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accession-icon GSE67973
Discrete Functions of Rev-erba Couple Metabolism to the Clock
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

GENE REGULATION. Discrete functions of nuclear receptor Rev-erbα couple metabolism to the clock.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE67964
Discrete Functions of Rev-erba Couple Metabolism to the Clock [array]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Illumina HiSeq 2000

Description

Circadian and metabolic physiology are intricately intertwined, as illustrated by Rev-erb , a transcription factor (TF) that functions both as a core repressive component of the cell autonomous clock and as a regulator of metabolic genes. Here we show that Rev-erb modulates the clock and metabolism by different genomic mechanisms. Clock control requires Rev-erb to bind directly to the genome at its cognate sites, where it competes with activating ROR TFs. By contrast, Rev-erb regulates metabolic genes primarily by recruiting the HDAC3 corepressor to sites to which it is tethered by cell type-specific transcription factors. Thus, direct competition between Rev-erb and ROR TFs provides a universal mechanism for self-sustained control of molecular clock across all tissues, whereas Rev-erb utilizes lineage-determining factors to convey a tissue-specific epigenomic rhythm that regulates metabolism tailored to the specific need of that tissue.

Publication Title

GENE REGULATION. Discrete functions of nuclear receptor Rev-erbα couple metabolism to the clock.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon SRP051500
Genetic Variation Determines PPAR? Function and Antidiabetic Drug Response In Vivo [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

SNPs affecting disease risk often reside in non-coding genomic regions. Here we show that SNPs are highly enriched at mouse strain-selective adipose tissue binding sites for PPAR?, a nuclear receptor for antidiabetic drugs. Many such SNPs alter binding motifs for PPAR? or cooperating factors, and functionally regulate nearby genes whose expression is strain-selective and imbalanced in heterozygous F1 mice. Moreover, genetically-determined binding of PPAR? accounts for mouse strain-specific transcriptional effects of TZD drugs, providing proof-of- concept for personalized medicine related to nuclear receptor genomic occupancy. In human fat, motif-altering SNPs cause differential PPAR? binding, provide a molecular mechanism for some expression quantitative trait loci, and are risk factors for dysmetabolic traits in genome- wide association studies. One PPAR? motif-altering SNP is associated with HDL levels and other metabolic syndrome parameters. Thus, natural genetic variation in PPAR? genomic occupancy determines individual disease risk and drug response. Overall design: Comparison of 5 RNA-seq experiments between 2 strains of mice differing in diet and fat depot. One of the experiments was evaluation of the response to a drug Rosiglitazone. Our RNA-seq data comprises primarily of 4 main experiments: The first experiment consists of samples taken from 2 strains of mice and their F1 progeny The samples are all taken from the same depot and when the mice were fed the same chow diet The second experiment has 2 parts, the first one involves samples taken from the 2 strains from the same eWAT depot when they were kept on a Low Fat Diet (LFD) This first part serves as a control for the second one in which the mice were treated with a drug, rosiglitazone in conjunction with a LFD The third experiment consists of samples taken from mice being fed on LFD. The samples are taken from the eWAT depot for both the strains. The fourth experiment consists of samples taken from mice being fed on LFD. The samples are taken from the iWAT depot for both the strains. We also have a solitary sample from a GRO-seq experiment which was done on eWAT in a B6 strain of mice being fed a LFD eWAT: epididymal White Adipose Tissue iWAT: inguinal White Adipose Tissue LFD-12w: mice were fed a control low fat diet (Research Diet D12450B) chow: mice were fed standard rodent chow Diet LFD w/rosiglitazone: Drug rosiglitazone (Cayman Chemicals) was incorporated into low fat diet D12450B by Research Diets at 36mg/kg of diet. Mice received control low fat diet for 10 weeks (age 6-16 weeks), and the rosiglitazone-containing diet versus control diet for the final 2 weeks (until sacrifice at 18 weeks) LFD control for rosi: mice were fed a control low fat diet (Research Diet D12450B)

