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accession-icon GSE82129
PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Genes regulated by miR-206 were identified by microarray analysis in RD cells transfected with a Negative Control (NC) or miR-206 Mimic

Publication Title

PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma.

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon SRP186572
RNAi Screening for Ubiquitin Ligases that Regulate Myofiber Size Identifies a Key Role for UBR4 in Myofiber Hypertrophy in Drosophila and Mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Sequencing of RNA isolated from the tibialis anterior muscles of 6 month old C57BL/6J mice that had been injected and electroporated with either a control non-targeting siRNA (NT) or two different UBR4 targeting siRNA sequences (UBR4 siRNA5 and siRNA7) to deplete UBR4. Muscles were harvested 7 days after electroporation and showed significant loss of UBR4 coincident with hypertrophy of type 2A and 2X myofibers. Overall design: 3 samples each of non targeting control and 2 siRNA UBR4 targeting constructs.

Publication Title

A Key Role for the Ubiquitin Ligase UBR4 in Myofiber Hypertrophy in Drosophila and Mice.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP184505
Transcriptional cofactors display core promoter class-specificity in human
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, NextSeq 550

Description

Transcriptional cofactors communicate regulatory cues from enhancers to promoters and are central effectors of transcription activation and gene expression, which is a hallmark of all multicellular organisms. However, the extent to which different cofactors display intrinsic specificity for distinct promoters is unclear. Testing intrinsic COF – core promoter (CP) compatibilities requires the systematic assessment of transcriptional activation for many CPs in the presence or absence of a given COF in an otherwise constant standardized reporter system. We therefore combined a plasmid-based high-throughput reporter assay, Self-Transcribing Active Core Promoter-sequencing (STAP-seq), with the specific recruitment of individual COFs to create a high-throughput activator bypass-like assay. Using this assay, we tested whether 5 different individually tethered human COFs (MED15, BRD4, EP300, MLL3 and EMSY) activate transcription from a selection of 12,000 candidate sequences encompassing different types of gene core promoters, enhancers and control sequences. In addition, we used the strong transcriptional activator P65 as a positive control and GFP as a negative control. We found that different COFs preferentially activate different CPs. For instance, MED15 prefers TATA-box containing CPs, while MLL3 preferentially activates CpG island promoters. The observed compatibilities between cofactors and promoters can explain how different enhancers specifically activate distinct sets of genes or alternative promoters within the same gene, and may underlie distinct transcriptional programs in human cells. Overall design: STAP-seq upon recruitment of individual transcriptional cofactor in HCT116 cells with 5 different cofactors and 2 controls, each in biological triplicate.

Publication Title

Transcriptional cofactors display specificity for distinct types of core promoters.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42299
Expression profiles of C2C12 myotubes in response to PGC-1 (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha) overexpression and/or iron chelation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mitochondria are centers of metabolism and signaling whose content and function must adapt to changing cellular environments. The biological signals that initiate mitochondrial restructuring and the cellular processes that drive this adaptive response are largely obscure. To better define these systems, we performed matched quantitative genomic and proteomic analyses of mouse muscle cells as they performed mitochondrial biogenesis. We find that proteins involved in cellular iron homeostasis are highly coordinated with this process, and that depletion of cellular iron results in a rapid, dose-dependent decrease of select mitochondrial protein levels and oxidative capacity. We further show that this process is universal across a broad range of cell types and fully reversed when iron is reintroduced. Collectively, our work reveals that cellular iron is a key regulator of mitochondrial biogenesis, and provides quantitative datasets that can be leveraged to explore post-transcriptional and post-translational processes that are essential for mitochondrial adaptation.

Publication Title

Complementary RNA and protein profiling identifies iron as a key regulator of mitochondrial biogenesis.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE53989
A genome-wide approach in Arabidopsis thaliana to assess the toxicity of cadmium sulfide quantum dots
  • organism-icon Arabidopsis thaliana
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Cadmium sulfide quantum dots (CdS QDs) are widely used in novel equipment. The relevance of the research lies in the need to develop risk assessments for nanomaterials, using as basis a model plant species.

Publication Title

Genome-wide approach in Arabidopsis thaliana to assess the toxicity of cadmium sulfide quantum dots.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE70901
Generation of Stem Cell-Derived Cells from Type 1 Diabetic Patients
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We recently reported the scalable in vitro production of functional stem cell-derived cells. Here we extend this approach to generate SC- cells from Type 1 diabetic patients (T1D), a cell type that is destroyed during disease progression and has not been possible to extensively study. These cells express cell markers, respond to glucose both in vitro and in vivo, prevent alloxan-induced diabetes in mice, and respond to anti-diabetic drugs. Furthermore, we use an in vitro disease model to demonstrate the cells respond to different forms of cell stress. Using these assays, we find no major differences in T1D SC- cells compared to SC- cells derived from non-diabetic patients (ND). These results show that T1D SC- cells can be used for the treatment of diabetes, drug screening, and the study of cell biology.

Publication Title

Generation of stem cell-derived β-cells from patients with type 1 diabetes.

Sample Metadata Fields

Specimen part

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accession-icon SRP100979
HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. Overall design: RNA-Seq was performed on mRNA isolated from quadriceps femoris muscle of 24 mice. These mice were of wild type, R6/2, and Hsf1-/- genotypes. Two mice of each genotype were tested in four conditions: (1) heat shock, (2) control heat shock, (3) HSP90 inhibition (NVP-HSP990), and (4) HSP90 inhibition vehicle.

Publication Title

HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.

Sample Metadata Fields

Age, Specimen part, Treatment, Subject

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accession-icon GSE55617
Gene expression of liver tissue from Pcyt2 mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Pcyt2 defient mice has metabolic syndrome and insulin resistance. We used microarray to study the gene expression of these mice to

Publication Title

Male-Specific Cardiac Dysfunction in CTP:Phosphoethanolamine Cytidylyltransferase (Pcyt2)-Deficient Mice.

Sample Metadata Fields

Specimen part

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accession-icon SRP038704
RNA-seq analysis of WT and blmp-1(tm548) mutant L3 larvae
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We performed RNA-seq analysis of WT and blmp-1(tm548) mutant L3 larvae to identify genes regulated by the zing-finger transcription factor BLMP-1. Overall design: We analyzed three WT and three blmp-1 mutant biological replicates

Publication Title

DRE-1/FBXO11-dependent degradation of BLMP-1/BLIMP-1 governs C. elegans developmental timing and maturation.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE53123
Expression data from MOLT-4 and CCRF-CEM cells grown in serum free medium, untreated, treated with direct (A-769662) and indirect (AICAR) AMPK activators.
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Two human acute lymphoblastic leukemia cell lines (Molt-4 and CCRF-CEM) were treated with direct (A-769662) and indirect (AICAR) AMPK activators. Molt-4 and CCRF-CEM cells were obtained from ATCC (CRL-1582 and CCL-119). Control samples were used for the analysis of metabolic differences between cell lines. Therefore the data was analyzed in combination with, metabolomic data, and the genome-scale reconstruction of human metabolism. For experiments cells were grown in serum-free medium containing DMSO (0.67%) at a cell concentration of 5 x 105 cells/mL.

Publication Title

Prediction of intracellular metabolic states from extracellular metabolomic data.

Sample Metadata Fields

Cell line, 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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