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accession-icon GSE56711
Mechanism of tissue-specific functional polarization of peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE56682
Genome wide transcriptional analysis of tissue macrophages and bone marrow derived macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Tissue macrophages from peritoneal cavity, lung, liver, spleen, small intestine and adipose tissue and M-CSF derived bone marrow derived macrophages (BMDMs) were determined for gene expression.

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE56683
Gene induction by all trans retinoic acid (ATRA) and/or omentum culture supernatant in bone marrow derived macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

BMDMs were stimulated with ATRA and/or omentum culture supernatant and gene expression was determined by Illumina microarray

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE56684
GATA6 dependent gene regulation in peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Peritoneal macrophages from control and Mac-Gata6 KO (LysM-cre;Gata6-floxed) mice were determined for genome wide gene expression.

Publication Title

Tissue-specific signals control reversible program of localization and functional polarization of macrophages.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE13589
Gene expression of E. coli MG1655 pOX38Km at the outside and inside of biofilms
  • organism-icon Escherichia coli
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Gene expression changes between outside and inside of biofilms were investigated. The gene expression was compared between the outside and inside of the biofilms. At the same time, the gene expressions were also compared with exponential phase and stationary phase in planktonic cells. The gene expression analysis showed that the physiological activities were higher at the outside of the biofilms than those at the inside of the biofilms. The genes induced at the ouside of the biofilms included genes involved in the stress responses and adhesions.

Publication Title

Localized expression profiles of rpoS in Escherichia coli biofilms.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE74304
Gene expression data of GBM146 and GBM157 at day0, 7, 30 after serum exposure
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Glioblastoma (GBM) is a lethal brain cancer composed of heterogeneous cellular populations including glioma stem cells (GSCs) and their progeny differentiated non-stem glioma cells (NSGCs). Although accumulating evidence points out the significance of GSCs for tumour initiation and propagation, the roles of NSGCs remain elusive. Here we demonstrate that, when patient-derived GSCs in GBM tumours undergo differentiation with diminished telomerase activity and shortened telomeres, they subsequently become senescent phenotype, thereby secreting angiogenesis-related proteins, including vascular endothelial growth factors. Interestingly, these secreted factors from senescent NSGCs promote proliferation of human umbilical vein endothelial cells and tumorigenic potentials of GSCs in immunocompromised mice. These experimental data are likely clinically-relevant, since immunohistochemistry of both patient tumours of GBM and the patient GSC-derived mouse xenografted tumours detected tumour cells that express a set of markers for the senescence phenotype. Collectively, our data suggest that the inter-cellular signals from senescent NSGCs promote GBM tumour angiogenesis thereby increasing malignant progression of GBM.

Publication Title

Senescence from glioma stem cell differentiation promotes tumor growth.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon SRP068733
HDAC inhibitor SAHA reverses inflammatory gene expression in diabetic endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

While histone deacetylase (HDAC) inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. While histone hyperacetylation has long been considered the paradigmatic mechanism of action, recent genome-wide profiles indicate more complex interactions with the epigenome. In particular, HDAC inhibitors also induce histone deacetylation at the promoters of highly active genes, resulting in gene suppression. This was linked to the loss of histone acetyltransferase (HAT) binding. To illustrate pre-clinical utility of the HDAC inhibitor SAHA as a therapeutic, we show reversal of diabetes-associated EP300 target genes in diabetic HAECs of primary origin. These results were confirmed using SAHA, C646 (EP300/CREBBP inhibitor) or EP300 siRNA. These findings suggest the inhibition of gene expression by SAHA is mediated by EP300 function and provide a rationale for clinical trials of safety and efficacy in patients with diabetes. Overall design: Human aortic endothelial cells from a diabetic and non-diabetic individual were stimulated with DMSO (control), SAHA (2 µM, HDAC inhibitor) or C646 (10 µM, EP300 inhibitor) for 12 hours, or EP300 siRNA or non-target siRNA (control) for 4 hours, followed by 48 hours in fresh media. Study performed in triplicate.

Publication Title

Systems approach to the pharmacological actions of HDAC inhibitors reveals EP300 activities and convergent mechanisms of regulation in diabetes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11670
Transcriptional profiling of ICL670 treated K562 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Iron plays a central role in the regulation of many cellular functions. Dysregulation of its metabolism leads an iron overload situation and iron depletion leads to an inhibition of cell proliferation. Recent reports demonstrated that ICL670 (Novartis) acts as a potent NF-kappa-B inhibitor and improves hematological data in a subset of MDS patients (Cilloni et al, Haematologica, s1: 238, 2007). However, the precise mechanism of anti-cancer effect of ICL670 is still uncertain.

