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accession-icon GSE65399
Epigenetic therapy for Friedreich ataxia.
  • organism-icon Homo sapiens
  • sample-icon 75 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We set out to investigate whether a histone deacetylase inhibitor (HDACi) would be effective in an in vitro model for the neurodegenerative disease Friedreich ataxia (FRDA) and to evaluate safety and surrogate markers of efficacy in a phase I clinical trial in patients. In the neuronal cell model, HDACi 109/RG2833 increases FXN mRNA levels and frataxin protein, with concomitant changes in the epigenetic state of the gene. Chromatin signatures indicate that histone H3 lysine 9 is a key residue for gene silencing through methylation and reactivation through acetylation, mediated by the HDACi. Drug treatment in FRDA patients demonstrated increased FXN mRNA and H3 lysine 9 acetylation in peripheral blood mononuclear cells. No safety issues were encountered.

Publication Title

Epigenetic therapy for Friedreich ataxia.

Sample Metadata Fields

Time

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accession-icon SRP008069
Genomic analyses of the RNA binding protein Hu Antigen R (HuR) identify a complex network of target genes and novel characteristics of its binding sites
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

The ubiquitously expressed RNA-binding protein Hu Antigen R (HuR) or ELAVL1 is implicated in a variety of biological processes as well as being linked with a number of diseases, including cancer. Despite a great deal of prior investigation into HuR, there is still much to learn about its function. We take an important step in this direction by conducting iCLIP (CrossLinking and ImmunoPreciptation) and RNA Sequencing experiments followed by an extensive computational analysis to determine the characteristics of the HuR binding site and impact on the transcriptome. We reveal that HuR targets predominantly uracil-rich single-stranded stretches of varying size, with a strong conservation of structure and sequence composition. Despite the fact that HuR sites are observed in intronic regions, our data does not support a role for HuR in regulating splicing. HuR sites in 3'UTRs overlap extensively with predicted miRNA target sites suggesting interplay between the functions of HuR and miRNAs. Network analysis showed that identified targets containing HuR binding sites in the 3' UTR are highly interconnected.

Publication Title

Genomic analyses of the RNA-binding protein Hu antigen R (HuR) identify a complex network of target genes and novel characteristics of its binding sites.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP022166
WTAP is a novel oncogenic protein in Acute Myeloid Leukemia
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Acute myeloid leukemia (AML) continues to have the lowest survival rates of all leukemias. Therefore, new therapeutic strategies are urgently needed to improve clinical outcomes for AML patients. Here, we report a novel role for Wilms’ tumor 1-associated protein (WTAP) in pathogenesis of AML. We have performed RNA-Seq in K562 cells with knockdown of WTAP to ascertain which genes it regulates. Overall design: We have 2 replicates of total RNA for K562 cells and 2 replicates with WTAP knocked down

Publication Title

WTAP is a novel oncogenic protein in acute myeloid leukemia.

Sample Metadata Fields

Subject

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accession-icon SRP058244
The RNA-binding protein Musashi1 is a central regulator of adhesion pathways in glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

The conserved RNA-binding protein Musashi1 (MSI1) has emerged as a key oncogenic factor in numerous solid tumors, including glioblastoma. However, its mechanism of action has not yet been established comprehensively. We set out to map its impact on the transcriptome in U251 cells using RNA-seq and iCLIP. Overall design: Examination of gene expression and splicing changes upon KD of Musashi1 in U251 cells and link to iCLIP-identified Musashi1 RNA binding sites

Publication Title

RNA-Binding Protein Musashi1 Is a Central Regulator of Adhesion Pathways in Glioblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE64123
Human embryonic stem cell based neuro-developmental toxicity assay: response to valproic acid and carbamazepine exposure
  • organism-icon Homo sapiens
  • sample-icon 90 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Here we studied the effects of anticonvulsant drug exposure in a human embryonic stem cell (hESC) based neuro- developmental toxicity test (hESTn). During neural differentiation the cells were exposed, for either 1 or 7 days, to non-cytotoxic concentration ranges of valproic acid (VPA) or carbamazepine (CBZ), anti-epileptic drugs known to cause neurodevelopmental toxicity.

