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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.

Sample Metadata Fields

No sample metadata fields

View Samples
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.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE10871
Differentiated, partially- and fully-reprogrammed MEFs/B-cells
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon

Description

Expression profiles generated during dissection of the molecular mechanisms underlying direct reprogramming of somatic cells to a pluripotent state (induced pluripotent stem cells, iPS).

Publication Title

Dissecting direct reprogramming through integrative genomic analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE25486
Nanoemulsion-Specific Gene Expression Data in Bone Marrow Derived Dendritic Cells and in Murine Nasal Epithelium
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE25485
Gene expression data in Bone Marrow Derived Dendritic Cells (BMDC) following nanoemulsion adjuvant exposure
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Antigen uptake, processing and presentation by dendritic cells are regulated by complex intra- and inter-cellular signalling events. Typical vaccine adjuvants lead to the transcription of pro-inflammatory cytokines and chemokines which relate to immune induction.

Publication Title

Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE109583
Epidermal fatty acid binding protein prevents chemical-induced skin tumorigenesis by inhibition of SOX2 expression in keratinocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

E-FABP expression in keratinocytes increase interferons, in particualur IFNlamda, expression, which activate P53, a critical tumor suppessor, to inhibit or prevent chemical-induced skin tumorigenesis.

Publication Title

Epidermal FABP Prevents Chemical-Induced Skin Tumorigenesis by Regulation of TPA-Induced IFN/p53/SOX2 Pathway in Keratinocytes.

Sample Metadata Fields

Specimen part

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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.

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.

Sample Metadata Fields

No sample metadata fields

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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.

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.

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)

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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