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accession-icon SRP079184
PRC2 represses transcriptionally competent genes on the inactive X-chromosome
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Polycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which characterizes many silenced genes including those on the inactive X-chromosome. Here we interrogate the role of core PRC2 protein EED in X-linked gene silencing by assessing allele-specific X-linked gene expression in WT and Eed-/- hybrid mouse trophoblast stem cells (TSCs) harboring a 129/S1-derived maternal X-chromosome and a JF1/Ms-derived paternal X-chromosome. This study generates mRNA-seq data for WT and Eed-/- TSCs, which undergo imprinted inactivation of the paternal X-chromosome. RNA-seq data was mapped allele-specifically to in silico strain-specific maternal and paternal reference genomes, generated based on known single nucleotide polymorphisms. We find that EED loss abrogates H3K27me3 and expression of Xist lncRNA, which is required for X-inactivation, however, despite the absence of H3K27me3 and Xist, only a subset of PRC2 target genes are derepressed in Eed-/- TSCs. Overall design: RNA-seq profiles of four WT (Eed +/+ and Eed fl/fl) and three EED null (Eed -/-) female TS cell lines were generated through strand-specific 100 bp paired-end sequencing on the Illumina HiSeq2000

Publication Title

PRC2 represses transcribed genes on the imprinted inactive X chromosome in mice.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE60578
Regulatory logic of the coupled diurnal and feeding cycles in the mouse liver
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This study is a follow-up to GSE35790.

Publication Title

Transcriptional regulatory logic of the diurnal cycle in the mouse liver.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon SRP064790
Transcriptome of ESCs, EpiSCs and reverted ES by MM401 (Mll1 inhibitor) #2
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

This study describes the transcriptome profiling of: 1) mouse ES cells in LIF/KSR medium; 2)EpiSCs in bFGF/serum-free (KSR) medium; 3) EpiSCs treated with MM401/LIF KSR at D3 and D6 (P2); 4) rES reverted form EpiSC by MM401/LIF KSR treatment at P6, P30 with or without MM401 . Overall design: RNA-Seq profiling on mouse pluripotent cells. Biological duplicates of each sample are labled as rep1/2.

Publication Title

MLL1 Inhibition Reprograms Epiblast Stem Cells to Naive Pluripotency.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE12508
Transcription patterns during wheat development
  • organism-icon Triticum aestivum
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

The analysis of gene expression during wheat development:

Publication Title

Comparative transcriptomics in the Triticeae.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP076395
Benomyl toxicity links histone H3 lysine 4 methylation to cell cycle control
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

The PAT-seq approach was utilised to determine the gene expression changes over the cell-cycle of wildtype and delta-set1 yeast strains. The cell were synchronised by alpha-factor arrest and cell-cycle release Overall design: Analysis gene expresson across the S. cerevisiae cell cycle.

Publication Title

Coordination of Cell Cycle Progression and Mitotic Spindle Assembly Involves Histone H3 Lysine 4 Methylation by Set1/COMPASS.

Sample Metadata Fields

Cell line, Subject, Time

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accession-icon GSE140746
Fractionated ionizing radiation evokes diverse patterns of long-term changes in gene expression and tumor-propagating capacity in human glioma stem cells.
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This study addresses long-term effects of clinically relevant regimens of radiation in human glioma stem cells. Our investigations reveal a strikingly diverse spectrum of changes in cell behavior, gene expression patterns and tumor-propagating capacities evoked by radiation in different types of glioma stem cells. Evidence is provided that degree of cellular plasticity but not the propensity to self-renew is an important factor influencing radiation-induced changes in the tumor-propagating capacity of glioma stem cells. Gene expression analyses indicate that paralell transcriptomic responses to radiation underlie similarity of clinically relevant cellular outcomes such as the ability to promote tumor growth after radiation. Our findings underscore the importance of longitudinal characterizations of molecular and cellular responses evoked by cytotoxic treatrments in glioma stem cells.

Publication Title

Diversity of Clinically Relevant Outcomes Resulting from Hypofractionated Radiation in Human Glioma Stem Cells Mirrors Distinct Patterns of Transcriptomic Changes.

