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accession-icon GSE31938
Hypothalamus
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

These arrays contain data from hypthalamus tissue of nestin-Pex5 -/- male mice

Publication Title

Peroxisome deficiency but not the defect in ether lipid synthesis causes activation of the innate immune system and axonal loss in the central nervous system.

Sample Metadata Fields

Specimen part

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accession-icon GSE34552
Expression data from mouse kidney tissue
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
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Description

The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage.

Publication Title

AT1 antagonism and renin inhibition in mice: pivotal role of targeting angiotensin II in chronic kidney disease.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE106981
Expression data from thymic non-hematopoietic stromal cells after damage
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
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Description

The thymus is extremely sensitive to damage but also has a remarkable ability to repair itself. However, the mechanisms underlying this endogenous regeneration remain poorly understood and this capacity diminishes considerably with age. To identify alternate regeneration pathways in the thymus, we performed an unbiased transcriptome analysis of the non-hematopoietic (CD45-) stromal cell compartment of the thymus, which is less sensitive to thymic damage compared to the CD45+ hematopoietic compartment.

Publication Title

Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE44563
Expression data from C2C12 myotubes infected with RML prions
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

Prion infection in animals results in neurodegeneration and eventually death. To examine the cellular impact of Prion disease, we profiled non-proliferative fully differentiated C2C12 cells, which can replicate prions to high levels. Results suggest that accumulation of high levels of PrPSc in C2C12 myotubes does not cause any overt cellular dysfunction or molecular pathology.

Publication Title

Infectious prions accumulate to high levels in non proliferative C2C12 myotubes.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

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accession-icon GSE55883
Expression Profiles of Primary Mouse Hepatocytes treated with Cyclosporin A and solvent control
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative cross-omics analysis in primary mouse hepatocytes unravels mechanisms of cyclosporin A-induced hepatotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE55881
Expression Profiles of Primary Mouse Hepatocytes treated with Cyclosporin A and solvent control [RNA]
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
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Description

The transcriptomics changes induced in Primary Mouse Hepatocytes by Cyclosporin A after treatment for 24h and 48h

Publication Title

Integrative cross-omics analysis in primary mouse hepatocytes unravels mechanisms of cyclosporin A-induced hepatotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE6134
Offsprings of crosses between hypercholesterolemic and normocholesterolemic parents LUMC-HKG-ApoE-Atherosclerosis
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

Enhanced prenatal fatty streak formation in human fetuses has been associated with maternal hypercholesterolemia. However, the possible roles of maternal genetic background and in utero environment on development of atherosclerosis in adult life have not been unraveled. We generated genetically identical heterozygous apoE-deficient mice offspring with a different maternal background to study the intrauterine effect of maternal genotype and associated hypercholesterolemia on the developing vascular system. As read out for increased atherosclerosis development in adult life, a constrictive collar was placed around the carotid artery to induce lesion formation. A significant increase in endothelial cell activation and damage was detected in the carotid arteries of heterozygous apoE-deficient fetuses with apoE-deficient mothers compared with offspring from wild type mothers, but no fatty streak formation was observed. Postnatally, all carotid arteries revealed normal morphology. In adult offspring with maternal apoE-deficiency, the constrictive collar resulted in severe lesion (9/10) development compared with no to only minor lesions (2/10) in offspring of wild type mothers. Microarray analysis showed no effect of maternal apoE-deficiency on gene expression in adult offspring. We conclude that maternal apoE-deficiency not only affects fetal arteries, but also increases the susceptibility for development of collar-induced atherosclerosis in adult life.

Publication Title

Intrauterine exposure to maternal atherosclerotic risk factors increases the susceptibility to atherosclerosis in adult life.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21048
Prednisolone-induced differential gene expression in liver of mice carrying the wild type or a dimerization-defective glucocorticoid receptor
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
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Description

Glucocorticoids control expression of a large number of genes after binding to the glucocorticoid receptor (GR). Transcription may be regulated either by binding of the GR dimer to DNA regulatory elements or by protein-protein interactions of GR monomers with other transcription factors. Although the type of regulation for a number of individual target genes is known, the relative contribution of both mechanisms to the regulation of the entire transcriptional program remains elusive.

Publication Title

Prednisolone-induced differential gene expression in mouse liver carrying wild type or a dimerization-defective glucocorticoid receptor.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE24207
mRNA analysis in different mouse tissues
  • organism-icon Mus musculus
  • sample-icon 72 Downloadable Samples
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Description

The functioning of a specific tissue depends on the expression pattern of the different genes. We used microarrays to compare gene expression across different murine tissues, to get a better understanding in the expression pattern and functioning of the different tissues. With this analysis, we were not only able to identify genes that were specifically expressed in a spicific tissue but, as important, we also identified genes that were specifically repressed in a tissue, compared to al the other analysed tissues.

Publication Title

Tissue-specific disallowance of housekeeping genes: the other face of cell differentiation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE34093
Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.

Sample Metadata Fields

Specimen part

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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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