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accession-icon GSE22307
Expression data from mouse colon tissue response to DSS induction at day 0, 2, 4 and 6
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

Temporal genome profiling of DSS colitis

Publication Title

Temporal genomewide expression profiling of DSS colitis reveals novel inflammatory and angiogenesis genes similar to ulcerative colitis.

Sample Metadata Fields

No sample metadata fields

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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 GSE37382
Subgroup specific somatic copy number aberrations in the medulloblastoma genome [mRNA]
  • organism-icon Homo sapiens
  • sample-icon 285 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Affymetrix Human Gene 1.1 ST Array profiling of 285 primary medulloblastoma samples.

Publication Title

Subgroup-specific structural variation across 1,000 medulloblastoma genomes.

Sample Metadata Fields

Sex, Age

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accession-icon GSE32422
Expression data from the dorsal and lateral lobes of the prostates of TRAMP mice treated with OSU-CG5
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Cells undergoing malignant transformation often shift their cellular metabolism from primarily oxidative phosphorylation to aerobic glycolysis (the Warburg effect). Energy restriction-mimetic agents (ERMAs), such as 2-deoxyglucose and resveratrol, that target this shift in cellular metabolism have been effective in inhibiting cancer cell growth in vitro, and xenograft tumor growth in vivo.

Publication Title

Suppression of prostate epithelial proliferation and intraprostatic progrowth signaling in transgenic mice by a new energy restriction-mimetic agent.

Sample Metadata Fields

Specimen part

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accession-icon GSE34773
Skeletal muscle PGC-1a mediates mitochondrial, but not metabolic, changes during calorie restriction.
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

Calorie restriction (CR) is a dietary intervention that extends lifespan and healthspan in a variety of organisms. CR improves mitochondrial energy production, fuel oxidation and reactive oxygen species scavenging in skeletal muscle and other tissues, and these processes are thought to be critical to the benefits of CR. PGC-1a is a transcriptional coactivator that regulates mitochondrial function and is induced by CR. Consequently, many of the mitochondrial and metabolic benefits of CR are attributed to increased PGC-1a activity. To test this model for the first time, we examined the metabolic and mitochondrial response to CR in mice lacking skeletal muscle PGC-1a (MKO). Surprisingly, MKO mice demonstrated a normal improvement in glucose homeostasis in response to CR, indicating that skeletal muscle PGC-1a is dispensable for the whole-body benefits of CR. In contrast, gene expression profiling and electron microscopy demonstrated that PGC-1a is required for the full CR-induced increases in mitochondrial gene expression and mitochondrial density in skeletal muscle. These results demonstrate that PGC-1a is a major regulator of the mitochondrial response to CR in skeletal muscle, but surprisingly show that neither PGC-1a nor mitochondrial biogenesis in skeletal muscle are required for the metabolic benefits of CR.

Publication Title

Skeletal muscle transcriptional coactivator PGC-1α mediates mitochondrial, but not metabolic, changes during calorie restriction.

Sample Metadata Fields

Specimen part

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accession-icon GSE61555
Treatment of C3H/HeJ grafted mice with baricitinib
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Reversal of Alopecia Areata Following Treatment With the JAK1/2 Inhibitor Baricitinib.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE61554
Treatment of C3H/HeJ grafted mice with baricitinib [topical]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

The C3H/HeJ grafted model of alopecia areata was used to determine the efficacy of systemic baricitinib at preventing alopecia or treating established disease.

Publication Title

Reversal of Alopecia Areata Following Treatment With the JAK1/2 Inhibitor Baricitinib.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE61552
Treatment of C3H/HeJ grafted mice with baricitinib [systemic]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

The C3H/HeJ grafted model of alopecia areata was used to determine the efficacy of systemic baricitinib at preventing alopecia or treating established disease.

Publication Title

Reversal of Alopecia Areata Following Treatment With the JAK1/2 Inhibitor Baricitinib.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE27309
SIRT3 opposes metabolic reprogramming of cancer cells through HIF1a destabilization
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Tumor cells exhibit aberrant metabolism characterized by high glycolysis even in the presence of oxygen. This metabolic reprogramming, known as the Warburg effect, provides tumor cells with the substrates and redox potential required for the generation of biomass. Here, we show that the mitochondrial NAD-dependent deacetylase SIRT3 is a crucial regulator of the Warburg effect. SIRT3 loss promotes a metabolic profile consistent with high glycolysis required for anabolic processes in vivo and in vitro. Mechanistically, SIRT3 mediates metabolic reprogramming independently of mitochondrial oxidative metabolism and through HIF1a, a transcription factor that controls expression of key glycolytic enzymes. SIRT3 loss increases reactive oxygen species production, resulting in enhanced HIF1a stabilization. Strikingly, SIRT3 is deleted in 40% of human breast cancers, and its loss correlates with the upregulation of HIF1a target genes. Finally, we find that SIRT3 overexpression directly represses the Warburg effect in breast cancer cells. In sum, we identify SIRT3 as a regulator of HIF1a and a suppressor of the Warburg effect.

Publication Title

SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization.

Sample Metadata Fields

Specimen part

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accession-icon GSE45551
Prevention of Mouse AA with IL-15 pathway inhibitors
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon

Description

Our goal was to identify gene expression patterns that correlated with prevention of autoimmune alopecia in C3H/HeJ mice following alopecic graft transplantation

Publication Title

Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

Sample Metadata Fields

Specimen part, Treatment

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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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