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accession-icon GSE13718
Alterations in Cell Growth and Signaling in ErbB3 Binding Protein -1 (Ebp1) Deficient Mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Background: The ErbB3 binding protein-1 (Ebp1) belongs to a family of DNA/RNA binding proteins implicated in cell growth, apoptosis and differentiation. However, the physiological role of Ebp1 in the whole organism is not known. Therefore, we generated Ebp1-deficient mice carrying a gene trap insertion in intron 2 of the Ebp1 (pa2g4) gene.

Publication Title

Alterations in cell growth and signaling in ErbB3 binding protein-1 (Ebp1) deficient mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE48600
Microarray expression analysis of wild type and Erg knockdown bone marrow hematopoietic stem and progenitor cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Erg is an ETS family transcription factor frequently overexpressed in human leukemias and has been implicated as a key regulator of hematopoietic stem cells (HSCs). However how Erg controls normal hematopoiesis, particularly at the stem cell level, remains poorly understood. Using homologous recombination, we generated an Erg knockdown allele (Ergkd) in which Erg expression can be restored upon Cre-mediated excision of a Stopper cassette. In Ergkd/+ mice, ~40% reduction in Erg dosage perturbed both fetal liver and bone marrow hematopoiesis by reducing the numbers of Lin-Sca-1+c-Kit+ (LSK) hematopoietic stem and progenitor cells (HSPCs) and megakaryocytic progenitors.

Publication Title

Reduced Erg Dosage Impairs Survival of Hematopoietic Stem and Progenitor Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE9630
Expression data from mouse liver
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon

Description

Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.

Publication Title

Laboratory diet profoundly alters gene expression and confounds genomic analysis in mouse liver and lung.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11056
Expression data from mouse lung
  • organism-icon Mus musculus
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon

Description

Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.

Publication Title

Chronic exposure to arsenic in the drinking water alters the expression of immune response genes in mouse lung.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39388
Distinct transcriptional programs controlled by ERG and ETV1 in prostate cells
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

ETV1 directs androgen metabolism and confers aggressive prostate cancer in targeted mice and patients.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE39355
Expression profiling of mouse primary prostate luminal cells from WT and T-ETV1 mice, which contains human ETV1 cDNA under the endogenous Tmprss2 promoter.
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

Chromosomal rearrangements involving ETS factors, ERG and ETV1, occur frequently in prostate cancer. We here examine mouse prostate cells from WT mice with s with T-ETV1 mice, which contains express the truncated human ETV1 under the endogenous Tmprss2 promoter. ETV1 expression can be tracked by GFP expression.

Publication Title

ETV1 directs androgen metabolism and confers aggressive prostate cancer in targeted mice and patients.

Sample Metadata Fields

Specimen part

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accession-icon GSE48622
Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
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Description

Gene expression analysis of 2-month-old APP/APLP2 double-conditional Knockout (N-dCKO) mice and littermate APLP2 knockout controls, APP knockout and wildtype controls.

Publication Title

Soluble amyloid precursor protein (APP) regulates transthyretin and Klotho gene expression without rescuing the essential function of APP.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE26912
Inflammation driven by tumor-specific Th1 cells protects against B-cell cancer
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered tumor-promoting. In contrast, the exact nature of protective antitumor immunity remains obscure. In this study, we have quantified locally secreted cytokines during primary immune responses against myeloma and B-cell lymphoma in mice. Strikingly, successful cancer immunosurveillance mediated by tumor-specific CD4+ T cells was consistently associated with elevated local levels of both proinflammatory (IL-1aplha, IL-1beta, and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-alpha, IL-2, IL-12). Cancer eradication was achieved by a collaboration between tumor-specific Th1 cells and tumor-infiltrating, antigen-presenting macrophages. Th1 cells induced secretion of IL-1? and IL-6 by macrophages. Th1-derived interferon-? was shown to render macrophages directly cytotoxic to cancer cells, and to induce macrophages to secrete the angiostatic chemokines CXCL9/MIG and CXCL10/IP-10. Thus, inflammation, when driven by tumor-specific Th1 cells, may prevent rather than promote cancer.

Publication Title

Inflammation driven by tumour-specific Th1 cells protects against B-cell cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE95283
Estrogen signaling and fatty liver disease
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

We propose comparing liver gene expression of WT and female ERKO mice early in the high-fat feeding period to animals fed a regular chow diet. Analyzing liver tissue before the fatty liver disease phenotype becomes severe will allow identification of target genes which may be causal.

Publication Title

Hormone signaling and fatty liver in females: analysis of estrogen receptor α mutant mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE112449
Microarray analysis comparing gene expression of callus tissue extracted from either Cyp24a1-null mice or their control heterozygous littermates
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The 24R,25-dihydroxyvitamin D metabolite (24R,25D) has long been suspected of participating to bone fracture repair. We used Cyp24a1-deficient mice, unable to produce 24R25D, to observe gene expression in callus tissue compared to that of control littermates.

Publication Title

Optimal bone fracture repair requires 24R,25-dihydroxyvitamin D3 and its effector molecule FAM57B2.

Sample Metadata Fields

Age, Specimen part, Treatment, 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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