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Mus musculus
40 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The sense of hearing depends on the faithful transmission of sound information from the ear to the brain by spiral ganglion (SG) neurons. However, how SG neurons develop the connections and properties that underlie auditory processing is largely unknown.
Publication Title
Developmental profiling of spiral ganglion neurons reveals insights into auditory circuit assembly.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 15 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
OBJECTIVE: To analyze genome-wide changes in chondrocyte gene expression in a surgically induced model of early osteoarthritis (OA) in rats, to assess the similarity of this model to human OA, and to identify genes and mechanisms leading to OA pathogenesis. METHODS: OA was surgically induced in 5 rats by anterior cruciate ligament transection and partial medial meniscectomy. Sham surgery was performed in 5 additional animals, which were used as controls. Both groups underwent 4 weeks of forced mobilization, 3 times per week. RNA was extracted directly from articular chondrocytes in the OA (operated), contralateral, and sham-operated knees. Affymetrix GeneChip expression arrays were used to assess genome-wide changes in gene expression. Expression patterns of selected dysregulated genes, including Col2a1, Mmp13, Adamts5, Ctsc, Ptges, and Cxcr4, were validated by real-time polymerase chain reaction, immunofluorescence, or immunohistochemistry 2, 4, and 8 weeks after surgery. RESULTS: After normalization, comparison of OA and sham-operated samples showed 1,619 differentially expressed probe sets with changes in their levels of expression >/=1.5-fold, 722 with changes >/=2-fold, 135 with changes >/=4-fold, and 20 with changes of 8-fold. Dysregulated genes known to be involved in human OA included Mmp13, Adamts5, and Ptgs2, among others. Several dysregulated genes (e.g., Reln, Phex, and Ltbp2) had been identified in our earlier microarray study of hypertrophic chondrocyte differentiation. Other genes involved in cytokine and chemokine signaling, including Cxcr4 and Ccl2, were identified. Changes in gene expression were also observed in the contralateral knee, validating the sham operation as the appropriate control. CONCLUSION: Our results demonstrate that the animal model mimics gene expression changes seen in human OA, supporting the relevance of newly identified genes and pathways to early human OA. We propose new avenues for OA pathogenesis research and potential targets for novel OA treatments, including cathepsins and cytokine, chemokine, and growth factor signaling pathways, in addition to factors controlling the progression of chondrocyte differentiation.
Publication Title
Global analyses of gene expression in early experimental osteoarthritis.
Sample Metadata Fields
No sample metadata fields
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GSE2154- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Primary micromass cultures derived from 11.5 day old mouse embryo limb buds were cultured for 15 days in differentiating conditions (beta-glycerophosphate and ascorbic acid). Total RNA from differentiating chondrocytes was isolated every three days i.e. days 3,6,9,12 and 15 and hybridized to MOE430A chips. Objective: Gain a view of the temporal gene expression changes occuring during chondrocyte differentiation.
Publication Title
Microarray analyses of gene expression during chondrocyte differentiation identifies novel regulators of hypertrophy.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 120 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Analysis of livers of male and female B6C3F1 mice exposed to prototype treatments from five classes of model hepatotoxicants. These hepatotoxicants include compounds that activate the peroxisome proliferator-activated receptor (PPAR), induce the inflammatory response, activate the constitutive androstane receptor (CAR), stimulate the hypoxia signal transduction pathway, and activate the aryl-hydrocarbon receptor (AHR). The results provide insights into the shared and unique pathways that are activated across these model hepatotoxicants.
Publication Title
Screening a mouse liver gene expression compendium identifies modulators of the aryl hydrocarbon receptor (AhR).
Sample Metadata Fields
Sex, Age, Compound, Time
View Samples- Mus musculus
- 47 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
PPAR-null and wild-type male mice treated with PFHxS or PFNA
Publication Title
Screening a mouse liver gene expression compendium identifies modulators of the aryl hydrocarbon receptor (AhR).
Sample Metadata Fields
Sex, Specimen part, Compound
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Many environmentally-relevant chemicals and drugs activate the nuclear receptor pregnane X receptor (PXR). Activation of PXR can lead to increases in liver weight in part through hepatocyte replication similar to a large number of compounds that activate other nuclear receptors such as the peroxisome proliferator-activated receptor alpha and the constitutive activated receptor (CAR). PXR controls the expression of a large battery of genes involved in xenobiotic metabolism. Identification of genes that are accurate predictors of PXR activation would be useful in high-throughput screens to assess potential toxicity and drug-drug interactions. Here, we identified PXR-dependent genes in the mouse liver after exposure to pregnenolone 16alpha-carbinonitrile (PCN), a chemical that is often used as a model PXR agonist.
Publication Title
Screening a mouse liver gene expression compendium identifies modulators of the aryl hydrocarbon receptor (AhR).
Sample Metadata Fields
Sex, Specimen part, Compound
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Growth hormone signaling in hepatocytes is fundamentally important. Disruptions in this pathway have led to fatty liver and other metabolic abnormalities. Growth hormone signals through the JAK2/STAT5 pathway. Mice with hepatocyte specific deletion of STAT5 were previously shown to develop fatty liver. Our aim in this study was to determine the effect of deleting JAK2 in hepatocytes on liver gene expression. To do so, we generated animals with hepatocyte specific deletion of JAK2.
Publication Title
Abrogation of growth hormone secretion rescues fatty liver in mice with hepatocyte-specific deletion of JAK2.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most aggressive human malignancies. In our studies, we find that the Gli transcription factors are required for Kras initiation of pancreatic tumorigenesis. In order to identify the downstream transcriptional targets of Gli in PDAC, we conducted gene expression analysis using Gli3T, a transcriptional repressor of Gli.
Publication Title
The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesis.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Activation of the canonical Wnt signaling pathway is commonly observed in pancreatic cancer. We therefore sought to identify a gene expression profile associated with the activation of this pathway in pancreatic cancer cells.
Publication Title
Activation of WNT/β-Catenin Signaling Enhances Pancreatic Cancer Development and the Malignant Potential Via Up-regulation of Cyr61.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 33 Downloadable Samples
Illumina HiSeq 4000
Description
TOX is selectively expressed in tumor-infiltrating CD8 T cells however the role of TOX in peripheral CD8 T cells is not known. The two goals of this study are to elucidate transcriptional changes between TOX-sufficient and TOX-deficient tumor infiltrating CD8 T cells and to elucidate the molecular program induced by TOX overexpression in peripheral CD8 T cells. Overall design: CD8 T cells were sorted by flow cytometry and RNA-seq was performed.
Publication Title
TOX is a critical regulator of tumour-specific T cell differentiation.
Sample Metadata Fields
Cell line, Subject
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