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accession-icon GSE18768
Transcriptome analysis of epithelial and stromal contributions to mammogenesis in prepartum dry cows
  • organism-icon Bos taurus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

Our overall objective is to identify key differences in gene expression signaling pathways in the epithelial and intralobular stromal compartments during prepartum mammary remodeling and development in the dry cow.

Publication Title

Transcriptome analysis of epithelial and stromal contributions to mammogenesis in three week prepartum cows.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE77084
Liver of MAT1A WT and MAT1A KO mice treated with placebo or SAMe during 8 weeks
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE77082
Gene expression analysis of the liver of MAT1A WT and MAT1A KO mice treated with placebo or SAMe during 8 weeks
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Methionine adenosyltransferase (MAT) enzymes generate SAMe (S-adenosylmethionine), the main biological methyl donor. There are two MAT encoding genes in mammals (Mat1a and Mat2a), which show different activities and cellular distribution. Mat1a encodes the enzyme mainly expressed in normal liver. Mat1a ablation in mice results in the spontaneous development of non-alcoholic steatohepatitis (NASH). We observed that SAMe depletion in Mat1a KO mice had three main effects on hepatic lipid metabolism: 1) impaired TG (triglyceride) export via VLDL; 2) impaired mitochondrial FA (fatty acid) oxidation (as evidenced by membrane depolarization, downregulation of Phb1 (prohibitin 1, a mitochondrial chaperone protein) and Mcj/Dnajc15 (endogenous mitochondrial repressor of respiratory chain), and accumulation of long-chain acylcarnitines); and 3) increased FA uptake. The convergence of these three factors induced TG accumulation in LD (lipid droplets). LD expansion confronts hepatocytes with a high demand of PC (phosphatidylcholine) molecules to cover the LD surface since other phospholipids, such as PE (phosphatidylethanolamine), cannot stabilize LD and prevent coalescence. In Mat1a KO this situation is aggravated, since SAMe-dependent PC synthesis via PE methylation is decreased, the PC/PE ratio reduced and mitochondrial FA oxidation impaired. To put a brake to this drain of PC molecules to LD, FA are rerouted in Mat1a KO mice liver to other catabolic (endoplasmic reticulum and peroxisome oxidation) and biosynthetic (ceramides synthesis) pathways, causing oxidative stress, inflammation and fibrosis. SAMe treatment for two months in 8-9 month old Mat1a KO mice ameliorated mitochondrial dysfunction (reduces membrane depolarization, improves Phb1 and Mcj expression, and increases SAMe transport to mitochondria) improving FA oxidation efficiency (FA and acylcarnitine levels decrease), which results in a drastic reduction in TG accumulation. SAMe treatment in Mat1a KO mice resulted in more PC available for proper membrane function, improving liver lipid homeostasis, histology (H&E, Sudan red, Sirius red) and liver injury (ALT, AST).

Publication Title

Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE33943
Gene expression profiles of pediatric IBD remission patients
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Clinical remission is apparent when laboratory markers of inflammation are normal and clinical symptoms are absent. However, sub-clinical inflammation can still be present. A detailed analysis of the immune status during this inactive state of disease may provide a useful tool to subcategorize patients with subclinical immune activation

Publication Title

Gene expression analysis of peripheral cells for subclassification of pediatric inflammatory bowel disease in remission.

Sample Metadata Fields

Specimen part

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accession-icon GSE97150
Genexpression of murine mesothelioma cell lines AC29 and AB1
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

RNA from two murine mesothelioma cell lines (AC29 and AB1) was extracted and hybridized to Affymetrix Microarrays to compare gene expression. Both mesothelioma cell lines were established following intraperitoneal introduction of crocidolite (asbestos) fibers (Davis et al. 1992) in CBA mice (AC29 cell line), and BALB/c mice (AB1).

Publication Title

Depletion of Tumor-Associated Macrophages with a CSF-1R Kinase Inhibitor Enhances Antitumor Immunity and Survival Induced by DC Immunotherapy.

