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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
  • Technology Badge Icon

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 GSE6540
Expression data from olfactory epithelium of Lip-C-treated mice compared to Lip-O-treated control mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Microarray analysis of gene expression in the olfactory epithelium of macrophage depleted mice to study the role of macrophages in regulating neurodegeneration, neuroprotection, and neurogenesis of olfactory sensory neurons

Publication Title

Macrophage-mediated neuroprotection and neurogenesis in the olfactory epithelium.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE51927
Expression analysis of murine primary and derived orthotopic SEOC tumors
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon

Description

We previously generated genetically engineered mouse (GEM) models based on perturbation of Tp53, Rb with or without Brca1 or Brca2 that develop serous epithelial ovarian cancer (SEOC) closely resembling the human disease on histologic and molecular levels. We have adapted these GEM models to orthotopic allografts that uniformly develop tumors with short latency in immunocompetent recipients and are ideally suited for routine preclinical studies. To monitor passaged tumors at the molecular level, we analyzed transcriptional profiles of a set of primary SEOC and matching derived passaged tumors. We have merged this dataset with previously published ( doi: 10.1158/0008-5472.CAN-11-3834; PMID 22617326) dataset of murine primary ovarian tumors from our GEM models (GSE46169) and merged and compared them to expression profiles of human dataset published previously (doi: 10.1038/nature10166).

Publication Title

Pathway-specific engineered mouse allograft models functionally recapitulate human serous epithelial ovarian cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE32937
MicroRNA-29 in Aortic Dilation: Implications for Aneurysm Formation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

We compared the aorta of 6-weeks-old mice (young) with 18-months-old mice (old). Using the publicly available tools Sylamer and DIANA-mirExTra, we identified an enrichment for miR-29 binding sites in the 3'UTR of genes downregulated in the aged aortas. We subsequently showed that inhibition of miR-29 in aged mice prevented dilation of the aorta.

Publication Title

MicroRNA-29 in aortic dilation: implications for aneurysm formation.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE18010
Pathogenicity of a disease-associated human IL-4 receptor allele in experimental asthma
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon

Description

Polymorphisms in the interleukin-4 receptor chain (IL-4R) have been linked to asthma incidence and severity, but a causal relationship has remained uncertain. In particular, a glutamine to arginine substitution at position 576 (Q576R) of IL-4R has been associated with severe asthma, especially in African Americans. We show that mice carrying the Q576R polymorphism exhibited intense allergen-induced airway inflammation and remodeling. The Q576R polymorphism did not affect proximal signal transducer and activator of transcription (STAT) 6 activation, but synergized with STAT6 in a gene target and tissue-specific manner to mediate heightened expression of a subset of IL-4 and IL-13responsive genes involved in allergic inflammation. Our findings indicate that the Q576R polymorphism directly promotes asthma in carrier populations by selectively augmenting IL-4Rdependent signaling.

Publication Title

Pathogenicity of a disease-associated human IL-4 receptor allele in experimental asthma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE27975
HL-1 cardiomyocyte response to hypoxia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.

Publication Title

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Sample Metadata Fields

Cell line

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accession-icon GSE65206
Comparison of gene expression in tumor ovarian surface epithelial cells with different p53 status
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

The impact of specific p53 mutations on ovarian tumor development and response to therapeutic treatment remain limited. Here, using transgenic mouse models of epithelial ovarian cancer (EOC), we demonstrated that the Trp53R172H mutation promotes EOC progression compared to wild-type p53, but with different consequences between heterozygous and homozygous mutation status. EOC expressing heterozygous Trp53R172H mutation has enhanced responsiveness to steroid hormones and at late stage developed mucinous cystadenocarcinoma. These findings open new realms for exploring the interaction between p53 and steroid receptor, and the allelic status of p53 in EOC development and treatment.

Publication Title

Mutant p53 Promotes Epithelial Ovarian Cancer by Regulating Tumor Differentiation, Metastasis, and Responsiveness to Steroid Hormones.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE21902
Expression Data from chemical induced tumors obtained from NDR1+/+, NDR1+/- and NDR1-/- mice
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon

Description

Loss and heterozygosity for NDR1 predisposes mice to T-cell lymphoma development. To analyze mechanisms of tumor development in these mice chemically (ENU)-induced tumors were collected and RNA was extracted.

Publication Title

Ablation of the kinase NDR1 predisposes mice to the development of T cell lymphoma.

Sample Metadata Fields

Sex, Specimen part, Disease, Treatment

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accession-icon GSE11732
Runx transcriptional program for control of cell adhesion and survival
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

The Runx genes are important in development and cancer, where they can act either as oncogenes or tumour supressors. We compared the effects of ectopic Runx expression in established fibroblasts, where all three genes produce an indistinguishable phenotype entailing epithelioid morphology and increased cell survival under stress conditions. Gene array analysis revealed a strongly overlapping transcriptional signature, with no examples of opposing regulation of the same target gene. A common set of 50 highly regulated genes was identified after further filtering on regulation by inducible RUNX1-ER. This set revealed a strong bias toward genes with annotated roles in cancer and development, and a preponderance of targets encoding extracellular or surface proteins reflecting the marked effects of Runx on cell adhesion.

Publication Title

Gene array analysis reveals a common Runx transcriptional programme controlling cell adhesion and survival.

Sample Metadata Fields

No sample metadata fields

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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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