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accession-icon GSE102958
Comparison of gene expression between high- and low-Sost/sclerostin expressing osteocytes
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Single-cell sorted cells from the osteocytic cell line Ocy454 were screened for high- and low-Sost/sclerostin expression to see changes in other gene expressions related to Sost/sclerostin.

Publication Title

Carbonic anhydrase III protects osteocytes from oxidative stress.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE5301
Expression data from yeast treated with enediynes compared to gamma radiation
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

We are investigating the transcriptional response of yeast to treatment with enediynes or gamma radiation, which generate different extents of double or single strand breaks in DNA.

Publication Title

The DNA-damage signature in Saccharomyces cerevisiae is associated with single-strand breaks in DNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11259
Role of epithelial to mesenchymal transition (EMT) in spontaneous breast cancer metastasis
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Epithelial-mesenchymal transition (EMT) has been linked to cancer progression and metastatic propensity. The 4T1 tumor is a clinically relevant model of spontaneous breast cancer metastasis. Here we characterize 4T1-derived cell lines for EMT, in vitro invasiveness and in vivo metastatic ability. Contrary to expectations, the 67NR cells, which form primary tumors but fail to metastasize, express vimentin and N-cadherin, but not E-cadherin. 4T1 cells, however, express E-cadherin, are highly migratory and invasive, and metastasize to multiple sites. The 66cl4 metastatic cells display mixed epithelial and mesenchymal markers, but are less migratory and invasive than 67NR cells. These findings demonstrate that the metastatic ability of breast cancer cells does not correlate with genotypic and phenotypic properties of EMT per se, and suggest that other processes may govern metastatic capability. Gene expression analysis also has not identified differences in EMT markers, but has identified several candidate genes that may influence metastatic ability.

Publication Title

Epithelial-mesenchymal transition (EMT) is not sufficient for spontaneous murine breast cancer metastasis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP055176
m6A level and isoform characterization sequencing (m6A-LAIC-seq) reveal the census and complexity of the m6A epitranscriptome
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

N6-methyladenosine (m6A) is a widespread reversible chemical modification of RNAs, implicated in many aspects of RNA metabolism. Little quantitative information exists as to either how many transcript copies of particular genes are m6A modified (“m6A levels”), or the relationship of m6A modification(s) to alternative RNA isoforms. To deconvolute the m6A epitranscriptome, we developed m6A level and isoform-characterization sequencing (m6A-LAIC-seq). We found that cells exhibit a broad range of non-stoichiometric m6A levels with cell type specificity. At the level of isoform characterization, we discovered widespread differences in use of tandem alternative polyadenylation (APA) sites by methylated and nonmethylated transcript isoforms of individual genes. Strikingly, there is a strong bias for methylated transcripts to be coupled with proximal APA sites, resulting in shortened 3’ untranslated regions (3’-UTRs), while nonmethylated transcript isoforms tend to use distal APA sites. m6A-LAIC-seq yields a new perspective on transcriptome complexity and links APA usage to m6A modifications. Overall design: m6A-LAIC-seq of H1-ESC and GM12878 cell lines, each cell line has two replicates

Publication Title

m(6)A-LAIC-seq reveals the census and complexity of the m(6)A epitranscriptome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP081219
RNA sequencing of mice fed a high fat/high sucrose diet or a low fat/low sucrose diet
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Publication Title: DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet. It is now well established that an intrauterine environment altered by overnutrition or malnutrition can change gene expression patterns through epigenetic mechanisms that may persist through generations. However, it is less clear if overnutrition alters epigenetic control of gene expression in adults, or if whether such mechanisms contribute to the pathology of obesity. Here we test the hypothesis that exposure to a high fat diet alters hepatic DNA methylation and gene expression patterns, and explore the contribution of such changes to the pathophysiology of overnutrition. RNA-seq and targeted high-throughput bisulfite DNA sequencing were used to undertake a systematic analysis of the hepatic response to a high fat diet. A subset of genes was found whose expression levels were altered in concert with DNA methylation changes. Using chromatin immunoprecipitation of RNA polymerase, we determined that hypermethylation correlated with decreased transcription of two of the genes, Phlda1 and Onecut1. A subnetwork of these genes and their nearest neighbors was generated from an existing Bayesian gene network that contained numerous hepatic regulatory genes involved in lipid and body weight homeostasis. Hepatic-specific depletion of Phlda1 in mice decreased the genes in the subnetwork, and led to increased oil droplet size in standard chow-fed mice, an early indicator of steatosis, validating the contribution of this gene to the phenotype. Overall design: 14 mice fed either a high fat/high sucrose (n=7) or low fat/low sucrose (n=7) diet.

