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accession-icon GSE22534
Expression data from PDK4 overexpressing (Ad-PDK4 infected) and control (Ad-control infected) mouse liver
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We identified PDK4 as a gene with adaptive transcriptional response to chemical stress. Although PDK4 is an energy resource regulator induced by starvation, expression of other fasting-inducible genes was unaffected, indicating additional physiological role of PDK4 for liver adaptation to the chemical stress.

Publication Title

Adaptive gene regulation of pyruvate dehydrogenase kinase isoenzyme 4 in hepatotoxic chemical-induced liver injury and its stimulatory potential for DNA repair and cell proliferation.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP078248
Adrenalectomy plus corticosterone treatment, rat hippocampal RNA-seq
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Male Sprague-Dawley rats 8 weeks old, were adrenalectomized, treated with 300ug/kg corticosterone or vehicle 3 days after surgery then sacrificed 1 hour later. Hippocampi were removed and RNA extracted and processed for sequencing at the Massachusetts General Hospital Nex-Generation Sequening Core. Overall design: Includes 6 cort treated and 6 control biological replicates

Publication Title

Stress and corticosteroids regulate rat hippocampal mitochondrial DNA gene expression via the glucocorticoid receptor.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7694
Cannabinoid receptor double knockout mice (Cnr1 -/- /Cnr2 -/-) in CHS model
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We evaluated cutaneous contact hypersensitivity (CHS) in Cnr1-/-/Cnr2-/- animals using the obligate contact allergen 2,4-dinitrofluorobenzene (DNFB), which generates a specific cutaneous T-cell mediated allergic response upon repeated allergen contact. Allergic contact dermatitis affects about 5% of men and 11% of women in industrialized countries and is one of the leading causes for occupational diseases. In an animal model for cutaneous contact hypersensitivity we show that mice lacking both known cannabinoid receptors display exacerbated allergic inflammation. In contrast, fatty acid amide hydrolase deficient mice, which have increased levels of the endocannabinoid anandamide, displayed reduced allergic responses in the skin. Cannabinoid receptor antagonists exacerbated whereas receptor agonists attenuated allergic inflammation. These results demonstrate a protective role of the endocannabinoid system in contact allergy in the skin, and suggest a novel target for therapeutic intervention.

Publication Title

Attenuation of allergic contact dermatitis through the endocannabinoid system.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12161
Transcriptome profiling of control and TNFalpha treated HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The proinflammatory cytokine, TNFalpha is critical in maintaining liver homeostasis since it is a major determiner of hepatocyte life and death. Considering this, gene transcription profiling was examined in control and TNFalpha treated HepG2 cells. Results indicated that TNFalpha could significantly alter the expression of a significant number of genes; most of them were functionally distributed among molecular functions like catalytic activity, binding, molecular transducer activity, transporter activity, translation and transcription regulator activities or enzyme regulator activity. Also, within genes up-regulated by TNFalpha, several GO terms related to lipid and fat metabolism were significantly overrepresented indicating global dysregulation of fat metabolism within the hepatocyte and those within the down-regulated dataset included genes involved in immunoglobulin receptor activity and IgE binding thereby indicating a compromise in immune defense mechanism(s) apart from those involved the DNA binding and protein binding categories. The interacting network of lipid metabolism, small molecule biochemistry was derived to be significantly affected that correlated well with the top canonical pathway of biosynthesis of steroids and molecular and cellular function of lipid metabolism. All these indicate TNFalpha to be significantly altering the transcriptome profiling within HepG2 cells with genes involved in lipid and steroid metabolism being the most favoured. This study suitably addresses the genes that determine TNFalpha mediated alterations within the hepatocyte mainly the phenotypes of hepatic steatosis and fatty liver that are associated with several hepatic pathological states.

Publication Title

Gene expression profiling and network analysis reveals lipid and steroid metabolism to be the most favored by TNFalpha in HepG2 cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE77533
Transcriptome profiling of SW480 cells treated or untreated with Floxuridine (FUdR)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Colorectal cancer cells with TP53 mutation are highly resistant to chemotherapeutics. In order to identify potential chemo-resistance signatures, here; we explored the global gene expression profiles of drug resistant colorectal cancer cell line SW480 upon Floxuridine (FdUrd) treatment using Illumina Human HT-12 v4.0 Expression Beadchip Array. Further, significantly altered genes were subjected to the pathway analysis in GeneCodis3 and crucial signaling pathways were found to be enriched. Upon further functional validations, these pathways could be targeted to enhance therapy in human cancers harboring mutant p53.

