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accession-icon GSE51089
Expression data from E12.5 and E14.5 mouse embryonic gonad of wild type (WT) and Wnt-4 knock-out (KO) mice. [Mouse430_2]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
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Description

Wnt-4 signaling is critical for embryonic female sexual development. When Wnt-4 gene is deleted during embryonic development, the knock-out females present a partial sex reversal.

Publication Title

Identification of the genes regulated by Wnt-4, a critical signal for commitment of the ovary.

Sample Metadata Fields

Specimen part

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accession-icon GSE95278
Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy.

Publication Title

Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE6514
Gene expression in the mouse brain during spontaneous sleep and prolonged wakefulness
  • organism-icon Mus musculus
  • sample-icon 86 Downloadable Samples
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Description

These studies address temporal changes in gene expression during spontaneous sleep and extended wakefulness in the mouse cerebral cortex, a neuronal target for processes that control sleep; and the hypothalamus, an important site of sleep regulatory processes. We determined these changes by comparing expression in sleeping animals sacrificed at different times during the lights on period, to that in animals sleep deprived and sacrificed at the same diurnal time.

Publication Title

Macromolecule biosynthesis: a key function of sleep.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE33744
Cross-species transcriptional networks in Diabetic Glomerulopathy in mouse and man
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
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Description

Murine models have been valuable instruments in defining the pathogenesis of diabetic nephropathy (DN), but they only partially recapitulate disease manifestations of human DN, limiting their utility . In order to define the molecular similarities and differences between human and murine DN, we performed a cross-species comparison of glomerular transcriptional networks. Glomerular gene expression was profiled in patients with early type 2 DN and in three mouse models (streptozotocin DBA/2 mice, db/db C57BLKS, and eNOS-deficient C57BLKS db/db mice). Species-specific transcriptional networks were generated and compared with a novel network-matching algorithm. Three shared, human-mouse cross-species glomerular transcriptional networks containing 143 (Human-STZ), 97 (Human- db/db), and 162 (Human- eNOS-/- db/db) gene nodes were generated. Shared nodes across all networks reflected established pathogenic mechanisms of diabetic complications, such as elements of JAK-STAT and VEGFR signaling pathways . In addition, novel pathways not formally associated with DN and cross-species gene nodes and pathways unique to each of the human-mouse networks were discovered. The human-mouse shared glomerular transcriptional networks will assist DN researchers in the selection of mouse models most relevant to the human disease process of interest. Moreover, they will allow identification of new pathways shared between mice and humans.

Publication Title

Identification of cross-species shared transcriptional networks of diabetic nephropathy in human and mouse glomeruli.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE27628
Expression data from affected skin from psoriasis mouse models and normal skin from control mice
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
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Description

Development of a suitable mouse model would facilitate the investigation of pathomechanisms underlying human psoriasis and would also assist in development of therapeutic treatments. However, while many psoriasis mouse models have been proposed, no single model recapitulates all features of the human disease, and standardized validation criteria for psoriasis mouse models have not been widely applied. In this study, whole-genome transcriptional profiling is used to compare gene expression patterns manifested by human psoriatic skin lesions with those that occur in five psoriasis mouse models (K5-Tie2, imiquimod, K14-AREG, K5-Stat3C and K5-TGFbeta1). While the cutaneous gene expression profiles associated with each mouse phenotype exhibited statistically significant similarity to the expression profile of psoriasis in humans, each model displayed distinctive sets of similarities and differences in comparison to human psoriasis. For all five models, correspondence to the human disease was strong with respect to genes involved in epidermal development and keratinization. Immune and inflammation-associated gene expression, in contrast, was more variable between models as compared to the human disease. These findings support the value of all five models as research tools, each with identifiable areas of convergence to and divergence from the human disease. Additionally, the approach used in this paper provides an objective and quantitative method for evaluation of proposed mouse models of psoriasis, which can be strategically applied in future studies to score strengths of mouse phenotypes relative to specific aspects of human psoriasis.

Publication Title

Genome-wide expression profiling of five mouse models identifies similarities and differences with human psoriasis.

Sample Metadata Fields

Specimen part

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accession-icon GSE42473
PGC-1 alpha isoforms and muscle hypertrophy
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
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Description

An alternative promoter of the PGC-1alpha gene gives rise to three new PGC-1alpha isoforms refered to as PGC-1a2 (A2), PGC-1a3 (A3) and PGC-1a4 (A4). The proximal PGC-1 alpha promotor transcribes the canonical PGC-1 alpha which is refered to as PGC-1a1 (A1).G1/G2/G3 samples refer to the Green fluorescent protein (GFP) control samples used in this experiment. Forced expression of the PGC-1a4 isoform results in muslce hypertrophy associated with increased IGF-1 signaling and repression of myostatin signaling.

Publication Title

A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy.

Sample Metadata Fields

Specimen part

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accession-icon GSE16454
Gene expression data from small intestines
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
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Description

Rb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo.

Publication Title

E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE16073
Expression Data from Pten Null Fibroblasts
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

The tumor stroma is believed to contribute to some of the most malignant characteristics of epithelial tumors. However, signaling between stromal and tumor cells is complex and remains poorly understood. Here we show that genetic inactivation of Pten in stromal fibroblasts of mouse mammary glands accelerated the initiation, progression and malignant transformation of mammary epithelial tumors.

Publication Title

Pten in stromal fibroblasts suppresses mammary epithelial tumours.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE57729
Differential expression of mouse Grem1+ Vs. Grem1- bone-marrow cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

The gene expression of bone marrow cells of mice enriched for

Publication Title

Gremlin 1 identifies a skeletal stem cell with bone, cartilage, and reticular stromal potential.

Sample Metadata Fields

Sex, 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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