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accession-icon GSE28515
Effect of acute ethanol on medidal prefrontal cortex across BXD genetic mapping panel and progenitors.
  • organism-icon Mus musculus
  • sample-icon 62 Downloadable Samples
  • Technology Badge Icon

Description

In order to elucidate the molecular mechanisms underlying individual variation in sensitivity to ethanol we profiled the prefrontal cortex transcriptomes of two inbred strains that exhibit divergent responses to acute ethanol, the C57BL6/J (B6) and DBA/2J (D2) strains, as well as 27 members of the BXD recombinant inbred panel, which was derived from a B6 x D2 cross. With this dataset we were able to identify several gene co-expression networks that were robustly altered by acute ethanol across the BXD panel. These ethanol-responsive gene-enriched networks were heavily populated by genes regulating synaptic transmission and neuroplasticity, and showed strong genetic linkage to discreet chromosomal loci. Network-based measurements of node importance identified several hub genes as established regulators of ethanol response phenotypes, while other hubs represent novel candidate modulators of ethanol responses.

Publication Title

Genetic dissection of acute ethanol responsive gene networks in prefrontal cortex: functional and mechanistic implications.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE20621
Immunoregulatory actions of epithelial cell PPAR g at the colonic mucosa
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in epithelial cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression.

Publication Title

Immunoregulatory actions of epithelial cell PPAR gamma at the colonic mucosa of mice with experimental inflammatory bowel disease.

Sample Metadata Fields

Specimen part

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accession-icon GSE13530
An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity.
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
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Description

Type I interferons were discovered as the primary antiviral cytokines and are now known to serve critical functions in host defense against bacterial pathogens. Accordingly, established mediators of interferon antiviral activity may mediate previously unrecognized antibacterial functions. RNase-L is the terminal component of an RNA decay pathway that is an important mediator of interferon-induced antiviral activity. Here we identify a novel role for RNase-L in the host antibacterial response. RNase-L-/- mice exhibited a dramatic increase in mortality following

Publication Title

An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16207
Expression data from mouse liver infected with Ft LVS (without or with LPS pretreatment)
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
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Description

Background: It has been shown previously that administration of Francisella tularensis (Ft) LVS lipopolysaccharide (LPS) protects mice against subsequent challenge with Ft LVS and blunts the pro-inflammatory cytokine response.

Publication Title

Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE20523
Immunoregulatory actions of T cell PPAR g at the colonic mucosa
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon

Description

BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression.

Publication Title

The role of T cell PPAR gamma in mice with experimental inflammatory bowel disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24789
Expression data from mouse ovarian surface epithelium cells at different stages of malignancy
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Ovarian cancer is one of the most deadly cancers accounting for only 3% of diagnosed cancers, but is the fifth leading cause of cancer deaths among woman; however, the progression of ovarian cancer is poorly understood. To study and further understand the early events that lead to epithelial derived ovarian cancer, we previously developed a cell model of progressive ovarian cancer. Mouse ovarian surface epithelial (MOSE) cells have undergone spontaneous transformation in cell culture and represent pre-neoplastic, non-tumorigenic to an aggressive malignant phenotype.

Publication Title

Changes in gene expression and cellular architecture in an ovarian cancer progression model.

Sample Metadata Fields

Specimen part

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accession-icon GSE46443
Expression data from mouse cerebral cortex
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
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Description

Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains

Publication Title

A novel genetic locus modulates infarct volume independently of the extent of collateral circulation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE10598
Transcriptional profile of rapidly stimulated atrial myocytes: Conservation with human atrial fibrillation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Atrial fibrillation (AF) is a progressive arrhythmia for which current therapy is inadequate. During AF, rapid stimulation causes atrial remodeling that promotes further AF. The cellular signals that trigger this process remain poorly understood, however, and elucidation of these factors would likely identify new therapeutic targets. We have previously shown that immortalized mouse atrial (HL-1) myocytes subjected to 24 hr of rapid stimulation in culture undergo remodeling similar to that seen in animal models of atrial tachycardia (AT) and human AF. This preparation is devoid of confounding in vivo variables that can modulate gene expression (e.g., hemodynamics). Therefore, we investigated the transcriptional profile associated with early atrial cell remodeling. RNA was harvested from HL-1 cells cultured for 24 hr in the absence and presence of rapid stimulation and subjected to microarray analysis. Data were normalized using Robust Multichip Analysis (RMA), and genes exhibiting significant differential expression were identified using the Significance Analysis of Microarrays (SAM) method. Using this approach, 919 genes were identified that were significantly altered with rapid stimulation (763 up-regulated and 156 down-regulated). For many individual transcripts, changes typical of AF/AT were observed, with marked up-regulation of genes encoding BNP and ANP precursors, heat shock proteins, and MAP kinases, while novel signaling pathways and molecules were also identified. Both stress and survival response were evident, as well as up-regulation of multiple transcription factors. Genes were also functionally classified based on cellular component, biologic process, and molecular function using the Gene Ontology database to permit direct comparison of our data with other gene sets regulated in human AF and experimental AT. For broad categories of genes grouped by functional classification, there was striking conservation between rapidly stimulated HL-1 cells and AF/AT. Results were confirmed using real-time quantitative RT-PCR on 13 genes selected by physiological relevance in AF/AT and regulation in the microarray analysis (up, down, and nonregulated). Rapidly-stimulated atrial myocytes provide a complementary experimental paradigm to explore the initial cellular signals in AT remodeling to identify novel targets in the treatment of AF.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44091
Genome-wide expression of the epithelial layer cells of mice injected with Clostridium difficile Toxin A and B
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon

Description

Toxin A (TcdA) and Toxin B (TcdB), of the pathogen Clostridium difficile, are virulence factors that cause gross pathologic changes (e.g. inflammation, secretion, and diarrhea) in the infected host, yet the molecular and cellular pathways leading to observed host responses are poorly understood. To address this gap, TcdA and/or TcdB were injected into the ceca of mice and the genome-wide transcriptional response of epithelial layer cells was examined. Bioinformatic analysis of gene expression identified sets of cooperatively expressed genes. Further analysis of inflammation associated genes revealed dynamic chemokine responses.

Publication Title

In vivo physiological and transcriptional profiling reveals host responses to Clostridium difficile toxin A and toxin B.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24225
Expression analysis of mouse embryo fibrobalsts lacking Tgif1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

Tgif1 is a transcriptional corepressor that limits TGF responsive gene expression. TGF signaling has antiproliferative effects in several cell types, generally resulting in a G1 arrest. Mouse embryo fibroblasts (MEFs) are primary cells with limited life-span, that senesce after several passages in culture.

Publication Title

Premature senescence and increased TGFβ signaling in the absence of Tgif1.

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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