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accession-icon GSE33302
Expression data from sleep deprivation experiment in mouse hippocampus
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression underlying the effect of sleep deprivation in the mouse hippocampus and identified distinct classes of regulated genes during this process.

Publication Title

Genomic analysis of sleep deprivation reveals translational regulation in the hippocampus.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon SRP049596
RNA-seq analysis of germline stem cell removal and loss of SKN-1 in C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In C. elegans, ablation of germline stem cells (GSCs) extends lifespan, but also increases fat accumulation and alters lipid metabolism, raising the intriguing question of how these effects might be related. Here we show that a lack of GSCs results in a broad transcriptional reprogramming, in which the conserved detoxification regulator SKN-1/Nrf increases stress resistance, proteasome activity, and longevity. SKN-1 also activates diverse lipid metabolism genes and reduces fat storage, thereby alleviating the increased fat accumulation caused by GSC absence. Surprisingly, SKN-1 is activated by signals from this fat, which appears to derive from unconsumed yolk that was produced for reproduction. We conclude that SKN-1 plays a direct role in maintaining lipid homeostasis, in which it is activated by lipids. This SKN-1 function may explain the importance of mammalian Nrf proteins in fatty liver disease, and suggests that particular endogenous or dietary lipids might promote health through SKN-1/Nrf. Overall design: Samples were prepared from ~5,000 synchronized, L1 arrested day-one adult animals cultured at 25°C. Worms were synchronized by sodium hypochlorite (bleach) treatment, as previously described (Porta-de-la-Riva et al., 2012). Bleach solution (9 mL ddH2O; 1 mL 1 N NaOH; 4 mL Clorox bleach) was freshly prepared before each experiment. Worms were bleached for 5 minutes, washed 5x in M9, and arrested at the L1 stage at 25°C in M9 containing 10 µg/mL cholesterol. Feeding RNAi was started at the L1 stage. This approach only partially reduces skn-1 function, but allows analysis of larger samples than would be feasible with skn-1 mutants, which are sterile (Bowerman et al., 1992). Because these animals were not treated with FUdR, the WT adults contained an intact germline and eggs. As is explained in the Results section, we therefore confined our analysis to genes that were overrepresented in glp-1(ts) animals, which lack eggs and most of the germline, and established a high-confidence cutoff for genes that were upregulated by GSC absence as opposed to simply being expressed specifically in somatic tissues. RNA was extracted using the same protocol for qRT-PCR samples. Purified RNA samples were DNase treated and assigned a RIN quality score using a Bioanalyzer 2100 (Agilent Technologies, Santa Clara, CA). Only matched samples with high RIN scores were sent for sequencing. Single read 50 bp RNA sequencing with poly(A) enrichment was performed at the Dana-Farber Cancer Institute Center for Computational Biology using a HiSeq 2000 (Illumina, San Diego, CA). FASTQ output files were aligned to the WBcel235 (Feb 2014) C. elegans reference genome using STAR (Dobin et al., 2013). These files have been deposited at the Gene Expression Omnibus (GEO) with the accession number GSE63075. Samples averaged 75% mapping of sequence reads to the reference genome. Differential expression analysis was performed using a custom R and Bioconductor RNA-seq pipeline (http://bioinf.wehi.edu.au/RNAseqCaseStudy/) (Gentleman et al., 2004; Anders et al., 2013; R Core Team, 2014). Quantification of mapped reads in the aligned SAM output files was performed using featureCounts, part of the Subread package (Liao et al., 2013, 2014). We filtered out transcripts that didn't have at least one count per million reads in at least two samples. Quantile normalization and estimation of the mean-variance relationship of the log-counts was performed by voom (Law et al., 2014). Linear model fitting, empirical Bayes analysis and differential expression analysis was then conducted using limma (Smyth, 2005). To identify genes that are upregulated in a SKN-1-dependent manner by GSC loss, we sought genes for which glp-1(ts) expression was higher than WT, and for which glp-1(ts);skn-1(-) expression was reduced relative to glp-1(ts). To test for this pattern, if a gene's expression change was higher in the comparison of glp-1(ts) vs. WT and lower in the comparison of glp-1(ts);skn-1(-) vs. glp-1(ts), then we calculated the minimum (in absolute value) of the t-statistics from these two comparisons, and assessed the significance of this statistic by comparing to a null distribution derived by applying this procedure to randomly generated t-statistics. We corrected for multiple testing in this and the differential expression analysis using the false discovery rate (FDR) (Benjamini and Hochberg, 1995). Heatmaps were generated using heatmap.2 in the gplots package (Warnes et al., 2014). Functional annotations and phenotypes were obtained from Wormbase build WS246. SKN-1 transcription factor binding site analysis of hits was conducted with biomaRt, GenomicFeatures, JASPAR, MotifDb, motifStack, MotIV, and Rsamtools (Sandelin et al., 2004; Durinck et al., 2005; Durinck et al., 2009; Lawrence et al., 2013; Ou et al., 2013; Mercier and Gottardo, 2014; Shannon, 2014). JASPAR analysis was performed with the SKN-1 matrix MA0547.1 using 2 kb upstream sequences obtained from Ensembl WBcel235 (Staab et al., 2013). modENCODE SKN-1::GFP ChIP-seq analysis of hits was performed using biomaRt, ChIPpeakAnno, IRanges, and multtest (Durinck et al., 2005; Durinck et al., 2009; Gerstein et al., 2010; Zhu et al., 2010; Niu et al., 2011; Lawrence et al., 2013). SKN-1::GFP ChIP-seq peaks were generated by Michael Snyder's lab. We used the peak data generated from the first 3 larval stages: L1 (modENCODE_2622; GSE25810), L2 (modENCODE_3369), and L3 (modENCODE_3838; GSE48710). Human ortholog matching was performed using Wormbase, Ensembl, and OrthoList (Shaye and Greenwald, 2011). Gene lists were evaluated for functional classification and statistical overrepresentation with Database for Annotation, Visualization and Integrated Discovery (DAVID) version 6.7 (Dennis et al., 2003).

