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accession-icon GSE70559
Gene expression patterns associated with histopathology in toxic liver injury
  • organism-icon Rattus norvegicus
  • sample-icon 94 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.1 ST Array (ragene21st)

Description

Predicting liver injury after exposure to toxic industrial chemicals is complicated by the large number of potential environmental contaminants, mixtures, and exposure dose and route scenarios. Identifying indicators of end organ injury can complement exposure-based assays and improve predictive power. A multiplexed approach was used to experimentally evaluate a panel of 67 genes predicted to be fibrogenic by computationally mining DrugMatrix, a publicly available repository of gene microarray data. Five-day oral gavage studies in male Sprague-Dawley rats dosed with varying concentrations of three fibrogenic compounds (allyl alcohol, carbon tetrachloride, and 4,4-methylenedianiline) and two non-fibrogenic compounds (bromobenzene and dexamethasone) were conducted. Fibrosis was definitively diagnosed by histopathology. Transcriptomics data matched the predictions made using the DrugMatrix data with greater than 90% accuracy. Microarray data were verified using a 67-plex panel Bioplex assay, confirming that the 67-plex panel constituted a biomolecular signature of hepatic fibrosis (Figure). Necrosis and inflammatory infiltration were comorbid with fibrosis. Interaction analysis identified 24 genes specific for the fibrosis phenotype. The protein product of the gene most strongly correlated with the fibrosis phenotype (Pcolce) was dose-dependently elevated in plasma from animals administered fibrogenic chemicals (p<0.05). PCOLCE is a novel biomarker candidate of fibrotic injury. These results support the development of gene panels for liver injury and may suggest bridging biomarkers for molecular mediators linked to histopathology.

Publication Title

Gene Expression Patterns Associated With Histopathology in Toxic Liver Fibrosis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP162537
AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose
  • organism-icon Mus musculus
  • sample-icon 111 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Purpose: To investigate alterations in subcutaneous white adipose gene expression induced by genetic AMPK activation in vivo, in mice fed a chow or a high-fat diet. Methods: Subcutaneous white adipose tissue mRNA profiles of wild-type transgenic (WT-Tg) mice and mice expressing a gain-of-function AMPK mutant gamma1 subunit (D316A-Tg) were generated by deep sequencing. Results: RNA sequencing revealed over 3000 differentially expressed genes between WT-Tg and D316A-Tg subcutaneous white adipose tissue (WATsc) from mice fed a high fat diet (HFD), of which many were classified as 'skeletal muscle-associated'. Interestingly, uncoupling protein 1 (UCP1), associated with 'beige' adipocyte formation in WATsc, was not differentially expressed. On a chow diet, many differentially expressed genes were also identified, with gene ontology analysis identifiying glycolysis, TCA cycle and brown fat differentiation as highly enriched; key features of brown adipocyte identity. HFD-associated skeletal-muscle associated gene expression was either not significantly altered, or significantly down-regulated on a chow diet, indicating a diet-induced gene signature in D316A-Tg WATsc. Conclusions: Our study revealed gene signatures indicative of brown adipocyte development on a chow diet, where no overt metabolic phenotype was observed in gain-of-function animals. When fed a HFD, WATsc from D316A-Tg mice displayed a muscle-like gene signature, expressing key components of creatine and calcium thermogenic cycles including Ckmt2 (creatine kinase, mitochondrial 2) Atp2a1 (SERCA1-sarco/endoplasmic reticulum ATPase 1) and ryr1 (ryanodine receptor 1). UCP1 expression was not altered between WT-Tg and D316A-Tg mice fed a HFD. Our findings suggest a novel role for AMPK in the regulation of white adipocyte identity and a potentially novel cell population that, when metabolically challenged, preferrentially utilise muscle-like thermogenic futile cycles independent of UCP1 to mediate whole organism energy expenditure. Overall design: Whole subcutaneous white adipose tissue mRNA profiles were generated from mice fed either chow or 45% high-fat diet.

Publication Title

AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose tissue.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE15840
Expression data for conditional Dnmt1knockout hematopoietic stem and progenitor cells
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

DNA methylation is essential for mammalian development and plays crucial roles in a variety of biological processes. The DNA methyltransferase Dnmt1 serves to maintain parental cell methylation patterns on daughter DNA strands in mitotic cells, however, the precise role of Dnmt1 in regulation of quiescent adult stem cells is not known.

Publication Title

DNA methyltransferase 1 is essential for and uniquely regulates hematopoietic stem and progenitor cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE49817
IL-2-dependent gene expression by human regulatory T cells
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This study determined the genes that are differetially expressed when regulatory T cells were stimulated in vitro with IL-2

Publication Title

Selective IL-2 responsiveness of regulatory T cells through multiple intrinsic mechanisms supports the use of low-dose IL-2 therapy in type 1 diabetes.

Sample Metadata Fields

Specimen part

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accession-icon GSE41005
HSF1 mediated Gene regulation in T cells at normal (37C) and febrile (40C) temperatures
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

HSF1 is a major transcriptional regulator of heat shock responses. Many cells activate HSF1 in response to heat shock temperatures (>42oC) and other cellular stress causing agents. Unlike other cell types, T cells activate HSF1 in response to T cell activation or when exposed to febrile (40oC) temperatures, suggesting a role for HSF1 beyond the heat-shock response.

Publication Title

Heat shock transcription factor 1 is activated as a consequence of lymphocyte activation and regulates a major proteostasis network in T cells critical for cell division during stress.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE9132
Identifying gene expression changes in adipose tissue of lipodystrophic mice
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A mouse model of conditional lipodystrophy.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE9130
aP2-nSREBP1c_white_Adipose_Tissue_expression_differentials
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Identifying gene expression changes in adipose tissue of lipodystrophic aP2-nSREBP1c trangenic mice

Publication Title

A mouse model of conditional lipodystrophy.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE9131
Pparg<ldi/+> white Adipose Tissue expression differentials
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Identifying gene expression changes in adipose tissue of lipodystrophic Pparg<ldi/+> targeted mice

Publication Title

A mouse model of conditional lipodystrophy.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP116949
Alveolar Injury and Regeneration Following Deletion of ABCA3
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Surfactant deficiency, diffuse alveolar damage and respiratory failure caused by loss of Abca3 in AT2 cells was followed by remarkable proliferation of alveolar cells and selective survival of ABCA3 sufficient cells resulting in regeneration of alveolar structure and function, providing the conceptual framework for the development of therapies to ameliorate lung diseases caused by mutations in ABCA3 and other genes critical for AT2 cell function or surfactant homeostasis. Overall design: Control and Abca3 cKO AT2 cell RNA-seq at 6 days post tamoxifen in adult mice.

Publication Title

Alveolar injury and regeneration following deletion of ABCA3.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP099844
Chemoprevention with COX2 and EGFR inhibition in FAP patients: mRNA signatures of duodenal neoplasia
  • organism-icon Homo sapiens
  • sample-icon 69 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNA sequencing of duodenal polyps in FAP patients treated with plabebo or the drug combination, erlotinib + sulindac Overall design: 69 duodenal RNA sequencing datasets (17 baseline uninvolved from 17 FAP patients, 10 endpoint uninvolved and 16 polyp from 10 FAP patients on placebo, 10 endpont uninvolved and 16 polyp from 10 FAP patients on drug)

Publication Title

Chemoprevention with Cyclooxygenase and Epidermal Growth Factor Receptor Inhibitors in Familial Adenomatous Polyposis Patients: mRNA Signatures of Duodenal Neoplasia.

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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