Publication Title

Genetic Variation Determines PPARγ Function and Anti-diabetic Drug Response In Vivo.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE25588
Liver-expressed antimicrobial peptide-2 is downregulated in Eimeria maxima-infected chickens
  • organism-icon Gallus gallus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

Avian coccidiosis is a major disease of poultry caused by the intestinal protozoa Eimeria. Aviagen line A and line B birds show differential susceptibility to Eimeria infection, with line B birds exhibiting higher lesion scores and mortality. The objective of this study was to examine differential intestinal gene expression between line A and B chicks in response to a challenge with Eimeria maxima. Following challenge with 1 x 10^4 oocysts/chick, greater than 40% of line A chicks had lesion scores of 0 to 1 (on 0 to 4 scale), similar to controls. In contrast, all line B challenged chicks at this same dose had lesion scores of 2 to 4.

Publication Title

An antimicrobial peptide is downregulated in the small intestine of Eimeria maxima-infected chickens.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE107333
Endogenous retrovirus-associated genes in a hypoxia-mimetic cobalt chloride neuroblastoma model
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

By using high-density DNA microarrays, we analyzed the gene-expression profile of SHSY5Y neuroblastoma cells after treatment with cobalt chloride

Publication Title

Investigation of Endogenous Retrovirus Sequences in the Neighborhood of Genes Up-regulated in a Neuroblastoma Model after Treatment with Hypoxia-Mimetic Cobalt Chloride.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE33426
Three-Dimensional Tumor Profiling Reveals Minimal mRNA Heterogeneity in Esophageal Squamous Cell Carcinoma
  • organism-icon Homo sapiens
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

We microdissected discrete sub-regions of esophageal squamous cell carcinoma (ESCC) and analyzed the transcriptomes throughout three-dimensional (3D) tumor space.

Publication Title

Identification of unique expression signatures and therapeutic targets in esophageal squamous cell carcinoma.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE29001
Identification of Unique Therapeutic Targets in Esophageal Squamous Cell Carcinoma
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

We utilized tissue microdissection and expression microarrays to measure ex vivo gene expression profiles in twelve cases of patient-matched normal basal epithelial cells, normal differentiated squamous epithelium, and cancer.

Publication Title

Identification of unique expression signatures and therapeutic targets in esophageal squamous cell carcinoma.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE108868
Expression data of the human colorectal cancer cell line HCT116 in response to MS-275 and hydroxyurea treatment
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

MS-275 and hydroxyurea treatment influences whole gene expression including DNA damage response and cell cycle checkpoint signaling.

Publication Title

HDAC1 and HDAC2 integrate checkpoint kinase phosphorylation and cell fate through the phosphatase-2A subunit PR130.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE49559
Gene expression data from PC3 prostate cells overexpressing control miR or miR-95
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

We used microarrays to detail the global changes in gene expression resulting from miR-95 overexpression

Publication Title

miRNA-95 mediates radioresistance in tumors by targeting the sphingolipid phosphatase SGPP1.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE107170
Molecular Signature of Hepatitis D Virus-Associated Hepatocellular Carcinoma
  • organism-icon Homo sapiens
  • sample-icon 298 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To investigate the role of viral and host factors in HDV-associated HCC we carried out an integrated clinicopathological and gene expression study of tissue specimens and laser microdissected hepatocytes obtained at the time of liver transplantation from livers with HDV-HCC, HDV-cirrhosis without HCC, HCV-HCC and HBV-HCC. References to GSM series of HDV and HBV livers, already deposited in GEO, are included in this series. Part of data of HCV livers are a re-analysis of GSE series GSE69715 and GSE78737, the re-analyzed GSM is indicated in the 'description' column and with a link at the bottom of the page.

Publication Title

Molecular Signature and Mechanisms of Hepatitis D Virus-Associated Hepatocellular Carcinoma.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Subject

View Samples

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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