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accession-icon GSE17865
Transcriptional profiling reveals divergent roles of PPARa and PPAR/d in regulation of gene expression in mouse liver
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) but not PPARalpha serves as a plasma free fatty acid sensor in liver.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE10682
Comparison of parental vs tumor-derived imortalized mouse kidney epithelial cell (iBMK) lines
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Most tumors are epithelial-derived, and although disruption of polarity and aberrant cellular junction formation is a poor prognosticator in human cancer, the role of polarity determinants in oncogenesis is poorly understood. Using in vivo selection, we identified a mammalian orthologue of the Drosophila polarity regulator crumbs as a gene whose loss of expression promotes tumor progression. Immortal baby mouse kidney epithelial (iBMK) cells selected in vivo to acquire tumorigenicity displayed dramatic repression of crumbs3 (crb3) expression associated with disruption of tight junction formation, apicobasal polarity, and contact-inhibited growth. Restoration of crb3 expression restored junctions, polarity and contact inhibition, while suppressing migration and metastasis. These findings suggest a role for mammalian polarity determinants in suppressing tumorigenesis that may be analogous to the well-studied polarity tumor suppressor mechanisms in Drosophila.

Publication Title

Role of the polarity determinant crumbs in suppressing mammalian epithelial tumor progression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE56352
Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays.

Publication Title

Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE25547
Profiling of promoter occupancy by PPAR in human hepatoma cells via ChIP-chip analysis
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transcription factor Peroxisome Proliferator-Activated Receptor (PPAR) is an important regulator of hepatic lipid metabolism. While PPAR is known to activate transcription of numerous genes, no comprehensive picture of PPAR binding to endogenous genes has yet been reported. To fill this gap, we performed ChIP-chip in combination with transcriptional profiling on HepG2 human hepatoma cells treated with the PPAR agonist GW7647. We found that GW7647 increased PPAR binding to 4220 binding regions. GW7647-induced binding regions showed a bias around the transcription start site and most contained a predicted PPAR binding motif. Several genes known to be regulated by PPAR, such as ACOX1, SULT2A1, ACADL, CD36, IGFBP1 and G0S2, showed GW7647-induced PPAR binding to their promoter. A GW7647-induced PPAR-binding region was also assigned to SREBP-targets HMGCS1, HMGCR, FDFT1, SC4MOL, and LPIN1, expression of which was induced by GW7647, suggesting cross-talk between PPAR and SREBP signaling. Our data furthermore demonstrate interaction between PPAR and STAT transcription factors in PPAR-mediated transcriptional repression, and suggest interaction between PPAR and TBP and C/EBP in PPAR-mediated transcriptional activation. Overall, our analysis leads to important new insights into the mechanisms and impact of transcriptional regulation by PPAR in human liver and highlight the importance of cross-talk with other transcription factors.

Publication Title

Profiling of promoter occupancy by PPARalpha in human hepatoma cells via ChIP-chip analysis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE46416
State- and trait-specific gene expression in euthymia and mania
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2,coreR3,A20071112,EP.cdf (huex10st)

Description

Gene expression profiles of bipolar disorder (BD) patients were assessed during both a manic and a euthymic phase and compared both intra-individually, and with the gene expression profiles of controls.

Publication Title

Investigation of manic and euthymic episodes identifies state- and trait-specific gene expression and STAB1 as a new candidate gene for bipolar disorder.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon GSE65945
Transcriptional profiling of proliferating and differentiating SPC04 human neural stem cell line
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Here we used microarray expression profiling to characterise global changes in gene expression during stages of proliferation and differentiation of human neural stem cells

Publication Title

Associations of the Intellectual Disability Gene MYT1L with Helix-Loop-Helix Gene Expression, Hippocampus Volume and Hippocampus Activation During Memory Retrieval.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP119455
Innate immune memory in the brain shapes neurological disease hallmarks [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Innate immune memory is a vital mechanism of myeloid cell plasticity that occurs in response to environmental stimuli and alters subsequent immune responses. Two types of immunological imprinting can be distinguished—training and tolerance. These are epigenetically mediated and enhance or suppress subsequent inflammation, respectively. Whether immune memory occurs in tissue-resident macrophages in vivo and how it may affect pathology remains largely unknown. Here we demonstrate that peripherally applied inflammatory stimuli induce acute immune training and tolerance in the brain and lead to differential epigenetic reprogramming of brain-resident macrophages (microglia) that persists for at least six months. Strikingly, in a mouse model of Alzheimer's pathology, immune training exacerbates cerebral beta-amyloidosis and immune tolerance alleviates it; similarly, peripheral immune stimulation modifies pathological features after stroke. Our results identify immune memory in the brain as an important modifier of neuropathology. Overall design: mRNA was isolated from FACS-purified microglia and prepared for RNA-sequencing.

Publication Title

Innate immune memory in the brain shapes neurological disease hallmarks.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

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accession-icon GSE66298
A DNA Hypomethylation Signature Predicts Novel Anti-Tumor Activity of LSD1 Inhibitors in SCLC
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A DNA Hypomethylation Signature Predicts Antitumor Activity of LSD1 Inhibitors in SCLC.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE66294
A DNA Hypomethylation Signature Predicts Novel Anti-Tumor Activity of LSD1 Inhibitors in SCLC (microarray)
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Epigenetic dysregulation has emerged as an important mechanism in cancer. Alterations in epigenetic machinery have become a major focus for new targeted therapies. The current report describes the discovery and biological activity of a cyclopropylamine containing inhibitor of Lysine Demethylase 1 (LSD1), GSK2879552. This small molecule is a potent, selective, orally bioavailable, mechanism-based irreversible inhibitor of LSD1. A proliferation screen of cell lines representing a number of tumor types indicated that small cell lung carcinoma (SCLC) is sensitive to LSD1 inhibition. The subset of SCLC lines and primary samples that undergo growth inhibition in response to GSK2879552 exhibit DNA hypomethylation of a signature set of probes suggesting this may be used as a predictive biomarker of activity. The targeted mechanism coupled with a novel predictive biomarker make LSD1 inhibition an exciting potential therapy for SCLC, a highly prevalent, rarely cured, tumor type representing approximately 15% of all lung cancers.

Publication Title

A DNA Hypomethylation Signature Predicts Antitumor Activity of LSD1 Inhibitors in SCLC.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE9116
Differential gene expression in primary ovarian tumors from depressed and non-depressed patients
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene expression profiling was carried out on primary ovarian carcinomas from 10 patients. The primary research question is whether gene expression differs in tissues from individuals with high vs low symptoms of psychological depression.

Publication Title

Depression, social support, and beta-adrenergic transcription control in human ovarian cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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