Publication Title

Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE28043
Bmpr2 mutation in murine PMVEC
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Pulmonary arterial hypertension (PAH) is thought to be driven by dysfunction of pulmonary vascular microendothelial cells (PMVEC). Most hereditary PAH is associated with BMPR2 mutations.

Publication Title

Physiologic and molecular consequences of endothelial Bmpr2 mutation.

Sample Metadata Fields

Specimen part

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accession-icon GSE149490
Transcriptional Profiling of Lung Macrophages from Preterm Infants Identifies Disease Related Programs
  • organism-icon Homo sapiens
  • sample-icon 218 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

To understand the molecular mechanisms of human lung macrophage development, function, and role in BPD pathogenesis, we conducted a clinical study using isolated tracheal aspirate macrophages from intubated preterm infants born before 30 wk gestation. One hundred twenty-eight patients intubated for respiratory distress syndrome and surfactant administration were consented for the study.

Publication Title

Transcriptional profiling of lung macrophages identifies a predictive signature for inflammatory lung disease in preterm infants.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE52322
Novel linkages between DCE-MRI and genomic profiling in locally advanced and inflammatory breast cancer
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression signatures have the capacity to identify clinically significant features of breast cancer and can predict which individual patients are likely to be resistant to neoadjuvant therapy, thus providing the opportunity to guide treatment decisions.

Publication Title

Gene expression profiles of multiple breast cancer phenotypes and response to neoadjuvant chemotherapy.

Sample Metadata Fields

Specimen part

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accession-icon SRP041929
RNAseq analysis of mouse lung transcriptome from allergic and non-allergic mice prior to and following lung Klebsiella pneumoniae infection
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We have demonstrated that allergic airway inflammation (induced by an ovalbumin sensitization and aerosol challenge protocol) decreases lung bacterial burden following lung infection with Klebsiella pneumoniae. The goals of this study are to indentify novel targets that are expressed during allergic airway inflammation in this model that contribute to enhanced lung bacterial immunity. Overall design: We isolated total RNA from the lungs of 4 groups of mice at both 0 hours (pre-infection) and 6 hours post-infection. WT and STAT6KO (BALB/c) mice were intraperitoneally sensitzed with alum or ovalbumin (OVA)-alum on day -18. Alum injected mice were not subsequently exposed to OVA aerosol. OVA-alum injected mice underwent aerosol sensitization on days -4, -3, -2, and -1. On day 0, four groups of mice were harvested (pre-infection). These included WT-ALUM, WT-OVA, STAT6KO-ALUM, and STAT6KO-OVA. On day 0, four groups of mice were infected with 10^4cfu of Klebsiella and then lungs were removed at 6 hours post-infection. These groups included WT-ALUM-KP, WT-OVA-KP, STAT6KO-ALUM-KP, and STAT6KO-OVA-KP. The right lung was removed for RNA isolation. Each group contained between 4 and 5 mice.

Publication Title

Allergic airway inflammation decreases lung bacterial burden following acute Klebsiella pneumoniae infection in a neutrophil- and CCL8-dependent manner.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP148786
A Transcriptomic Analysis of the Development of Skeletal Muscle Atrophy in Cancer-Cachexia in Tumor-Bearing Mice
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We recently demonstrated mitochondrial degenerations precede muscle wasting in time course progression of CC. However, the extent of muscle perturbations prior to wasting in CC is unknown. Therefore, we performed global gene expression analysis in CC-induced muscle wasting to enhance understanding of intramuscular perturbations across the development of CC. Overall design: Lewis Lung Carcinoma (LLC) was injected into the hind-flank of C57BL6/J mice at 8 wks age with tumor allowed to develop for 1, 2, 3, or 4 wks and compared to PBS injected control. Muscle wasting was evident at 4 wks LLC. Animals were anesthetized using isoflourane and gastrocnemius muscles were collected for analysis. Conclusions: Current findings present novel evidence of transcriptomic shifts and altered cellular pathways in CC-induced muscle wasting.

Publication Title

Transcriptomic analysis of the development of skeletal muscle atrophy in cancer-cachexia in tumor-bearing mice.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE104335
Whole transcriptome (gene expression and splice isoform changes) profiling using Affymetrix Human Transcriptome Array 2.0
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Transcriptome analysis of total RNA samples from human cell line (LAM 621-101, female)

Publication Title

Post-transcriptional Regulation of De Novo Lipogenesis by mTORC1-S6K1-SRPK2 Signaling.

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon GSE93371
Transcriptomic comparison of FVB mouse strain lung Cells one week upon injecting mice intraperitoneally with urethane and with the mouse lung adenocarcinoma cell line FULA 1
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Transcriptomic comparison of FVB mouse strain lung Cells one week upon injecting mice intraperitoneally with either saline or Urethane. Mouse lung cell were also compared at the transcriptomic level with the mouse lung adenocarcinoma cell line FULA 1, which was established in our lab

Publication Title

IκB Kinase α Is Required for Development and Progression of <i>KRAS</i>-Mutant Lung Adenocarcinoma.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE94060
Human lung MPC
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

A comparison of gene expression between control versus IPF human lung MPC using human Affy 1.0st chips.

Publication Title

Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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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