Publication Title

DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP142535
Single-cell transcriptomics confirms heterogeneity of contractile cells in large skin wounds
  • organism-icon Mus musculus
  • sample-icon 364 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report transcriptomes of pre-sorted skin wound dermal cells. Post-wounding day (PWD) 12, 15 and 21 Zombie-neg;tdTomatoHi cells were FACS sorted from Sm22-Cre;TdTomato mice. Overall design: Examination of single cell heteregeneity in large skin wounds on PWD 12, 15 and 21

Publication Title

Single-cell analysis reveals fibroblast heterogeneity and myeloid-derived adipocyte progenitors in murine skin wounds.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP067567
Genome-wide responses to extracellular actin in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report the transcriptional changes in Drosophila after administration of Actin or buffer control Overall design: Examination of transcriptional responses to actin versus buffer injected flies at 3,6 and 24 hours post injection (each time point includes triplicate samples)

Publication Title

Actin is an evolutionarily-conserved damage-associated molecular pattern that signals tissue injury in <i>Drosophila melanogaster</i>.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP033269
m6A RNA modification controls cell fate transition in mammalian embryonic stem cells (RNA methylation)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Here we determine the map of RNA methylation (m6A) in mouse embrionic stem cells, and Mettl3 knock out cells Overall design: Examination of m6A modification sites on the transcriptome of mouse Embryonic stem cells and Embryonic Mettl3 knock out cells, using a m6A specific antibody.

Publication Title

m(6)A RNA modification controls cell fate transition in mammalian embryonic stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20713
Epigenetic portraits of human breast cancers
  • organism-icon Homo sapiens
  • sample-icon 108 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

DNA methylation profiling reveals a predominant immune component in breast cancers.

Sample Metadata Fields

Specimen part, Disease stage, Cell line, Treatment

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accession-icon GSE20711
Epigenetic portraits of human breast cancers (expression data)
  • organism-icon Homo sapiens
  • sample-icon 90 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Breast cancer is a molecularly, biologically and clinically heterogeneous group of disorders. Understanding this diversity is essential to improving diagnosis and optimising treatment. Both genetic and acquired epigenetic abnormalities participate in cancer, but information is scant on the involvement of the epigenome in breast cancer and its contribution to the complexity of the disease. Here we used the Infinium Methylation Platform to profile at single-CpG resolution (over 14,000 genes interrogated) the methylomes of 119 breast tumours. It emerges that many genes whose expression is linked to the ER status are epigenetically controlled (or/ we show that the two major phenotypes of breast cancers determined by ER status are widely involving epigenetic regulatory mechanisms), offering the prospect of a novel approach to treating ER-positive tumours. We have distinguished methylation-profile-based tumour clusters, some coinciding with known expression subtypes but also new entities that may provide a meaningful basis for refining breast tumour typology. We show that methylation patterns may reflect the cellular origins of tumours. Having highlighted an unexpectedly strong epigenetic component in the regulation of key immune pathways, we show that a set of immune genes have high prognostic value in specific tumour categories. By laying the ground for better understanding of breast cancer heterogeneity and improved tumour taxonomy, the precise epigenetic portraits drawn here should contribute to better management of breast cancer patients.

Publication Title

DNA methylation profiling reveals a predominant immune component in breast cancers.

Sample Metadata Fields

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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Developed by the Childhood Cancer Data Lab

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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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