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Mus musculus, Homo sapiens
4 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.
Sample Metadata Fields
Treatment, Time
View Samples- Mus musculus
- 4 Downloadable Samples
Description
C2C12 mouse myoblasts expressing RAS mutants identified in human tumors fail to differentiate in low serum media.
Publication Title
MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
The perinatal period and early infancy are considered critical periods for lung development, and adversities during this period are believed to impact lung health in adulthood.The main factors affecting postnatal lung development and growth include environmental exposures, cigarette smoking, (viral) infections, allergic sensitization, and asthma.Therefore, we hypothesized that concomitant exposure in the early postnatal period in mice would cause more profound alterations in lung alveolarization and growth in adult life, quantified by stereology, and differently modulate lung inflammation and gene expression than either insult alone.Five-day-old male mice were immunized intraperitoneally (i.p.) with 10 µg of ovalbumin (OVA). This procedure was repeated at the 7th day of life, animals from the control group received i.p. injection of PBS only. Mice were exposed to either ambient PM2.5 or filtered air from the 5th to the 39th day of life, using an ambient particle concentrator developed at the Harvard School of Public Health (HAPC).Total RNA of lung samples (n=3 animals per group) was extracted using RNeasy Mini Kit (Qiagen, Hilden, Germany), according to manufacturer's instructions. The microarray analysis was performed using three RNA samples for each studied group (Control, OVA, PM2.5, OVA+PM2.5), totalizing 12 samples. One hundred nanograms of total RNA was amplified with the Ambion WT Expression Kit and hybridized onto the GeneChip Mouse Gene 2.0 ST Array (Thermo Scientific, Massachusetts, USA), following manufacturer’s protocol. The comparison between the control and OVA group exhibit 32 DEGs (28 up-regulated and 4 down-regulated), between the control and PM2.5 group had 6 DEGs (4 up and 2 down) and between the control and OVA+PM2.5 group had 5 DEGs (4 up and 1 down). The comparison between OVA and PM2.5 group showed 97 DEGS (22 up and 75 down) and between OVA and OVA+PM2.5 group had 7 DEGs (4 up and 3 down). Finally, the comparison between the PM2.5 and OVA+PM2.5 group exhibit 34 DEGs (2 up and 32 down).Our experimental data provide pathological support for the hypothesis that either allergic or environmental insults in early life have permanent adverse consequences to lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice.
Publication Title
Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 2 Downloadable Samples
Description
TGF-beta/Smads signaling plays important roles in vascular integrity. To identify potential Smad4 target genes in brain endothelial cells that control cerebrovascular integrity, the microarray assay was performed to compare the gene expression profiles of bEnd3 transfected with Smad4-siRNA and control-siRNA.
Publication Title
Endothelial Smad4 maintains cerebrovascular integrity by activating N-cadherin through cooperation with Notch.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Hopx appears to be needed for persistence of Th1 effector memory cells. IFN-gamma-producing Th cells are significantly reduced in Hopx-deficient mice compared to Hopx-expressing littermates and Hopx-deficient Th1 cells show a defective persistence upon adoptive transfer. Moreover, Hopx protects Th1 cells from Fas-mediated cell death in vitro. To further dissect the role of Hopx and to identify target genes of Hopx, we have performed transcriptome analysis to compare gene expression in Hopx-deficient versus Hopx-competent Th1 cells. In agreement with the role of Hopx in supporting survival of Th1 effector memory cells, anti-apoptotic cells were up-regulated and pro-apoptotic genes were down-regulated in Hopx-competent compared to Hopx-deficient Th1 cells.
Publication Title
Persistence of effector memory Th1 cells is regulated by Hopx.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
Description
BACKGROUND: p53 is an important tumor suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated.
Publication Title
A limited role for p53 in modulating the immediate phenotype of Apc loss in the intestine.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 10 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
WAMIDEX: a web atlas of murine genomic imprinting and differential expression.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
Description
Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Moreover, we analyzed differential gene expression patterns between Gprc5a knockout normal lung epithelial cells as well as lung adenocarcinoma cells isolated and cultured from tumors of NNK-exposed Gprc5a knockout mice.
Publication Title
A Gprc5a tumor suppressor loss of expression signature is conserved, prevalent, and associated with survival in human lung adenocarcinomas.
Sample Metadata Fields
Specimen part
View Samples
GSE10085- Mus musculus
- 2 Downloadable Samples
Description
Comparison of gene expression levels between matUPD18 and patUPD18 8.5 dpc whole embryo samples (maternal versus paternal uniparental disomy of Chr 18). Identification of highly differentially expressed transcripts.
Publication Title
WAMIDEX: a web atlas of murine genomic imprinting and differential expression.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 10 Downloadable Samples
Description
Dysregulated Wnt signalling is seen in approximately 30% of hepatocellular cancers, thus finding pathways downstream of activation of Wnt signalling is key. Using cre lox technology we have deleted the the adenomatous polyposis coli tumour suppressor protein (Apc) within the adult mouse liver and observed a rapid increase in nuclear beta-catenin and C-Myc. This is associated with an induction of proliferation leading to hepatomegally within 4 days of gene deletion. To investigate the downstream pathways responsible for these phenotypes we analysed the impact of inactivating Apc in the context of deficiency of the potentially key effectors beta-catenin and c-Myc. beta-catenin loss rescues both the proliferation and hepatomegally phenotypes following Apc loss. However c-Myc deletion, which rescues the phenotypes of Apc loss in the intestine, had no effect on the phenotypes of Apc loss. The consequences of deregulation the Wnt pathway within the liver are therefore strikingly different to those observed within the intestine, with the vast majority of Wnt targets beta-catenin dependent but c-Myc independent in the liver.
Publication Title
B-catenin deficiency, but not Myc deletion, suppresses the immediate phenotypes of APC loss in the liver.
Sample Metadata Fields
No sample metadata fields
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