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accession-icon GSE35378
adipose tissue Glut4 overexpression or knockout
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

The goal of this study is to determine the effects of adipose-specific Glut4 overexpression or knockout on changes in adipose tissue global gene expression

Publication Title

A novel ChREBP isoform in adipose tissue regulates systemic glucose metabolism.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE8505
Isolated adipocytes and stromo-vascular fraction (SVF) of subcutaneous and intraabdominal adipose tissue in mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Obesity is an epidemic health problem worldwide that impacts the risk and prognosis of many diseases. However, not all obese patients have the same risk of developing these disorders. Individuals with peripheral obesity, i.e., fat distributed subcutaneously, are at little or no risk of the common medical complications of obesity, whereas individuals with central obesity, i.e., fat accumulated in visceral depots, are prone to these complications.

Publication Title

Evidence for a role of developmental genes in the origin of obesity and body fat distribution.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP110814
Hepatic Expression of Ectodysplasin (ED) A Increases in Obesity and Impairs Insulin Sensitivity in Skeletal Muscle
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We screened intronic microRNAs dysregulated in liver of obese mouse models to identify previously uncharacterized coding host genes that may contribute to the pathogenesis of obesity-associated insulin resistance and type 2 diabetes mellitus. Our approach identified the expression of Ectodysplasin A (Eda), the causal gene of X-linked hypohidrotic ectodermal dysplasia (XLHED; MIM 305100) was strongly increased in liver of obese mouse models both in rodents and humans.Eda expression in murine liver is controlled via PPAR? activation, increases in circulation and promotes JNK activation and inhibitory serine phosphorylation of IRS1 in skeletal muscle. Consistently, bi-directional modulation of hepatic Eda expression in mouse models affects systemic glucose metabolism with alterations of muscle insulin signaling, revealing a novel role of EDA as an obesity-associated hepatokine, which impairs insulin sensitivity in skeletal muscle. Overall design: Soleus muscle mRNA profiles of db/db mice at 3 weeks after injection of AAV encoding shRNA targeting mouse Eda or the control scrambled shRNA sequence at the titer of 2-3x10e10 particles/body.

Publication Title

A microRNA screen reveals that elevated hepatic ectodysplasin A expression contributes to obesity-induced insulin resistance in skeletal muscle.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon SRP076519
Next Generation Sequencing of liver and subcutaneous fat tissues obtained from obese subjects
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Patients had low calorie diet weight reduction run in prior to the day of surgery. The human liver and subcutaneous fat tissue samples were obtained from 12 obese subjects undergoing bariatric surgery and then used for the mRNA expression analyses. Overall design: mRNA profiles of human liver and subcutaneous fat tissue samples were generated by RNA sequencing using Illumina HiSeq 2500.

Publication Title

Integrated Network Analysis Reveals an Association between Plasma Mannose Levels and Insulin Resistance.

Sample Metadata Fields

Age, Specimen part, Subject

View Samples
accession-icon GSE49030
Genome-wide profiling of the activity-dependent hippocampal transcriptome
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Activity-dependent gene expression is central for sculpting neuronal connectivity in the brain. Despite the importance for synaptic plasticity, a comprehensive analysis of the temporal changes in the transcriptomic response to neuronal activity is lacking. In a genome wide survey we identified genes that were induced at 1, 4, 8, or 24 hours following neuronal activity in the hippocampus.

Publication Title

Genome-wide profiling of the activity-dependent hippocampal transcriptome.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE93611
Time-course expression data from HEK293RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF and labelled with 4SU
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An immediate-late gene expression module decodes ERK signal duration.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE72919
Time-course expression data from HEK293RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We integrate experimental data and mathematical modelling to unveil how ERK signal duration is relayed to mRNA dynamics.

