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accession-icon GSE14906
The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample.

Publication Title

Cardiac expression of Tnnt1 requires the GATA4-FOG2 transcription complex.

Sample Metadata Fields

Specimen part

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accession-icon GSE11314
Ovarian Development in Mice Requires GATA4/FOG2 Transcriptional Complex
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We have demonstrated previously that mammalian sexual differentiation requires both GATA4 and FOG2 transcription regulators to assemble the functioning testis. We have now determined that the sexual development of female mice is profoundly affected by the loss of GATA4-FOG2 interaction. We have also identified the Dkk1 gene, encoding a secreted inhibitor of canonical -catenin signaling as a target of GATA4/FOG2 repression in the developing ovary. The tissue-specific ablation of the -catenin gene in the gonads disrupts female development while in the Gata4ki/ki/Dkk1-/- or Fog2-/-/Dkk1-/- embryos the normal ovarian gene expression pattern is partially restored. Control of ovarian development by the GATA4/FOG2 complex presents a novel insight into the crosstalk of transcriptional regulation and extracellular signaling in ovarian development.

Publication Title

Ovarian development in mice requires the GATA4-FOG2 transcription complex.

Sample Metadata Fields

Specimen part

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accession-icon SRP092098
Analysis of genes differencially expressed depending on Myc expression
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal is to examine the transcriptome of ESCs with different Myc levels Overall design: In order to analyse the transcriptome, mESC population was sorted in 3 groups depending on Myc levels

Publication Title

Pluripotency Surveillance by Myc-Driven Competitive Elimination of Differentiating Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP110619
RNA-Seq analysis of iMOS T1-Myc ESC mosaic cultures
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

The goal of this study is to analyse the transcriptome of WT and Myc-overexpressing ESCs in iMOS T1-Myc mosaic cultures. Overall design: Homozygous iMOS T1-Myc ESC cultures (Claveria et al., 2013) were treated with 20µM 4-hydroxytamoxifen for 24 hours to generate a mosaic of cell populations containing two, one or no extra Myc and EYFP copies. 24 hours after tamoxifen removal, cells were sorted according to their EYFP expression levels and populations with two extra Myc and EYFP copies and with no extra Myc and EYFP copies were collected. Uninduced homozygous iMOS T1-Myc ESC cultures were also sorted and collected as a control. Three biological replicas were included for each condition.

Publication Title

Pluripotency Surveillance by Myc-Driven Competitive Elimination of Differentiating Cells.

Sample Metadata Fields

Subject

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accession-icon GSE8646
The Hay Wells Syndrome-Derived TAp63alphaQ540L Mutant Has Impaired Transcriptional and Cell Growth Regulatory Activity
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

p63 mutations have been associated with several human hereditary disorders characterized by ectodermal dysplasia such as EEC syndrome, ADULT syndrome and AEC syndrome . The location and functional effects of the mutations that underlie these syndromes reveal a striking genotype-phenotype correlation. Unlike EEC and ADULT that result from missense mutations in the DNA-binding domain of p63, AEC is solely caused by missense mutations in the SAM domain of p63. We report a study on the TAp63a isoform, the first to be expressed during development of the embryonic epithelia, and on its naturally occurring Q540L mutant derived from an AEC patient. To assess the effects of the Q540L mutation, we generated stable cell lines expressing TAp63a wt, DeltaNp63 alpha or the TAp63 alpha-Q540L mutant protein and used them to systematically compare the cell growth regulatory activity of the mutant and wt p63 proteins and to generate, by microarray analysis, a comprehensive profile of differential gene expression. We found that the Q540L substitution impairs the transcriptional activity of TAp63a and causes misregulation of genes involved in the control of cell growth and epidermal differentiation.

