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accession-icon GSE18460
Lactobacillus acidophilus induces virus immune defense genes in murine dendritic cells by a TLR-2 dependent mechanism
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Lactobacilli are probiotics that, among other health promoting effects, have been ascribed immunostimulating and virus preventive properties. Certain lactobacilli species have been shown to possess strong IL-12 inducing properties. As IL-12 production depends on the up-regulation of type I interferons, we hypothesized that the strong IL-12 inducing capacity of L. acidophilus NCFM in murine bone marrow derived DC is caused by an up-regulation of IFN-, which subsequently stimulates the induction of IL-12 and the dsRNA binding toll like receptor (TLR)-3. The expression of the genes encoding IFN-, IL-12, IL-10 and TLR-3 in DC upon stimulation with L. acidophilus NCFM was measured. L. acidophilus NCFM induced a much stronger expression of ifn-, il-12 and il-10 compared to the synthetic dsRNA ligand Poly I:C, whereas the levels of expressed tlr-3 were similar. By the use of whole genome microarray gene expression, we investigated whether other genes related to the viral defence were up-regulated in DC upon stimulation with L. acidophilus NCFM and found that various virus defence related genes, both early and late, were among the strongest up-regulated genes. The IFN- stimulating capability was also detected in another L. acidophilus strain, but was not a property of other probiotic bacteria tested (B. bifidum and E. coli nissle).The IFN- inducing capacity was markedly reduced in TLR-2 -/- DCs, dependent on endocytosis and the major cause of the induction of il-12 and tlr-3 in L. acidophilus NCFM stimulated cells. Collectively, our results reveal that certain lactobacilli trigger the expression of viral defence genes in DC in a TLR-2 manner through induction of IFN- .

Publication Title

Lactobacillus acidophilus induces virus immune defence genes in murine dendritic cells by a Toll-like receptor-2-dependent mechanism.

Alternate Accession IDs

E-GEOD-18460

Sample Metadata Fields

Treatment, Time

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accession-icon GSE8621
LPS tolerance in macrophages
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Among the multiple mechanisms that control the intensity and duration of macrophage activation, the development of a state of refractoriness to a second stimulation in cells treated with LPS has long been recognized. Release of inhibitory cytokines and alterations in intracellular signaling pathways may be involved in the development of LPS tolerance. Although a number of molecules have been implicated, a detailed picture of the molecular changes in LPS tolerance is still missing. We have used a genome-wide gene expression analysis approach to (i) define which fraction of LPS target genes are subject to tolerance induction and (ii) identify genes that are expressed at high levels in tolerant macrophages. Our data show that in LPS tolerant macrophages the vast majority of LPS-induced gene expression is abrogated. The extent of tolerance induction varies for individual genes, and a small subset appears to be excepted. Compared to other negative control mechanisms of macrophages, e.g. IL-10-induced deactivation, LPS-tolerance inhibits a much wider range of transcriptional targets. Some previously described negative regulators of TLR-signaling (e.g. IRAK-M) were confirmed as expressed at higher levels in LPS-tolerant macrophages. In addition, we discuss other potential players in LPS tolerance identified in this group of genes.

Publication Title

A genome-wide analysis of LPS tolerance in macrophages.

Alternate Accession IDs

E-GEOD-8621

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15433
The PPARg2 A/B-domain plays a gene specific role in transactivation and co-factor recruitment
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

We have previously shown that adenoviral expression of peroxisome proliferator-activated receptors (PPARs) leads to rapid establishment of transcriptionally active complexes and activation of target gene expression within 5-8 h following transduction. Here we have used the adenoviral delivery system combined with expression array analysis to identify novel putative PPARgamma target genes in murine fibroblasts and to determine the role of the A/B-domain in PPARgamma mediated transactivation of genomic target genes. Of the 257 genes found to be induced by PPARgamma2 expression, only 25 displayed A/B-domain dependency, i.e. significantly reduced induction in the cells expressing the truncated PPARgamma lacking the A/B-domain (PPARgammaCDE). Nine of the 25 A/B-domain dependent genes were involved in lipid storage and in line with this, triglyceride accumulation was considerably decreased in the cells expressing PPARgammaCDE compared to cells expressing full length PPARgamma2. Using chromatin immunoprecipitation (ChIP) we demonstrate that PPARgamma binding to genomic target sites and recruitment of the mediator component TRAP220/MED1/PBP/DRIP205 is not affected by the deletion of the A/B-domain. By contrast, the PPARgamma-mediated CBP and p300 recruitment to A/B-domain dependent target genes is abolished by deletion of the A/B-domain. These results indicate that the A/B-domain of PPARgamma2 is specifically involved in the recruitment or stabilization of CBP and p300 containing co-factor complexes to a subset of target genes.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-15433

Sample Metadata Fields

Cell line

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accession-icon GSE24451
Knockout of the Acyl CoA binding protein (ACBP) in mice - expression profile from the liver of 21 days old ACBP-/- and +/+ mice.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am

Publication Title

Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.

Alternate Accession IDs

E-GEOD-24451

Sample Metadata Fields

Specimen part

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accession-icon GSE84767
Genetics of the hippocampal transcriptome in mouse: a systematic survey and online neurogenomics resource
  • organism-icon Mus musculus
  • sample-icon 67 Downloadable Samples
  • Technology Badge Icon

Description

The Hippocampus Consortium data set provides estimates of mRNA expression in the adult hippocampus of 99 genetically diverse strains of mice including 67 BXD recombinant inbred strains, 13 CXB recombinant inbred strains, a diverse set of common inbred strains, and two reciprocal F1 hybrids.

Publication Title

Genetics of the hippocampal transcriptome in mouse: a systematic survey and online neurogenomics resource.

Alternate Accession IDs

E-GEOD-84767

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE40540
IP of 5-hydroxymethylcytosine (5-hmC) and 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Dynamic changes in 5-hydroxymethylation signatures underpin early and late events in drug exposed liver.

Alternate Accession IDs

E-GEOD-40540

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE9444
Sleep deprivation and the brain
  • organism-icon Mus musculus
  • sample-icon 93 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Homer1a is a core brain molecular correlate of sleep loss.

Alternate Accession IDs

E-GEOD-9444

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16387
Licensing of PPARg-regulated gene expression by IL-4-induced alternative macrophage activation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.

Alternate Accession IDs

E-GEOD-16387

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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accession-icon GSE10026
High resolution gene expression profiling for simultaneous analysis of RNA synthesis, abundance and decay
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Conserved principles of mammalian transcriptional regulation revealed by RNA half-life.

Alternate Accession IDs

E-GEOD-10026

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10744
Copy number variation and gene expression in the mouse
  • organism-icon Mus musculus
  • sample-icon 108 Downloadable Samples
  • Technology Badge Icon

Description

Copy number variation (CNV) of DNA segments has recently been identified as a major source of genetic diversity, but a more comprehensive understanding of the extent and phenotypic effect of this type of variation is only beginning to emerge. In this study we generated genome-wide expression data from 6 mouse tissues to investigate how CNVs influence gene expression.

Publication Title

Segmental copy number variation shapes tissue transcriptomes.

Alternate Accession IDs

E-GEOD-10744

Sample Metadata Fields

No sample metadata fields

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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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