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accession-icon GSE17478
Particulate Matter effect on Mouse Model of Cardiac Failure: Lung and Heart Left Ventricle
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

Particulate Matter Triggers Carotid Body Dysfunction, Respiratory Dysynchrony and Cardiac Arrhythmias in Mice with Cardiac Failure

Publication Title

Particulate matter induces cardiac arrhythmias via dysregulation of carotid body sensitivity and cardiac sodium channels.

Alternate Accession IDs

E-GEOD-17478

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE7528
Gene expression of Wt vs CYP26A1-/- murine ES cells treated with control or 100 nM RA for 8 or 72 hr.
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

The goal of this study was to identify genes that are differentially expressed after genetic deletion of both alleles of the Cyp26a1 gene in murine embryonic stem cells. Cyp26a1 codes for the CYP26A1 enzyme which metabolizes RA to polar RA metabolites, such as 4-oxo-RA and 4-OH-RA. CYP26A1-/- ES cells do not metabolize RA within 48 hours of RA treatment while in Wt ES cells, polar RA metabolites are already detectable by 8 hr. In addition, the absence of CYP26A1 enzyme increases intracellular RA levels. By gene microarray analysis, we wanted to identify genes that would be affected by the lack of the Cyp26a1 gene.

Publication Title

CYP26A1 knockout embryonic stem cells exhibit reduced differentiation and growth arrest in response to retinoic acid.

Alternate Accession IDs

E-GEOD-7528

Sample Metadata Fields

No sample metadata fields

View Samples
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 GSE13125
Identification of PU.1 target genes by expression profiling of PUER cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

PU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation.

Publication Title

Transcriptomic profiling identifies a PU.1 regulatory network in macrophages.

Alternate Accession IDs

E-GEOD-13125

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE51678
Microarray profiling of STEP knockout mouse striatum
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon

Description

STEP (striatal-enriched tyrosine phosphatase) is a brain-specific phosphatase named for its robust expression in striatum. Brains from homozygous and heterozygous STEP knockout mice and wild-type littermates were harvested, and striatum microdissected. RNA was extracted and hybridized to Affymetrix 230_2 microarray chips.

Publication Title

Downstream effects of striatal-enriched protein tyrosine phosphatase reduction on RNA expression in vivo and in vitro.

Alternate Accession IDs

E-GEOD-51678

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE51994
Spatial Regulation of Gene Expression in Articular Cartilage Assessed by Laser Captured Microdissection and Microarray
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

We used laser capture microdissection to isolate different zones of the articular cartilage from proximal tibiae of 1-week old mice, and used microarray to analyze global gene expression. Bioinformatic analysis corroborated previously known signaling pathways, such as Wnt and Bmp signaling, and implicated novel pathways, such as ephrin and integrin signaling, for spatially associated articular chondrocyte differentiation and proliferation. In addition, comparison of the spatial regulation of articular and growth plate cartilage revealed unexpected similarities between the superficial zone of the articular cartilage and the hypertrophic zone of the growth plate.

Publication Title

Gene expression profiling reveals similarities between the spatial architectures of postnatal articular and growth plate cartilage.

Alternate Accession IDs

E-GEOD-51994

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE24291
Expression data from differentiating ES cells expressing Snail during Wnt inhibition
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

ES cells differentiated in the presence of the Wnt inhibitor DKK1 fail to express the transcription factor Snail and undergo EMT. We generated an ES cell line, A2.snail, that induced Snail expression upon addition of doxycycline addition.

Publication Title

Snail and the microRNA-200 family act in opposition to regulate epithelial-to-mesenchymal transition and germ layer fate restriction in differentiating ESCs.

Alternate Accession IDs

E-GEOD-24291

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon GSE2873
Burden-2R01NS036193-06A1
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

These experiments are designed to discover genes that are expressed selectively by synaptic nuclei in skeletal muscle with the particular goal of identifying genes that regulate motor axon growth and differentiation.

Publication Title

CD24 is expressed by myofiber synaptic nuclei and regulates synaptic transmission.

Alternate Accession IDs

E-GEOD-2873

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54678
A pivotal role of SRC-2 in Metastatic and Castration Resistant Prostate Cancer
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

SRC-2 is frequently amplified or overexpressed in metastatic prostate cancer patients. In this study, we used genetically engineered mice, overexpressing SRC-2 specifically in the prostate epithelium as a mouse model to examine the role of SRC-2 in prostate tumorigenesis. Over-expression of SRC-2 in PTEN heterozygous mice accelerates PTEN mutation induced tumor progression and develops a metastasis-prone cancer.

Publication Title

Androgen deprivation-induced NCoA2 promotes metastatic and castration-resistant prostate cancer.

Alternate Accession IDs

E-GEOD-54678

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE28515
Effect of acute ethanol on medidal prefrontal cortex across BXD genetic mapping panel and progenitors.
  • organism-icon Mus musculus
  • sample-icon 62 Downloadable Samples
  • Technology Badge Icon

Description

In order to elucidate the molecular mechanisms underlying individual variation in sensitivity to ethanol we profiled the prefrontal cortex transcriptomes of two inbred strains that exhibit divergent responses to acute ethanol, the C57BL6/J (B6) and DBA/2J (D2) strains, as well as 27 members of the BXD recombinant inbred panel, which was derived from a B6 x D2 cross. With this dataset we were able to identify several gene co-expression networks that were robustly altered by acute ethanol across the BXD panel. These ethanol-responsive gene-enriched networks were heavily populated by genes regulating synaptic transmission and neuroplasticity, and showed strong genetic linkage to discreet chromosomal loci. Network-based measurements of node importance identified several hub genes as established regulators of ethanol response phenotypes, while other hubs represent novel candidate modulators of ethanol responses.

Publication Title

Genetic dissection of acute ethanol responsive gene networks in prefrontal cortex: functional and mechanistic implications.

Alternate Accession IDs

E-GEOD-28515

Sample Metadata Fields

Sex, Specimen part

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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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