Publication Title

Gene Expression Regulation and Pathway Analysis After Valproic Acid and Carbamazepine Exposure in a Human Embryonic Stem Cell-Based Neurodevelopmental Toxicity Assay.

Sample Metadata Fields

Time

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accession-icon GSE55618
Toxicogenomic profiling in the whole zebrafish embryo after exposure to reference hepatotoxicants.
  • organism-icon Danio rerio
  • sample-icon 188 Downloadable Samples
  • Technology Badge Icon Affymetrix Genechip Zebrafish ST Genome Array 1.1 (zebgene11st)

Description

Zebrafish embryos have been proposed as an attractive alternative model system for hepatotoxicity testing.

Publication Title

A transcriptomics-based hepatotoxicity comparison between the zebrafish embryo and established human and rodent in vitro and in vivo models using cyclosporine A, amiodarone and acetaminophen.

Sample Metadata Fields

Compound

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accession-icon SRP095625
Generation of muscle stem cells from pluripotent stem cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We have developed a method to generate muscle stem cells from pluripotent stem cells via teratoma formation. The goal of this study is to compare the transcriptome of a7+ VCAM+ myogenic cells derived from pluripotent stem cells versus satellite cells Overall design: RNA from a7+ VCAM+ myogenic cells derived from teratoma, transplanted muscles, E14.5 mouse embryos, and hindlimbs of 8-week-old mice. In 3 biological replicates

Publication Title

Skeletal Muscle Stem Cells from PSC-Derived Teratomas Have Functional Regenerative Capacity.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE18397
Expression profiling of NB4 cells after treatment with ATRA
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

In acute promyelocytic leukemia (APL), differentiation therapy with all-trans retinoic acid (ATRA)

Publication Title

Chemokine induction by all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia: triggering the differentiation syndrome.

Sample Metadata Fields

Specimen part

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accession-icon SRP165285
RNA-Seq of WT and constitutively methylated mESCs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

WT J1 and 3B3L cells (in which Dnmt3B and Dnm3L are constitutively expressed from an exogenous construct) were cultured under both serum/LIF and 2i/LIF conditions. 3B3L cells do not show ground state-associated hypomethylation phenotype. This experiment sought to analyse the gene expression changes between the two conditions. Overall design: Three biological replicates per condition J1 serum, J1 2i, 3B3-3l serum, 3B3-3l 2i.

Publication Title

DNA Methylation Directs Polycomb-Dependent 3D Genome Re-organization in Naive Pluripotency.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE73001
Immediate dysfunction of vaccine-elicited CD8+ T cells primed in the absence of CD4+ T cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

CD4+ T cell help is critical for optimal CD8+ T cell expansion after priming in many experimental systems. However, a role for CD4+ T cells in regulating the initial steps of CD8+ T cell effector differentiation is not well established. Here we demonstrate that absence of CD4+ T cells at the time of replication-incompetent adenovirus vector immunization of C57BL/6 mice led to immediate CD8+ T cell dysfunction characteristic of exhaustion at the first detectable timepoints as well as impaired expansion of antigen-specific CD8+ T cells. The absence of CD4+ T cell help resulted in antigen-specific CD8+ T cells that had reduced ex vivo cytotoxicity and decreased capacity to produce IFN- and TNF-. CD8+ T cells primed in the absence of CD4+ T cells expressed elevated levels of the inhibitory receptors PD-1, LAG-3, and Tim-3, and these cells exhibited transcriptomic exhaustion profiles by gene set enrichment analysis. This dysfunctional state was imprinted within 3 days of immunization and could not be reversed by provision of CD4+ T cell help after priming. Partial rescue of unhelped CD8+ T cell expansion and effector differentiation could be achieved by PD-1 pathway blockade or recombinant IL-2 administration.

Publication Title

Immediate Dysfunction of Vaccine-Elicited CD8+ T Cells Primed in the Absence of CD4+ T Cells.

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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