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accession-icon SRP155044
Differential expression data between E15.5 outflow tracts of Gata4 G295S mutant embryos and littermate controls
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

E15.5 embryos were micro-disscted from Gata4 G295S mutant mice and littermate controls, RNA was isolated using Norgen total RNA isolation, and libraries were generated with the RNA TruSeq Stranded Total RNA kit. 50 base pair paired end reads were obtained on an illumina high seq 2500. Fastq files were aligned to the mouse genome using STAR aligner. QC was performed using RNASeQC and RSeQC. BAM files were processed using cufflinks pipeline. Overall design: The project aims to assess the differential gene expression at E15.5 between the outflow tracts of Gata4 G295S mutant embryos and wildtype littermate controls.

Publication Title

Developmental origins for semilunar valve stenosis identified in mice harboring congenital heart disease-associated <i>GATA4</i> mutation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP046290
Transcriptional Program of Kpna2 (Importin-alpha2) Regulates Cellular Differentiation-Coupled Circadian Clock Development in Mammalian Cells
  • organism-icon Mus musculus
  • sample-icon 78 Downloadable Samples
  • Technology Badge IconIllumina HiScanSQ

Description

The circadian clock in mammalian cells is cell-autonomously generated during the cellular differentiation process, but the underlying mechanisms are not understood. Here we show that perturbation of transcriptional program by constitutive expression of c-Myc and Dnmt1 ablation disrupts the differentiation-coupled emergence of the clock from mouse embryonic stem cells (ESCs). Using these model ESCs, 484 genes are identified by global gene expression analysis as correlating factors with differentiation-coupled circadian clock development. Among them, we find the misregulation of Kpna2 (Importin-alpha2) during the differentiation of the c-Myc over-expressed and Dnmt1-/- ESCs, in which sustaining cytoplasmic accumulation of PER proteins is observed. Moreover, constitutive expression of Kpna2 during the differentiation culture of ESCs significantly impairs clock development and KPNA2 facilitates cytoplasmic localization of PER1/2. These results suggest that the programmed gene expression network regulates the differentiation-coupled circadian clock development in mammalian cells, at least in part via post-transcriptional regulation of clock proteins. Overall design: Examination of whole transcriptome in ES cells and in vitro differentiated cells.

Publication Title

Transcriptional program of Kpna2/Importin-α2 regulates cellular differentiation-coupled circadian clock development in mammalian cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE46295
Effects of a Tricaprylin Emulsion on Anti-glomerular Basement Membrane Glomerulonephritis in Rats
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Expression data from rat with anti-glomerular basement membrane nephritis (anti-GBM). We used microarrays to analyze the transcriptome of kidney from anti-GBM model rat with or without drug treatment

Publication Title

Effects of a Tricaprylin Emulsion on Anti-glomerular Basement Membrane Glomerulonephritis in Rats: In Vivo and in Silico Studies.

Sample Metadata Fields

Specimen part

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accession-icon GSE4600
Identifying targets of MeCP2 during neuronal maturational differentiation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rett syndrome (RTT) is an X-linked dominant neurodevelopmental disorder caused by mutations in MECP2, encoding methyl-CpG binding protein 2. MeCP2 is a transcriptional repressor elevated in mature neurons and is predicted to be required for neuronal maturation by regulating multiple target genes. Identifying primary gene targets in either Mecp2-deficient mice or human RTT brain has proven to be difficult, perhaps because of the transient requirement for MeCP2 during neuronal maturation. In order to experimentally control the timing of MeCP2 expression and deficiency during neuronal maturation, human SH-SY5Y cells undergoing mature neuronal differentiation were transfected with methylated MeCP2 oligonucleotide decoy to disrupt the binding of MeCP2 to endogenous targets. Genome-wide expression microarray analysis identified all four known members of the inhibitors of differentiation or inhibitors of DNA binding (ID1, ID2, ID3 and ID4) subfamily of helix-loop-helix (HLH) genes as novel neuronal targets of MeCP2. Chromatin immunoprecipitation analysis confirmed binding of MeCP2 near or within the promoters of ID1, ID2 and ID3, and quantitative RT-PCR confirmed increased expression of all four Id genes in Mecp2-deficient mouse brain. All four ID proteins were significantly increased in Mecp2-deficient mouse and human RTT brain using immunofluorescence and laser scanning cytometric analyses. Because of their involvement in cell differentiation and neural development, ID genes are ideal primary targets for MeCP2 regulation of neuronal maturation that may explain the molecular pathogenesis of RTT.

Publication Title

Inhibitors of differentiation (ID1, ID2, ID3 and ID4) genes are neuronal targets of MeCP2 that are elevated in Rett syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE48029
Expression data of Jurkat cells stably expressing HBZ with or without stimulation
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human T-cell leukemia virus type 1 (HTLV-1) encodes HTLV-1 bZIP factor (HBZ), which is thought to be crucial for neoplastic and inflammatory diseases caused by HTLV-1. So, we analyzed the transcriptional profile of HBZ expressing cells and how HBZ affect the expression of apoptosis-related genes.

Publication Title

HTLV-1 bZIP factor suppresses apoptosis by attenuating the function of FoxO3a and altering its localization.

Sample Metadata Fields

Specimen part

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accession-icon GSE57194
In Vitro Transformation of Primary Human CD34+ Cells by AML Fusion Oncogenes: Early Gene Expression Profiling Reveals Possible Drug Target in AML
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation. Here we compare the in vitro effects of representatives of major groups of AML fusion oncogenes on primary human CD34+ cells.

Publication Title

In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML.

Sample Metadata Fields

Specimen part

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accession-icon GSE95278
Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy.

Publication Title

Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE7501
Genes in nonpermissive temperature-induced cell growth arrest and differentiation of astrocyte RCG-12 cells
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in astrocyte RCG-12 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Astrocyte RCG-12 cells used in this study were derived from primary cultured rat cortical glia cells infecting with a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Of the 15,923 probe sets analyzed, nonpermissive temperature differentially expressed 556 probe sets by >2.0-fold.

Publication Title

Identification of genetic networks involved in the cell growth arrest and differentiation of a rat astrocyte cell line RCG-12.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41146
Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection
  • organism-icon Drosophila melanogaster
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells

Publication Title

Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.

Sample Metadata Fields

Cell line

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accession-icon GSE41242
Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells
  • organism-icon Drosophila melanogaster
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection

Publication Title

Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.

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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