Sample Metadata Fields

Sex

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accession-icon GSE65472
Identification of IL-22 regulated genes in the ileum after infection with Toxoplasma gondii
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

IL-22 acts on epithelial cells and has been shown to induce tissue protective and wound healing responses in these cells. But it has recently been decribed that IL-22 exacerbates ileatis after infection with T. gondii.

Publication Title

Interleukin-22 induces interleukin-18 expression from epithelial cells during intestinal infection.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE50572
Gene signature of CLL cells cultured with activated T cells or CD40L-expressing cells
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Chronic Lymphocytic Leukemia (CLL) cells multiply in secondary lymphoid tissue but the mechanisms leading to their proliferation are still uncertain. In addition to BCR-triggered signals, other microenvironmental factors might well be involved. In proliferation centres, leukemic B cells are in close contact with CD4+CD40L+T cells. Therefore, we here dissected the signals provided by autologous activated T cells (Tact) to CLL cells. Although the gene expression profile induced by Tact was highly similar to that induced by sole CD40 signaling, an obvious difference was that Tact induced proliferation of CLL cells. We determined that stimulation with only CD40L+IL-21 was sufficient to induce robust proliferation in CLL cells. We then defined an IL-21-induced gene signature in CLL, containing components of JAK-STAT and apoptosis pathways, and this signature could be detected in lymph node (LN) samples from patients. Finally, we could detect IL-21 RNA and protein in LN, and IL-21 productionex vivoby LN CD4+CXCR5+ follicular helper T cells. These results indicate that, in addition to BCR signaling, activated T cells might contribute to CLL cell proliferation via CD40 and IL-21. Targeting these signaling pathways might offer new venues for treatment of CLL.

Publication Title

IL-21 and CD40L signals from autologous T cells can induce antigen-independent proliferation of CLL cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP094007
Quantitative Proteomics Reveals a Unique Wiring of Signaling Pathways that Protects Human Regulatory T Cell Identity
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Regulatory CD4+ T cells (Tregs) are functionally distinct from conventional CD4+ T cells (Tconvs). To understand Treg identity, we have compared by proteomics and transcriptomics human naïve (n) and effector (e)Tregs, Tconvs and transitional FOXP3+ cells. Among these CD4+ T cell subsets, we detected differential expression of 421 proteins and 640 mRNAs, with only 48 molecules shared. Fifty proteins discriminated Tregs from Tconvs. This common Treg protein signature indicates altered signaling by TCR-, TNF receptor-, NFkB-, PI3 kinase/mTOR-, NFAT- and STAT pathways and unique cell biological and metabolic features. Another protein signature uniquely identified eTregs and revealed active cell division, apoptosis sensitivity and suppression of NFkB- and STAT signaling. eTreg fate appears consolidated by FOXP3 outnumbering its partner transcription factors. These features explain why eTregs cannot produce inflammatory cytokines, while transitional FOXP3+ cells can. Our collective data reveal that Tregs protect their identity by a unique “wiring” of signalling pathways Overall design: mRNA profiles of 5 CD4+ T cell populations were generated by deep sequencing, in triplicate

Publication Title

Proteomic Analyses of Human Regulatory T Cells Reveal Adaptations in Signaling Pathways that Protect Cellular Identity.

Sample Metadata Fields

Subject

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accession-icon GSE101973
Comparisonof kPSCs versus cMSC
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

expression profiles kPSCs versus cMSC

Publication Title

The human kidney capsule contains a functionally distinct mesenchymal stromal cell population.

Sample Metadata Fields

Specimen part

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accession-icon GSE36244
Transcriptomic response to benzo[a]pyrene treatment in HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

RNA-Seq provides new insights in the transcriptome responses induced by the carcinogen benzo[a]pyrene.

Sample Metadata Fields

Cell line, Compound, 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)

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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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