Sample Metadata Fields

Treatment

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accession-icon SRP137808
Kinetic analysis of TGFbeta-induced EMT in NMuMG/E9 cells
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To investigate the transcriptional remodelling during EMT, we treated normal murine mammary gland epithelial cells with TGFbeta for 0, 2h, 6h, 12h, 24h, 36h, 48h, 60h, 72h, 96h, 168h and 240h. Using WGCNA and pathway enrichment analysis we identified multiple gene expression modules that were enriched in general, signaling, metabolic or stuctural pathways highly relevant for EMT. Overall design: RNA sequencing of NMuMG/E9 cells induced to undergo EMT by treatment with TGFbeta from 0-10 days.

Publication Title

PyMT-1099, a versatile murine cell model for EMT in breast cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP070670
FOXF1 inhibits endothelial barrier function in the lung and transcriptionally activates the gene for the S1PR1 receptor
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Multiple signaling pathways, structural proteins and transcription factors are involved in regulation of endothelial barrier function. The Forkhead protein FOXF1 is a key transcriptional regulator of lung embryonic development, and we use a conditional knockout approach to examine the role of FOXF1 in adult lung homeostasis and lung injury and repair. Tamoxifen-regulated deletion of both Foxf1 alleles in endothelial cells of adult mice (Pdgfb-iCreER/Foxf1 caused lung inflammation and edema, leading to respiratory insuffency and uniform mortality. Deletion of a single foxf1 allele was sufficient to increase susceptibility of heterozygous mice to acute lung injury. FOXF1 abundance was decreased in pulmonary endothelial cells of human patients with acute lung injury. Gene expression analysis of pulmonary endothelial cells of FOXF1 deletion indicated reduced expression for genes critical for maintance and regulation of adherens junctions. FOXF1 knockdown in vitro and in vivo disrupted adherens junctions, increased lung endothelial permeability, and the abundance of mRNA and protein for sphingosine 1 phosphate receptor 1 (S1PR1), a key regulator of endothelial barrier function. Chromatin immunoprecipitation and luciferase reporter assay demonstrated that FOXF1 directly bound to and induced the tanscriptional activity of the S1pr1 promoter. Pharmacological administratiion of S1P to injured pdgfb-iCreER/Foxf1 mice restored endothelial barrier function, decreased lung edema and improved survival. Thus, FOXF1 promotes normal lung homeostasis and lung repair, at least in part, by enhancing endothelial barrier function through transcriptional activation of the S1P/S1PR1/ signaling pathway. Overall design: RNA was isolated and pooled from the lungs of multiple mice with either the Foxf1 floxed alleles alone or Pdgfb-iCreER Foxf1 floxed mice.

Publication Title

FOXF1 maintains endothelial barrier function and prevents edema after lung injury.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE49248
KrasG12D partially compensates for the loss of beta-catenin in MLL-AF9 AML
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The Wnt/beta-catenin pathway is required for the development of leukemia stem cells in MLL-AF9 AML.

Publication Title

KRas(G12D)-evoked leukemogenesis does not require β-catenin.

Sample Metadata Fields

Specimen part

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accession-icon GSE48991
Myotonic dystrophy type 1 (DM1) leads to altered mRNA expression in heart tissue
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Myotonic dystrophy type 1 (DM1) is a dominantly inherited disease that affects multiple organ systems. Cardiac dysfunction is the second leading cause of death in DM1. We quantified gene expression in heart tissue from a heart-specific DM1 mouse model (EpA960/MCM) which inducibly expresses human DMPK exon 15 containing 960 CUG expanded repeats and that reproduced Celf1 up regulation. To assess if, in addition to splicing and miRNA defects, CUGexp RNA also perturbed the steady state mRNA levels of genes, we carried out a microarray study on wildtype E14, adult, MCM controls and DM1 mouse hearts. As anticipated we noted a large number of genes to be developmentally regulated in wildtype hearts, however, within 72h of induction of CUGexp RNA there appeared to be a coordinate adult-to-embryonic shift in steady state levels of many genes.

Publication Title

The Mef2 transcription network is disrupted in myotonic dystrophy heart tissue, dramatically altering miRNA and mRNA expression.

Sample Metadata Fields

Specimen part, Time

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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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