Publication Title

Transcriptome profiling identifies genes and pathways deregulated upon floxuridine treatment in colorectal cancer cells harboring GOF mutant p53.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Treatment

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accession-icon GSE36933
Regulation of Pattern Recognition Receptors by the Apolipoprotein A-I Mimetic Peptide 4F
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The apolipoprotein A-I (apoA-I) mimetic peptide 4F displays prominent anti-inflammatory properties, including the ability to reduce vascular macrophage content. Macrophages are a heterogenous group of cells, represented by two principal phenotypes, the classically activated M1 macrophage and an alternatively activated M2 phenotype. We recently reported that 4F favors the differentiation of human monocytes to an anti-inflammatory phenotype similar to that displayed by M2 macrophages. In the current study, microarray analysis of gene expression in monocyte-derived macrophages (MDMs) was carried out to identify inflammatory pathways modulated by 4F treatment. ApoA-I treatment of MDMs served as a control. Transcriptional profiling revealed that 4F and apoA-I modulated expression of 113 and 135 genes that regulate inflammatory responses, respectively. Cluster heat maps revealed that 4F and apoA-I induced similar changes in expression for 69 common genes. Modulation of other gene products, including STAT1 and PPARG, were unique for 4F treatment. Besides modulating inflammatory responses, 4F was found to alter gene expression in cell-to-cell signaling, cell growth/proliferation, lipid metabolism and cardiovascular system development. These data suggest that the protective effects of 4F in a number of disease states may be due to underlying changes in monocyte/macrophage gene expression.

Publication Title

Regulation of pattern recognition receptors by the apolipoprotein A-I mimetic peptide 4F.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP110478
mRNA sequencing of wild type Columbia and serrate-1 globular stage embryos of Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Wild type Columbia and serrate-1 globular stage embryos were sequenced in order to profile miRNAs which are expressed in embryogenesis in Arabidopsis thaliana Overall design: Two biological replicates, two conditions

Publication Title

Arabidopsis thaliana miRNAs promote embryo pattern formation beginning in the zygote.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE71219
Gene Expression in Human Vastus Lateralis after PrimaVie Shilajit Supplementation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Changes in Gene exporession after 8 weeks of PrimaVie Shilajit Supplementation were measured in vastus lateralis

Publication Title

The Human Skeletal Muscle Transcriptome in Response to Oral Shilajit Supplementation.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE59338
Expression data from Dnmt3a-deficient and control mouse MYC induced T-cell lymphomas
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dnmt3a catalyzes DNA methylation of gDNA, which contributes to the transriptional regulations of genes and genomic stability.

Publication Title

Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE33892
Comparison of TEX and M9-ENL1 cell lines to HL60 and THP1 cell lines
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Gene regulatory networks that govern hematopoietic stem cells (HSC) and leukemiainitiating cells (L-IC) are deeply entangled. Thus, the discovery of compounds that target L-IC while sparing HSC is an attractive but difficult endeavor. Presently, most drug discovery approaches fail to counter-screen compounds against normal hematopoietic stem/progenitor cells (HSPC) to assess therapeutic index. Here, we present a combined in vitro and in vivo strategy to identify compounds specific to L-IC in acute myeloid leukemia (AML). A high-throughput screen of 4000 compounds on novel leukemia cell lines derived from human experimental leukemogenesis models yielded 80 hits, of which most were toxic to normal HSPC. Of the 10 compounds that passed this initial filter, we chose to characterize a single compound, kinetic riboside (KR), on AML L-IC and HSPC. KR demonstrated comparable efficacy to standard therapies against 63 primary AMLs. In vitro, KR effectively targeted the L-IC-enriched CD34+CD38- AML fraction, while sparing normal HSPC enriched fractions, although these effects were mitigated on HSC assayed in vivo, and highlights the importance of in vivo L-IC and HSC assays to measure function. Overall, we provide a novel approach to screen large drug libraries for the discovery of anti-L-IC compounds for human leukemias.

Publication Title

A small molecule screening strategy with validation on human leukemia stem cells uncovers the therapeutic efficacy of kinetin riboside.

Sample Metadata Fields

Cell line, 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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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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