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SRP125702
Mus musculus
4 Downloadable Samples
Illumina HiSeq 2000
Description
Purpose: Analyze the function of the transcription factors Hand2 and Gata3 in adult sympathetic neurons by induced knockout and RNAseq analysis Overall design: Method and Result: Hand2flx/del::DbhCreERT2 (referred to as mutant) and Hand2flx/+::DbhCreERT2 (referred to a control) were injected for 10 days with tamoxifen to activate Cre. Animals were killed, sympathetic ganglia (SCG+Stellate) collected and processed for RNA isolation and RNAseq (Stanzel et al., 2016). Gata3flx/flx::DbhCerERT2 (mutant) and Gata3flx/+::DbhCreERT2 (controls) were treated as Hand2 animals. 16 ganglia from 4 mice were pooled for Hand2 mutant and controls and Gata3 controls. As only rudimentary ganglia were present in Gata3 mutant mice (Tsarovina et al., 2010) ganglia from 8 mice were pooled. The specific effects of the Hand2 knockout are decribed in Stanzel et al., 2016. The analysis of ganglion rudiments in the Gata3 knockout revealed that Gata3 was not reduced, indicating that the remaining cells had escaped the knockout.
Publication Title
Distinct roles of hand2 in developing and adult autonomic neurons.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 31 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Neuroblastoma is an embryonal neoplasm that remains of dramatic prognosis in its aggressive forms. Activating mutations of the ALK tyrosine kinase receptor have been identified in sporadic and familial cases of this cancer. We generated knock-in mice carrying the two most frequent Alk mutations observed in neuroblastoma patients. We used microarrays to detail the global programme of gene expression underlying the impact of ALK mutations on neuroblastoma formation in a MYCN amplified background.
Publication Title
Activated Alk triggers prolonged neurogenesis and Ret upregulation providing a therapeutic target in ALK-mutated neuroblastoma.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Atrial identity is determined by a COUP-TFII regulatory network.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Atria and ventricles exhibit distinct molecular profiles that produce structural and functional differences between the two cardiac compartments. However, factors that determine these differences remain largely undefined. Cardiomyocyte-specific COUP- TFII ablation produces ventricularized atria that exhibit ventricle-like action potentials, increased cardiomyocyte size, and development of extensive T-tubules.
Publication Title
Atrial identity is determined by a COUP-TFII regulatory network.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
COUP-TFII, a member of the nuclear receptor superfamily plays a critical role in angiogenesis and organogenesis during embryonic development. Our results indicate that COUP-TFII expression is profoundly upregulated in prostate cancer patients and might serves as biomarker for recurrence prediction. Thus we conduct transcriptome comparison of control and COUP-TFII depleted PC3 cells to gain genomic insights on the biological processes that COUP-TFII is involved in prostate cancer cells. Ingenuity Pathway Analysis (IPA) shows that the most prominent altered pathways in the COUP-TFII depleted cells are related to cell growth; cell cycle progression and DNA damage response. Indeed many growth related genes including E2F1, p21, CDC25A, Cyclin A and Cyclin B are changed in COUP-TFII knockdown cells, suggesting that COUP-TFII might be an important regulator for prostate cancer cell growth. Further functional assays from cells and mice genetic studies confirm the hypothesis that COUP-TFII serve as the major regulator to control prostrate cancer growth. Together, results provide insight into the role of COUP-TFII in prostate tumorigenesis.
Publication Title
COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Homo sapiens
- 3 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Early EPCs (eEPCs) appear at less than 1 week in culture dishes, whereas late EPCs (LEPCs) appear late at 2-4 weeks. Distinct angiogenic properties between these two EPC subpopulations have been disclosed by the angiogenesis assay: late EPCs, but not eEPCs, form vascular networks de novo and are able to incorporate into vascular networks. On the contrary, eEPCs, but not late ones, indirectly augment tubulogenesis even when physically separated by a Transwell membrane, implying the involvement of a cytokine-based paracrine mechanism.
Publication Title
Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
High glucose impairs the angiogenic activities of late endothelial precursor cells (EPC). We found that far infrared (FIR) treatment restored partially the activity of late EPC. However, the mechanisms are unclear. We performed gene expression microarray analysis to assess the expression profiles of high glucose-treated late EPC with or without FIR treatment.
Publication Title
Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tazarotene-induced gene 1 (TIG1), also named as retinoic acid receptor responder 1 (RARRES1), is a retinoid inducible type II tumor suppressor gene; the TIG1B isoform inhibits growth and invasion of cancer cells. Expression of TIG1B is frequently downregulated in various cancer tissues; however, the expression and activities of the TIG1A isoform has yet to be analyzed. This study investigated the effects of TIG1A and TIG1B isoforms on gene expression profiles of colon cancer cells. TIG1A, TIG1B and control stable clones derived from HCT116 colon cells were established using the GeneSwitch system. TIG1 isoform expression was induced upon 5 micro Molar of mifepristone (MFP) treatment for 24 hr. Biological triplicate samples were prepared and gene expression profiles were determined by microarray using human genome HGU133 plus 2 array (Affymatrix). Upon induction of TIG1A and TIG1B expression for 24 hr, a total of 129 and 55 genes were significantly altered, respectively. Of the genes analyzed, 23 and 6 genes were up- and downregulated, respectively in both TIG1A and TIG1B expressing cells.
Publication Title
G protein-coupled receptor kinase 5 mediates Tazarotene-induced gene 1-induced growth suppression of human colon cancer cells.
Sample Metadata Fields
Cell line, Time
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
COUP-TFII plays a critical role in angiogenesis during development. It has also been shown to suppress Notch signaling pathway to confer vein identity. However, the downstream targets and the mechanism mediate COUP-TFII function to regulate these processes remain elusive. To identify the downstream targets and the mechanism by which COUP-TFII regulates agiogenesis and vein specification, we knocked down COUP-TFII in HUVEC cells using COUP-TFII specific siRNA and used microarray analysis to identify downstream targets. Interestingly, we found the expression of many genes in the cell cycle pathway and Notch signaling pathway are significantly altered in the COUP-TFII depleted cells.
Publication Title
COUP-TFII is a major regulator of cell cycle and Notch signaling pathways.
Sample Metadata Fields
Specimen part
View Samples