Publication Title

The oral iron chelator deferasirox represses signaling through the mTOR in myeloid leukemia cells by enhancing expression of REDD1.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP096177
Deep sequencing reveals novel Set7 networks
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Methyl-dependent regulation of transcription has expanded from a traditional focus on histones to encompass transcription factor modulation. While the Set7 lysine methyltransferase is associated with pro-inflammatory gene expression in vascular endothelial cells, genome-wide regulatory roles remain to be investigated. From initial characterization of Set7 as specific for methyl-lysine 4 of H3 histones (H3K4m1), biochemical activity toward non-histone substrates has revealed additional mechanisms of gene regulation. mRNA-Seq revealed transcriptional deregulation of over 8,000 genes in an endothelial model of Set7 knockdown. Gene ontology identified up-regulated pathways involved in developmental processes and extracellular matrix remodeling, whereas pathways regulating the inflammatory response as well as nitric oxide signaling were down-regulated. Chromatin maps derived from ChIP-Seq profiling of H3K4m1 identified several hundred loci with loss of H3K4m1 at gene regulatory elements associated with an unexpectedly subtle effect on gene expression. Transcription factor network analysis implicated six previously described Set7 substrates in mRNA-Seq changes, and we predict that Set7 post-translationally regulates other transcription factors associated with vascular endothelial gene expression through the presence of Set7 amino acid methylation motifs. We describe a role for Set7 in regulating developmental pathways and response to stimuli (inflammation/immune response) in human endothelial cells of vascular origin. Set7-dependent gene expression changes that occurred independent of H3K4m1 may involve transcription factor lysine methylation events. The method of mapping measured transcriptional changes to transcription factors to identify putative substrates with strong associations to functional changes is applicable to substrate prediction for other broad-substrate histone modifiers. Overall design: We used lentiviral delivered shRNA to knock down the expression of Set7 protein in HMEC-1 cells. As a control, we used a non-targeting shRNA. RNA-seq was performed in biological triplicate. Set7 knock down datasets are labeled “Set7KD” and non-targeting control datasets are labeled “NTC”

Publication Title

Deep sequencing reveals novel Set7 networks.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP071610
REV-ERBa influences stability and nuclear localization of the glucocorticoid receptor
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report here that REV-ERBa influences nuclear localization of the glucocorticoid receptor and vice versa. As a consequence these two nuclear receptors influence each others transcriptome. REV-ERBa (Nr1d1) is a nuclear receptor that is part of the circadian clock mechanism and regulates metabolism and inflammatory processes. The glucocorticoid receptor (GR, Nr3c1) influences similar processes, but is not part of the circadian clock mechanism although glucocorticoid signaling affects resetting of the circadian clock in peripheral tissues. Because of their similar impact on physiological processes we studied the interplay between these two nuclear receptors. We found that REV-ERBa competes with GR for binding to HSP90, a chaperone responsible for the activation of substrate proteins to ensure survival of a cell. This competition affected stability and nuclear localization of GR, thereby affecting GR target gene expression such as I?B and alcohol dehydrogenase 1 (Adh1). Our findings highlight an important interplay between two nuclear receptors that influence each others transcritpional potential indicating that the transcriptional landscape is strongly dependent on dynamic processes at the protein level.  Overall design: In this dataset, we isolated livers at Zeitgebertime (ZT) 8 and ZT20 of wild type and Rev-erb alpha knock-out animals. Liver samples were immediately flash frozen in liquid N2 and stored at -80?°C. RNA was extracted using NucleoSpin RNA (Machery-Nagel, Düren, Germany) according to the instructions of the manufacturer. Quality of the RNA samples was analysed with a spectrophotometer, agarose gel electrophoresis and reverse transcription-PCR. Library construction starting from the poly(A)-tail and multiplexing was performed according to the instructions of the manufacturer (Illumina). The samples were organized as follows: Three replicas (1-WT, 2-WT, 3-WT) correspond to genotype WT at ZT8. Three replicas (4-Rev, 5-Rev, 6-Rev) correspond to genotype Rev-/- at ZT8. Three replicas (7-WT, 8-WT, 9-WT) correspond to genotype WT at ZT20. Three replicas (10-Rev, 11-Rev, 12-Rev) correspond to genotypeRev-/- at ZT20. For the experiment, complementary DNA (cDNA) libraries were barcoded using Illumina primers and loaded onto one lane of an IlluminaHS2000 machine. cDNA libraries were diluted and loaded onto each lane. The samples were sequenced for a maximum sequencing length of 75?bp. Sequences were aligned to the mouse genome (UCSC version mm10 database). Numbers of the sequences obtained for each library can be found in Supplementary Table 3. Sequences (fastq format) were mapped with Tophat (Trapnell, C. 2009), uniquely mapped sequences from the output files (bam format) were then used for further analysis, percentage of the mapping obtained for each sample can be found in Supplementary Table 3. For all files the reads were counted with HTSeq-count using the following criteria: samtools view sample.bam | htseq-count -m union -a 10 -s no -i gene_name Mus_Musculus.gtf > sample_counts.txt Tests for differential expression between the samples were performed in R software (R Core Team, 2014 http://www.R-project.org/) using the DESeq2 package (Version 1.6.3) (Love, M. 2014). A threshold on the corrected P value was used to call for differentially expressed genes (P.adjust<0.05).    

Publication Title

REV-ERBα influences the stability and nuclear localization of the glucocorticoid receptor.

Sample Metadata Fields

Age, Specimen part, Subject, Time

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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