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accession-icon GSE97627
Comparative cardiac induction time-courses using WT, EOMES KO, and EOMES TET-ON human ES cells
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This study compares cardiac induction time-courses using (i) wild-type hESCs subjected to a standard directed differentiation protocol, (ii) EOMES knockout hESCs subjected to the same protocol, and (iii) EOMES KO / TET-ON hESCs subjected to a TET-ON protocol.

Publication Title

Cardiogenic programming of human pluripotent stem cells by dose-controlled activation of EOMES.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE97625
Analysis of immediate-early induced target genes of the BMP and WNT pathways in human ES cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Human ES cells respond to activation of the BMP and WNT signaling by upregulating target genes. A 4h time-point following signaling factor stimulation was chosen to reveal immediate-early induced genes which are likely to be direct targets.

Publication Title

Cardiogenic programming of human pluripotent stem cells by dose-controlled activation of EOMES.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon SRP098622
Control of plant cell fate transitions by transcriptional and hormonal signals [RNA-seq: mock_vs_dex_14h]
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Plant meristems carry pools of continuously active stem cells, whose activity is controlled by developmental and environmental signals. After stem cell division, daughter cells that exit the stem cell domain acquire transit amplifying cell identity before they are incorporated into organs and differentiate. In this study, we used an integrated approach to elucidate the role of HECATE (HEC) genes in regulating developmental trajectories of shoot stem cells in Arabidopsis thaliana. Our work reveals that HEC function stabilizes cell fate in distinct zones of the shoot meristem thereby controlling the spatio-temporal dynamics of stem cell differentiation. Importantly, this activity is concomitant with the local modulation of cellular responses to cytokinin and auxin, two key phytohormones regulating cell behaviour. Mechanistically, we show that HEC factors directly modulate auxin signal transduction by physical interaction with MONOPTEROS (MP), a key regulator of auxin signalling, and thus interfere with the autocatalytic stabilization of auxin signalling. Overall design: p16:HEC1-linker-GR;inflorescence meristems; 14hours; mock1,mock2,mock3,dex1,dex2,dex3

Publication Title

Control of plant cell fate transitions by transcriptional and hormonal signals.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon SRP119825
The vertebrate protein Dead end maintains primordial germ cell fate by inhibiting somatic differentiation
  • organism-icon Danio rerio
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Maintaining cell fate relies on robust mechanisms that prevent the differentiation of specified cells into other cell types. This is especially critical during embryogenesis, when extensive cell proliferation, patterning and migration events take place. Here we show that vertebrate primordial germ cells (PGCs) are protected from reprogramming into other cell types by the RNA-binding protein Dead end (Dnd). PGCs knocked down for Dnd lose their characteristic morphology and adopt that of various somatic cell types. Concomitantly, they gain a gene expression profile reflecting differentiation into cells of different germ layers, in a process that we could direct by expression of specific cell-fate determinants. Importantly, we visualized these events within live zebrafish embryos, which provide temporal information regarding cell reprogramming. Our results shed light on the mechanisms controlling germ cell fate maintenance and are relevant for the formation of teratoma, a tumor class composed of cells from more than one germ layer. Overall design: Transcriptome profiling of 13hpf sorted germ cells of zebrafish embryos injected with either control or dead end Morpholino

Publication Title

The Vertebrate Protein Dead End Maintains Primordial Germ Cell Fate by Inhibiting Somatic Differentiation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE83129
RNA profiling in metastatic colorectal cancer patients treated first-line with oxaliplatin
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major medical problem, and predictive markers are urgently needed. Recently, miR-625-3p was reported as a promising predictive marker. Here, we have used in vitro models to show that miR-625-3p functionally induces oxPt resistance in CRC cells, and have identified signalling networks affected by miR-625-3p. The p38 MAPK activator MAP2K6 was shown to be a direct target of miR-625-3p, and, accordingly, was downregulated in patients not responding to oxPt therapy. miR-625-3p resistance could be reversed in CRC cells by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. In addition, by reducing p38 MAPK signalling using either siRNA technology, chemical inhibitors to p38 or by ectopic expression of dominant negative MAP2K6 protein we induced resistance to oxPt. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signalling as one likely mechanism a possible driving force behind of oxPt resistance. Our study shows that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks, and corroborates the predictive power of miR-625-3p

Publication Title

miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signalling in human colorectal adenocarcinoma cells.

Sample Metadata Fields

Subject

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accession-icon GSE39491
GLOBAL CHANGES IN GENE EXPRESSION OF BARRETT'S ESOPHAGUS COMPARED TO NORMAL SQUAMOUS ESOPHAGUS AND GASTRIC CARDIA TISSUES
  • organism-icon Homo sapiens
  • sample-icon 117 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Barretts esophagus (BE) is a metaplastic precursor lesion of esophageal adenocarcinoma (EA), the most rapidly increasing cancer in western societies. While the prevalence of BE is increasing, the vast majority of EA occurs in patients with undiagnosed BE. Thus, we sought to identify genes that are altered in BE compared to the normal mucosa of the esophagus, and which may be potential biomarkers for the development or diagnosis of BE.

Publication Title

Global changes in gene expression of Barrett's esophagus compared to normal squamous esophagus and gastric cardia tissues.

Sample Metadata Fields

Specimen part

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accession-icon GSE154028
High fat diet inhibits EV-Mediated angiogenisis
  • organism-icon Sus scrofa
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Porcine Gene 1.0 ST Array (porgene10st)

Description

Mesenchymal stem cell-derived extracellular vesicles (EVs) have been shown to promote angiogenesis in the ischemic myocardium. This study examines the difference in vascular density, myocardial perfusion, molecular signaling, and gene expression between normal diet (ND) and high fat diet (HFD) groups at baseline and following intra-myocardial injection of EVs

Publication Title

Effects of High Fat Versus Normal Diet on Extracellular Vesicle-Induced Angiogenesis in a Swine Model of Chronic Myocardial Ischemia.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE100211
Expression data from primary hepatocytes from mouse
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Retinol Saturase (RetSat) is an oxidoreductase expressed at high levels in the hepatocyte fraction of liver.

Publication Title

Retinol saturase coordinates liver metabolism by regulating ChREBP activity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26020
Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE26019
Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuGene-1_0-st]
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This is one of expressional parts of the study. These data were correlated to epigenetic marks and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively.

Publication Title

Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks.

Sample Metadata Fields

Specimen part, Cell line

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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