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.
Gene expression profiling reveals similarities between the spatial architectures of postnatal articular and growth plate cartilage.
Age, Specimen part
View SamplesThese 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.
CD24 is expressed by myofiber synaptic nuclei and regulates synaptic transmission.
No sample metadata fields
View SamplesExpression profiles generated during dissection of the molecular mechanisms underlying direct reprogramming of somatic cells to a pluripotent state (induced pluripotent stem cells, iPS).
Dissecting direct reprogramming through integrative genomic analysis.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.
Sex, Age, Specimen part, Time
View SamplesAntigen 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.
Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.
Sex, Age, Specimen part, Time
View SamplesE-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.
Epidermal FABP Prevents Chemical-Induced Skin Tumorigenesis by Regulation of TPA-Induced IFN/p53/SOX2 Pathway in Keratinocytes.
Specimen part
View SamplesParticulate Matter Triggers Carotid Body Dysfunction, Respiratory Dysynchrony and Cardiac Arrhythmias in Mice with Cardiac Failure
Particulate matter induces cardiac arrhythmias via dysregulation of carotid body sensitivity and cardiac sodium channels.
Age, Specimen part
View SamplesThe 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.
CYP26A1 knockout embryonic stem cells exhibit reduced differentiation and growth arrest in response to retinoic acid.
No sample metadata fields
View SamplesAmong 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.
A genome-wide analysis of LPS tolerance in macrophages.
No sample metadata fields
View SamplesPU.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.
Transcriptomic profiling identifies a PU.1 regulatory network in macrophages.
No sample metadata fields
View Samples