In this study, we report that global changes in 5hmC mark chondrogenic differentiation.

Publication Title

Stable 5-Hydroxymethylcytosine (5hmC) Acquisition Marks Gene Activation During Chondrogenic Differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE56612
Genetic deletion or pharmacologic blockade of the amino acid transporter Slc6a14 in mice suppresses breast cancer induced by Polyoma middle T oncogene
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Tumor cells have an increased need for amino acids. Mammalian cells cannot synthesize essential amino acids; they must obtain these amino acids via specific transporters. Glutamine, though a non-essential amino acid, is critical for tumor cells (glutamine addiction). Entry of amino acids into tumor cells is enhanced by upregulation of specific transporters. If the transporters that are specifically induced in tumor cells are identified, blockade of the induced transporters would constitute a logical strategy for cancer treatment.

Publication Title

Deletion of the amino acid transporter Slc6a14 suppresses tumour growth in spontaneous mouse models of breast cancer.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP004448
Genome-wide identification of Ago2 binding sites from mouse embryonic stem cells with and without mature microRNAs
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

MicroRNAs (miRNAs) are a large family of 19-22nt non-coding RNAs that post-transcriptionally regulate their mRNA targets. Computational algorithms predict that over half of all genes are regulated by miRNAs, yet approaches for experimental identification of miRNA binding sites are now emerging. To directly identify endogenous miRNA binding sites, we performed photo-crosslinking immunoprecipitation using antibodies against Ago2, followed by deep-sequencing of RNA tags (CLIP-seq) in mouse embryonic stem cells (mESCs). We also performed parallel CLIP-seq in Dicer null mESCs that lack mature miRNAs, allowing us to define whether the association of Ago2 with the identified sites was mediated by miRNAs. We include the exon-array expression data obtained from three sets of Dicer WT and Dicer Null mESCs.These data are used to determine genes that are differentially expressed between Dicer WT and Dicer Null conditions. Overall design: Six samples (3 Dicer wild-type CLIP RNA libraries representing two biological replicates, 2 Dicer null CLIP RNA libraries, 1 short-RNA library from Dicer wild-type mESCs) were analyzed. Six total mESC samples were analyzed (3 Dicer WT, 3 Dicer Null). Expression values for probesets were summarized into a single per-gene value. The log fold change for Dicer_WT/Dicer_Null was defined as the difference between the mean expression in Dicer WT mESCs and the mean expression in the Dicer Null mESCs.

Publication Title

Genome-wide identification of Ago2 binding sites from mouse embryonic stem cells with and without mature microRNAs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041414
Dicer knockout NSCLC RNAseq and miRseq
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Dicer knockout NSCLC mRNAseq profiles the transcriptome, Dicer knockout NSCLC miRseq profiles the miRnome Overall design: DicerHet and DicerKO NSCLC, 2 biological reps each genotype for mRNAseq, 1 biological rep each for miRseq

Publication Title

Global microRNA depletion suppresses tumor angiogenesis.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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