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Mus musculus
2 Downloadable Samples
Description
In order to explore molecules whose expression is controlled by Slc39a13, we investigated gene expression profiling of primary osteoblast isolated from wild-type and Slc39a13 knockout mice.
Publication Title
The zinc transporter SLC39A13/ZIP13 is required for connective tissue development; its involvement in BMP/TGF-beta signaling pathways.
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No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Description
A control vs. genetic knockout experiment aimed at determining what RNAs are upregulated or downregulated in e11.5 mouse proximal limb tissue lacking the Lmx1b gene. Because Lmx1b is required for dorsal-ventral patterning of the limb, this screen gives insight into what putative downstream targets of Lmx1b contribute to dorsal-ventral patterning.
Publication Title
Identification of genes controlled by LMX1B in the developing mouse limb bud.
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Sample Metadata Fields
No sample metadata fields
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GSE28130- Mus musculus
- 4 Downloadable Samples
Description
Induced and activated regulatory CD4+ Foxp3+ cells compared
Publication Title
Connexin 43 signaling enhances the generation of Foxp3+ regulatory T cells.
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Specimen part
View Samples- Mus musculus
- 17 Downloadable Samples
Description
Proteinases play a pivotal role in wound healing by degrading molecular barriers, regulating cell-matrix interactions and availability of bioactive molecules. Matrix metalloproteinase-13 (MMP-13, collagenase-3) is a wide spectrum proteinase. Its expression and function is linked to the growth and invasion of many epithelial cancers such as squamous cell carcinoma. Moreover, the physiologic expression of MMP-13 is associated e.g. to scarless healing of human fetal skin and adult gingival wounds. While MMP-13 is not found in the normally healing skin wounds in human adults, it is expressed in mouse skin during wound healing. Thus, mouse wound healing models can be utilized for studying the role of MMP-13 in the events of wound healing. As the processes such as the migration and proliferation of keratinocytes, angiogenesis, inflammation and activation of fibroblasts are components of wound repair as well as of cancer, many results received from wound healing studies are also adaptable to cancer research.
Publication Title
MMP-13 regulates growth of wound granulation tissue and modulates gene expression signatures involved in inflammation, proteolysis, and cell viability.
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Time
View Samples- Mus musculus
- 6 Downloadable Samples
Description
To identify gene(s) that are modified in their relative expression levels in the Potocki-Lupski Syndrome mouse model and map to the rearranged region, i.e. possible candidate genes at the source of the PTLS-like phenotypes shown by the PTLS mouse, we comp
Publication Title
Abnormal social behaviors and altered gene expression rates in a mouse model for Potocki-Lupski syndrome.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
Description
Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells.
Publication Title
Asymmetric PI3K Signaling Driving Developmental and Regenerative Cell Fate Bifurcation.
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Specimen part, Treatment
View Samples- Mus musculus
- 11 Downloadable Samples
Description
Oxidative stress is a hallmark of inflammation in infection or sterile tissue injury. We show that partially oxidized phospholipids of microvesicles (MVs) from plasma of patients with rheumatoid arthritis or cells exposed to oxidative stress induce activation of TLR4. MVs from healthy donors or reconstituted synthetic MVs can be converted to TLR4 agonists by limited oxidation, while prolonged oxidation abrogates the activity. Activation by MVs mimics the mechanism of TLR4 activation by LPS. However, LPS and MVs induce significantly different transcriptional response profile in mouse BMDMs with a strong inflammation-resolving component induced by the endogenous signals. MVs thus represent a ubiquitous endogenous danger signal released under the oxidative stress, which underlies the pervasive role of TLR4 signaling in inflammation.
Publication Title
Toll-like receptor 4 senses oxidative stress mediated by the oxidation of phospholipids in extracellular vesicles.
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Sex
View Samples- Mus musculus
- 14 Downloadable Samples
Description
CD38, a multi-functional membrane receptor and enzyme, consumes NAD+ to generate products such as cyclic-ADP-ribose. CD38 knockout mice show elevated tissue and blood NAD+ level. Chronic feeding of high-fat, high-sucrose diet to wild type mice leads to exercise intolerance and reduced metabolic flexibility. Loss of CD38 by genetic mutation protects mice from diet-induced metabolic deficit. These animal model results suggest that elevation of tissue NAD+ through genetic ablation of CD38 can profoundly alter energy homeostasis in animals that are maintained on a calorically-excessive Western diet.
Publication Title
Genetic Ablation of CD38 Protects against Western Diet-Induced Exercise Intolerance and Metabolic Inflexibility.
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Sample Metadata Fields
Specimen part
View Samples- Danio rerio
- 6 Downloadable Samples
Description
Identification of genes differentially regulated after treatment of zebrafish embryos from 50% epiboly to 24hpf with 6.5uM leflunomide A six chip study comparing expression levels of zebrafish embryos treated with leflunomide 6.5uM
Publication Title
DHODH modulates transcriptional elongation in the neural crest and melanoma.
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Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 558 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Establishing reliable biomarkers for assessing and validating clinical diagnosis at early prodromal stages of Parkinson’s disease is crucial for developing therapies to slow or halt disease progression. Here, we present the largest study to date using whole blood gene expression profiling from over 500 individuals to identify an 87-gene blood-based signature. Our gene signature effectively differentiates between idiopathic PD patients and controls in both a validation cohort and an independent test cohort, and further highlights mitochondrial metabolism and ubiquitination/proteasomal degradation as potential pathways disrupted in Parkinson’s disease.
Publication Title
Analysis of blood-based gene expression in idiopathic Parkinson disease.
Alternate Accession IDs
Sample Metadata Fields
Sex, Specimen part, Subject
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