Publication Title

An immediate-late gene expression module decodes ERK signal duration.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP079368
TADs emerge as a functionally, but not structurally privileged scale in the hierarchical folding of chromosomes
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Understanding how regulatory sequences interact in the context of chromosomal architecture is a central challenge in biology. Chromosome conformation capture revealed that mammalian chromosomes possess a rich hierarchy of structural layers, from multi-megabase compartments to sub-megabase topologically associating domains (TADs), and further down to sub-TAD loop domains. TADs appear to act as regulatory microenvironments by constraining and segregating regulatory interactions across discrete chromosomal regions. However, it is unclear whether other (or all) folding layers share similar properties, or rather TADs constitute a privileged folding scale with maximal impact on the organization of regulatory interactions. Here we present a novel parameter-free algorithm (CaTCH) that identifies hierarchical trees of chromosomal domains in Hi-C maps, stratified through their reciprocal physical insulation which is a simple and biologically relevant property. By applying CaTCH to published Hi-C datasets, we show that previously reported folding layers appear at different insulation levels. We demonstrate that although no structurally privileged folding level exists, TADs emerge as a functionally privileged scale defined by maximal enrichment of CTCF at boundaries, and maximal cell-type conservation. By measuring transcriptional output in embryonic stem cells and neural precursor cells, we show that TADs also maximize the likelihood that genes in a domain are co-regulated during differentiation. Finally, we observe that regulatory sequences occur at genomic locations corresponding to optimized mutual interactions at the scale of TADs. Our analysis thus suggests that the architectural functionality of TADs arises from the interplay between their ability to partition interactions and the genomic position of regulatory sequences. Overall design: The hybrid mouse ESC line F1-21.6 (129Sv-Cast/EiJ), previously described in (Jonkers et al., 2009), were grown on mitomycin C-inactivated MEFs in ES cell media containing 15% FBS (Gibco), 10-4 M b-mercaptoethanol (Sigma), and 1000U/ml of leukaemia inhibitory factor (LIF, Chemicon). Mouse ES cells were differentiated into neural progenitor cells (NPC) as previously described (Conti et al., 2005; Splinter et al., 2011). Total RNAs were prepared by Trizol extraction from the mouse ESC line, and for one NPC clone derived from it. Two biological replicates were collected for ESCs and NPCs. After ribosomal RNA depletion with Ribo-Zero (Illumina), RNA-seq libraries were prepared using ScriptSeq v2 kit (Illumina) following the manufacturer’s instructions. Libraries were prepared in two technical replicates per biological replicate. 50 bp single-end sequencing was performed on Illumina HiSeq 2000 instruments according to manufacturer’s instructions.

Publication Title

Reciprocal insulation analysis of Hi-C data shows that TADs represent a functionally but not structurally privileged scale in the hierarchical folding of chromosomes.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP104287
Perturbation-response genes reveal signaling footprints in cancer gene expression
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Aberrant cell signaling can cause cancer and other diseases and is a focal point of drug research. A common approach is to infer signaling activity of pathways from gene expression. However, mapping gene expression to pathway components disregards the effect of post-translational modifications, and downstream signatures represent very specific experimental conditions. Here we present PROGENy, a method that overcomes both limitations by leveraging a large compendium of publicly available perturbation experiments to yield a common core of Pathway RespOnsive GENes. Unlike existing methods, PROGENy can (i) recover the effect of known driver mutations, (ii) provide or improve strong markers for drug indications, and (iii) distinguish between oncogenic and tumor suppressor pathways for patient survival. Collectively, these results show that PROGENy accurately infers pathway activity from gene expression. Overall design: HEK293?RAF1:ER cells were treated with different stimuli (4OHT, Ly29002, TNFa, TGF1b, IFNg) for different periods of time (1h, 4h).

Publication Title

Perturbation-response genes reveal signaling footprints in cancer gene expression.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE38614
Hierarchical regulation in a KRAS pathway-dependent transcriptional network revealed by a reverse-engineering approach
  • organism-icon Rattus norvegicus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Reverse engineering a hierarchical regulatory network downstream of oncogenic KRAS.

Sample Metadata Fields

Cell line, Treatment

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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