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accession-icon SRP008223
Neuronal activity regulates hippocampal miRNA expression
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Small RNA fractions from 6-8 week old C57BL/6 mouse hippocampus following electroconvulsive shock (ECS) Overall design: Size selected RNA clones using Illumina v1.0 DGE small RNA kit, sequenced using Illumina

Publication Title

Neuronal activity regulates hippocampal miRNA expression.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE18334
Profiling oxidative stress in Saccharomyces cerevisiae by oxidation of transcription factor Swi6p
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Cell cycle sensing of oxidative stress in Saccharomyces cerevisiae by oxidation of a specific cysteine residue in the transcription factor Swi6p.

Publication Title

Cell cycle sensing of oxidative stress in Saccharomyces cerevisiae by oxidation of a specific cysteine residue in the transcription factor Swi6p.

Sample Metadata Fields

Treatment

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accession-icon GSE31666
Identification of a molecular network of DNA damage-induced neural cell death
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

DNA damage plays a major role in neural cell death by necrosis and/or apoptosis. However, our understanding of the molecular mechanisms of neural cell death remains still incomplete. To acquire a global understanding of the various mediators related to DNA damage-induced neural cell death pathways, we performed a whole genomic wide screen in neural stem cells by using a siRNA library. We identified 80 genes required for DNA damage-induced cell death. 14 genes (17.5%) are directly related to cell death and/or apoptosis. 66 genes have not been previously directly linked to DNA damage-induced cell death. Using an integrated approach with functional and bioinformatics analysis, we have uncovered a molecular network containing several partially overlapping and interconnected pathways and/or protein complexes that are required for DNA damage-induced neural cell death. The identification of the network of neural cell death mediators will greatly enhance our understanding of the molecular mechanisms of neural cell death and provide therapeutic targets for nervous system disorders.

Publication Title

High-Content Genome-Wide RNAi Screen Reveals <i>CCR3</i> as a Key Mediator of Neuronal Cell Death.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE16855
Expression data from OBGF400 cell line (porcine olfactory bulb neuroblast origin)
  • organism-icon Sus scrofa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

The phenotypically characterized hTERT immortalized porcine olfactory bulb neuroblast cell line (OBGF400) was subjected to an extensive whole genome-scaled expression profile for establishing their use as an in vitro neuronal disease model system.

Publication Title

Transcriptome profile and cytogenetic analysis of immortalized neuronally restricted progenitor cells derived from the porcine olfactory bulb.

Sample Metadata Fields

Cell line

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accession-icon SRP070946
Transcriptome of liver tissue in 5 week old Stabilin-1 knock-out mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Stabilin-1/CLEVER-1 is a multidomain protein present in lymphatic and vascular endothelial cells and in M2 immunosuppressive macrophages. Stabilin-1 functions in scavenging, endocytosis and leukocyte adhesion to and transmigration through the endothelial cells. Overall design: The transcriptome of liver tissue in 5wk old Stab1 knock-out mice was compared to that of corresponding wild type mice

Publication Title

Stabilin-1 expression defines a subset of macrophages that mediate tissue homeostasis and prevent fibrosis in chronic liver injury.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE58252
Expression data from breast cancer cell line MCF-7 with ectopic expression of the transcription factor Snail
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transcription factor Snail has been proposed to mediate epithelial-to-mesenchymal transition (EMT) and confer mesenchymal invasive phenotype to epithelial cancer cells

Publication Title

SNAIL-induced epithelial-to-mesenchymal transition produces concerted biophysical changes from altered cytoskeletal gene expression.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE63683
iBET resistance
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

BET inhibitor resistance emerges from leukaemia stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE63575
Genome wide expression analysis of BET inhibitor resistance
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. Using primary murine stem and progenitor cells immortalised with MLL-AF9, we have used an innovative approach to generate 20 cell lines derived from single cell clones demonstrating stable resistance, in vitro and in vivo, to the prototypical BET inhibitor, I-BET. Resistance to I-BET confers cross-resistance to chemically distinct BET inhibitors such as JQ1, as well as resistance to genetic knockdown of BET proteins. Resistance is not mediated through increased drug efflux or metabolism but is demonstrated to emerge from leukaemia stem cells (LSC). Resistant clones display a leukaemic granulocyte-macrophage progenitor (L-GMP) phenotype (Lin-, Sca-, cKit+, CD34+, FcRII/RIII+) and functionally exhibit increased clonogenic capacity in vitro and markedly shorter leukaemia latency in vivo. Chromatin bound BRD4 is globally reduced in resistant cells, however expression of key target genes such as MYC remains unaltered, highlighting the existence of alternative mechanisms to regulate transcription. We demonstrate that resistance to BET inhibitors is in part a consequence of increased Wnt/-catenin signaling. Negative regulation of this pathway results in differentiation of resistant cells into mature leukaemic blasts, inhibition of MYC expression and restoration of sensitivity to I-BET in vitro and in vivo. Finally, we show that the sensitivity of primary human AML cells to I-BET correlates with the baseline expression of Wnt/-catenin target genes. Together these findings provide novel insights into the biology of AML, highlight the potential therapeutic limitations of BET inhibitors and identify strategies that may overcome resistance and enhance the clinical utility of these unique targeted therapies.

Publication Title

BET inhibitor resistance emerges from leukaemia stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP075272
Splicing towards noncoding isoforms in colorectal carcinoma is associated with tumor hypoxia and the DNA damage response
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Tumor hypoxia is associated with poor patient outcome and resistance to therapy. It is associated with a rapid decline in protein production mediated through mTOR signalling. Here we show that it also leads to widespread changes in splicing and a global shift towards the expression of noncoding isoforms, thus providing a novel and orthogonal mechanism by which cells can modulate protein expression. Overall design: Examination of mRNA levels in HCT116 cells after 0 hr, 1 hr, 2 hr and 24 hr in hypoxia. Three biological replicates each.

Publication Title

Hypoxia-driven splicing into noncoding isoforms regulates the DNA damage response.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject, Time

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accession-icon GSE62204
Transcription in wounded rat vocal folds and vocal fold fibroblasts
  • organism-icon Rattus norvegicus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

We used microarrays to characterize transcriptome profiles of rat vocal fold tissue following surgical injury (vs. naive tissue); rat vocal fold fibroblasts harvested from scar tissue at the 60 d time point (vs. naive fibroblasts); rat vocal fold scar fibroblasts treated with siRNA against the collagen chaperone protein rat gp46 (vs. scramble siRNA).

Publication Title

Microarray-based characterization of differential gene expression during vocal fold wound healing in rats.

Sample Metadata Fields

Specimen part, Treatment

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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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