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accession-icon GSE70262
The impact of P53 loss on transcriptome changes following loss of Apc in the intestine
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

BACKGROUND: p53 is an important tumor suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated.

Publication Title

A limited role for p53 in modulating the immediate phenotype of Apc loss in the intestine.

Sample Metadata Fields

Specimen part

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accession-icon GSE65476
B-catenin deficiency, but not c-Myc deletion, suppresses the immediate phenotypes of Apc loss in the liver
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Dysregulated Wnt signalling is seen in approximately 30% of hepatocellular cancers, thus finding pathways downstream of activation of Wnt signalling is key. Using cre lox technology we have deleted the the adenomatous polyposis coli tumour suppressor protein (Apc) within the adult mouse liver and observed a rapid increase in nuclear beta-catenin and C-Myc. This is associated with an induction of proliferation leading to hepatomegally within 4 days of gene deletion. To investigate the downstream pathways responsible for these phenotypes we analysed the impact of inactivating Apc in the context of deficiency of the potentially key effectors beta-catenin and c-Myc. beta-catenin loss rescues both the proliferation and hepatomegally phenotypes following Apc loss. However c-Myc deletion, which rescues the phenotypes of Apc loss in the intestine, had no effect on the phenotypes of Apc loss. The consequences of deregulation the Wnt pathway within the liver are therefore strikingly different to those observed within the intestine, with the vast majority of Wnt targets beta-catenin dependent but c-Myc independent in the liver.

Publication Title

B-catenin deficiency, but not Myc deletion, suppresses the immediate phenotypes of APC loss in the liver.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE88994
Analysis of mRNA from Gli1 expressing stromal cells of mice given SAG21k versus vehicle
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Comparison of mRNA expression from FACS isolated Gli1 expressing stromal cells from mice given SAG21k versus vehicle

Publication Title

Control of inflammation by stromal Hedgehog pathway activation restrains colitis.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE13061
Comparative transcriptomic analysis of BA- or BL-
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Bifidobacteria can protect from enteropathogenic infection through production of acetate.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17936
Nkx2.5 regulates Jarid2 during outflow tract morphogenesis
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon

Description

The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression.

Publication Title

Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE17910
In vitro differentiation of P19CL6 cardiogenic embryonic carcinoma cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Pluripotent P19CL6 embryonic carcinoma cells can be differentiated to a cardiac lineage by culture in the presence of DMSO. The goal of this study was to characterize temporal gene expression patterns associated with cardiogenic differentiation. Gene expression analysis was conducted on differentiating P19CL6 cells at several time points following induction with 1% DMSO. Samples were processed for analysis by Affymetrix GeneChip.

Publication Title

Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.

Sample Metadata Fields

Cell line

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accession-icon GSE26299
Gene expression profiling in DBA/2J glaucoma
  • organism-icon Mus musculus
  • sample-icon 107 Downloadable Samples
  • Technology Badge Icon

Description

In this study that was specifically designed to identify early stages of glaucoma in DBA/2J mice, we used genome-wide expression profiling and a series of computational methods. Our methods successfully subdivided eyes with no detectable glaucoma by conventional assays into molecularly defined stages of disease. These stages represent a temporally ordered sequence of glaucoma states. Using an array of tools, we then determined networks and biological processes that are altered at these early stages. Our strategy proved very sensitive, suggesting that similar approaches will be valuable for uncovering early processes in other complex, later-onset diseases. Early changes included upregulation of both the complement cascade and endothelin system, and so we tested the therapeutic value of separately inhibiting them. Mice with a mutation in the complement component 1a gene (C1qa) were robustly protected from glaucoma with the protection being among the greatest reported. Similarly, inhibition of the endothelin system was strongly protective. Since EDN2 is potently vasoconstrictive and was produced by microglial/macrophages, our data provide a novel link between these cell types and vascular dysfunction in glaucoma. Targeting early events such as the upregulation of the complement and endothelin pathways may provide effective new treatments for human glaucoma.

Publication Title

Molecular clustering identifies complement and endothelin induction as early events in a mouse model of glaucoma.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE35805
Gene expression analysis of WT and Flt3-ITD multipotent progenitors
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

FLT3-ITDs Introduce a Myeloid Differentiation and Transformation Bias in Lympho-myeloid Multipotent Progenitors

Publication Title

FLT3-ITDs instruct a myeloid differentiation and transformation bias in lymphomyeloid multipotent progenitors.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE25423
LSD1 knockdown in 3T3-L1 preadipocytes
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Obesity is often associated with a low-grade systemic inflammation state that contributes to the development of insulin resistance and atherosclerotic complications. This is usually coupled with increased macrophage infiltration in the adipose tissue and a defect in adipocyte differentiation that results in accumulation of hypertrophic fat cells characterized by a deregulated pattern of adipokine expression. Here we show that knockdown of histone demethylase lsd1 in 3T3-L1 preadipocytes results in defective adipogenesis and derepression of an inflammatory program in these cells.

Publication Title

Histone demethylase KDM1A represses inflammatory gene expression in preadipocytes.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP008976
Personal Omics Profiling Reveals Dynamic Molecular Phenotypes and Actionable Medical Risks
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Illumina Genome Analyzer IIx

Description

We have determined the whole genome sequence of an individual at high accuracy and performed an integrated analysis of omics profiles over a 1.5 year period that included healthy and two virally infected states. Omics profiling of transcriptomes, proteomes, cytokines, metabolomes and autoantibodyomes from blood components have revealed extensive, dynamic and broad changes in diverse molecular components and biological pathways that occurred during healthy and disease states. Many changes were associated with allele- and edit-specific expression at the RNA and protein levels, which may contribute to personalized responses. Importantly, genomic information was also used to predict medical risks, including Type II Diabetes (T2D), whose onset was observed during the course of our study using standard clinical tests and molecular profiles, and whose disease progression was monitored and subsequently partially managed. Our study demonstrates that longitudinal personal omics profiling can relate genomic information to global functional omics activity for physiological and medical interpretation of healthy and disease states. Overall design: Examination of blood component in 20 different time points over 1.5 years which includes 2 disease state and 18 healty state Related exome studies at: SRX083314 SRX083313 SRX083312 SRX083311

Publication Title

Personal omics profiling reveals dynamic molecular and medical phenotypes.

Sample Metadata Fields

Specimen part, Disease, Subject

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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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