Publication Title

The Hay Wells syndrome-derived TAp63alphaQ540L mutant has impaired transcriptional and cell growth regulatory activity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE61839
The Ubiquitin Ligase Siah2 Regulates Obesity-induced Adipose Tissue Inflammation
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Chronic, low-grade adipose tissue inflammation associated with adipocyte hypertrophy is an important link in the relationship between obesity and insulin resistance. Although ubiquitin ligases are essential regulators of inflammatory processes, the role of these enzymes in metabolically driven adipose tissue inflammation is relatively unexplored. In this study, we found that the ubiquitin ligase Siah2 is a central factor in obesity-related adipose tissue inflammation. When challenged with chronic excess energy intake, Siah2-null mice become obese with enlarged adipocytes, but do not develop obesity-induced insulin resistance. Proinflammatory gene expression is substantially reduced in the Siah2-null epididymal adipose tissue of the obese Siah2KO mice.

Publication Title

The ubiquitin ligase Siah2 regulates obesity-induced adipose tissue inflammation.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE2852
Ochratoxin A study on rat liver and kidney gene expression
  • organism-icon Rattus norvegicus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Ochratoxin A gene expression profiling in liver and kidney, with time points of exposure from 7 days to 12 motnhs

Publication Title

A toxicogenomics approach to identify new plausible epigenetic mechanisms of ochratoxin a carcinogenicity in rat.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE59201
Gene expression changes during retinal development and rod specification.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Photoreceptor disorders are collectively known as retinal degeneration (RD), and include retinitis pigmentosa (RP), cone-rod dystrophy and age related macular degeneration (AMD). These disorders are largely genetic in origin; individual mutations in any one of >200 genes cause RD, making mutation specific therapies prohibitively expensive. A better treatment plan, particularly for late stage disease, may involve stem cell transplants into the photoreceptor or ganglion cell layers of the retina. Stem cells from young mouse retinas can be transplanted, and can form photoreceptors in adult retinas. These cells can be grown in tissue culture, but can no longer form photoreceptors. We have used microarrays to investigate differences in gene expression between cultured retinal progenitor cells (RPCs) that have lost photoreceptor potential, postnatal day 1 (pn1) retinas and the postnatal day 5 (pn5) retinas that contain transplantable photoreceptors. We have also compared FACS sorted Rho-eGFP expressing rod photoreceptors from pn5 retinas with Rho-eGFP negative cells from the same retinas. We have identified over 300 genes upregulated in rod photoreceptor development in multiple comparisons, 37 of which have been previously identified as causative of retinal disease when mutated. It is anticipated that this research should bring us closer to growing photoreceptors in culture and therefore better treatments for RD. This dataset is also a resource for those seeking to identify novel retinopathy genes in RD patients.

Publication Title

Gene expression changes during retinal development and rod specification.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP039089
RNA-seq based characterization of long non-coding RNA involved in respiratory viruses pathogenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

This dataset includes both whole transcriptome (WT) and mRNA-seq data for interferon-treated mouse samples. This is part of a larger study (GSE52405), where these interferon datasets were used as validation. Overall design: 6-week-old C57BL/6J mice were treated with 10,000 U of recombinant interferon (Universal Type I IFN, Recombinant Human IFN-alpha A/D [BglII], R&D Systems) dissolved in endotoxin-free phosphate-buffered saline (EF-PBS), or with EF-PBS alone. For this study, the mice at 12 hours post-treatment were used.

Publication Title

Annotation of long non-coding RNAs expressed in collaborative cross founder mice in response to respiratory virus infection reveals a new class of interferon-stimulated transcripts.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE60350
Expression Profiles of Responders versus Non-Responders with AML or MDS to the Novel Mitochondrial Inhibitor CPI-613
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

To determine if there are differences in the gene expression profile of peripheral blood mononuclear cells in patients with Acute Myeloid Leukemia (AML) or Myelodysplastic Syndrome (MDS) who responded to CPI-613 when compared to those patients who did not respond we generated gene expression profiles from four responding patients and compared them to four non-responders. None of the gene expression profiles have been previously published. Here we describe the origins and provide associated clinical annotations with the hope that other investigators will be able to utilize this data in their own research.

Publication Title

A phase I study of the first-in-class antimitochondrial metabolism agent, CPI-613, in patients with advanced hematologic malignancies.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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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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