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accession-icon E-CBIL-24
Transcription profiling of liver from B6 and 129 mice fed on low and high fat diets
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Both environmental and genetic factors play important roles in the development of the metabolic syndrome. To elucidate how these factors interact under normal conditions, C57Bl/6 (B6) and 129S6/SvEvTac (129) mice were placed on a low-fat or high-fat diet. Liver samples were extracted and hybridized to Affymetrix Genome U74 (version 2) arrays.

Publication Title

Effects of diet and genetic background on sterol regulatory element-binding protein-1c, stearoyl-CoA desaturase 1, and the development of the metabolic syndrome.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE2926
Gene Expression Profiles of Scd1 knockout mice vs wild type mice on chow diet: Liver.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Array (mgu74a)

Description

Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity.

Publication Title

Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3889
Scd1 Knockout Mice on very low fat diet
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat, high-carbohydrate (VLF-HC) diet, SCD1-/- mice develop severe hypercholesterolemia characterized by an increase in apolipoprotein B-containing lipoproteins and the appearance of lipoprotein-X. Additionally, high-density lipoprotein cholesterol is dramatically reduced in VLF-HC SCD1-/- mice. The concomitant presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF-HC SCD1-/- mouse are indicative of hepatic dysfunction. Supplementation of the VLF-HC diet with unsaturated fat (canola oil), but not saturated fat (coconut oil), prevents these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing low-density lipoprotein cholesterol, signifying an additional role for dietary polyunsaturated fatty acid deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction.

Publication Title

Cholestasis and hypercholesterolemia in SCD1-deficient mice fed a low-fat, high-carbohydrate diet.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP127399
Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

This study demonstrates that arthritis and heart valve stenosis comorbidity, the most common condition among RA and SpA patients, share common mesenchymal requirements converging in the pathogenic activation of resident mesenchymal origin fibroblasts in the Tnf?ARE mouse model. TNFR2 signaling, in this context, orchestrates the molecular mechanisms underlying arthritis and heart valve stenosis manifestation by regulating fibroblasts pathogenic activation status, cell proliferation and pro-inflammatory milieu. Finally this work highlights the complexity of TNFR2 functions since mesenchymal signaling is detrimental, whereas systemic TNFR2 provides protective signals that contain both pathologies Overall design: 3' RNA-Seq (QuantSeq) profiling of 2 cell types (SFs,VICs) in two different genotypes (TNF-DeltaARE, ColVIp75f/f-TNF-DeltaARE) and Wild type as control. 3 replicates per group.

Publication Title

Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE56285
N-octanoyl dopamine treatment of endothelial cells induces the unfolded protein response and results in hypometabolism and tolerance to hypothermia
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

N-octanoyl dopamine (NOD), but not dopamine dose dependently induces the UPR. This was also found for other synthetic N-Acyl dopamine derivates (NADD). Induction of the UPR was dependent on the redox activity of NADD and was not caused by selective activation of a particular UPR sensor. UPR induction did not result in cell apoptosis, yet NOD strongly impaired cell proliferation by attenuation of cells in the S-G2/M phase. Long-term treatment of HUVEC with low NOD concentration showed decreased intracellular ATP concentration paralleled with activation of AMPK. These cells were significantly more resistant to cold inflicted injury.

Publication Title

N-octanoyl dopamine treatment of endothelial cells induces the unfolded protein response and results in hypometabolism and tolerance to hypothermia.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP174055
Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Lung adenocarcinoma (LUAD)-derived oncogenic Wnts increase cancer cell proliferative/stemness potential, but whether they also impact the immune microenvironment is unknown. Here we show that LUAD cells use paracrine Wnt1 signaling to induce immune resistance. Wnt1 correlated strongly with tolerogenic genes on the TCGA expression data. In another cohort, Wnt1 was inversely associated with T cell abundance. Altering Wnt1 expression profoundly affected growth of murine lung adenocarcinomas and this was strongly dependent on conventional dendritic cells and T cells. Mechanistically, Wnt1 lead to transcriptional silencing of CC/CXC chemokines in dendritic cells and T cell cross-tolerance. Wnt-target genes were up-regulated in human intratumoral dendritic cells and decreased upon silencing Wnt1, accompanied by enhanced T cell cytotoxicity. siWnt1-loaded nanoparticles as single therapy or part of combinatorial immunotherapies acted at both arms of the cancer-immune ecosystem to halt tumor growth. Collectively, our studies show that Wnt1 enhances adaptive immune rejection of lung adenocarcinomas and highlight its potential targeting as a novel therapeutic strategy  Overall design: RNAseq data of two DC subsets of 4 patients with lung adenocarcinomas (LUADs).

Publication Title

Wnt1 silences chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon SRP171054
Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

This study showed that the oncogenic ligand Wnt1 silences chemokine genes in dendritic cells, leading to impaired cross-priming of T cells in lung adenocarcinoma. Blocking Wnt1 enhanced rejection of tumors by acting concomitantly at the cancer and immune cell level. Overall design: 3' RNA-Seq (QuantSeq) profiling of sorted cDCs populations from WNT1 overexpressing and control (Empty) lung tumors.

Publication Title

Wnt1 silences chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE74309
Comparison of wild type mouse lung cancer cell lines to transfected cell lines with Nras sh RNA
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

We compared different mouse cancer cell lines to identify their unique cell signatures.

Publication Title

<i>NRAS</i> destines tumor cells to the lungs.

Sample Metadata Fields

Specimen part, Cell line

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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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