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Homo sapiens
12 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Alveolar rhabdomyosarcoma (aRMS) is a soft tissue sarcoma associated with the skeletal muscle lineage. The majority of aRMS tumors express the fusion protein PAX3-FOXO1 (PF), which has proven chemically intractable. As such, we identified proteins downstream from or cooperate with PF to support tumorigenesis, including SFRP3 (FRZB). Suppression of SFRP3 using lentivirally transduced shRNAs inhibits cell growth in vitro and tumor growth in vivo. This study aims to identify the genetic changes that underlie the SFRP3 suppression-mediated decreased cell growth. We analyzed changes using Gene Ontology (GO) enrichment and found the induced genes were enriched in striated muscle development/differentiation. In contrast, the repressed genes were enriched in response to stimulus and cell cycle/mitosis genes. We also observed as expected downregulation of SFRP3 (FRZB) but also downregulation of Wnt pathway-repressing genes such as CTBP2 (a transcriptional repressor of TCF, similar to CTBP1 ) and NAV2 (which is downstream from APC). Conversely, we noted upregulation of genes including CCND1 (cyclin D1) and SNAI2 (SLUG), both Wnt signaling target genes and WNT6, which is known to inhibit myoblast proliferation but induce myoblast elongation.
Publication Title
Secreted Frizzled-Related Protein 3 (SFRP3) Is Required for Tumorigenesis of PAX3-FOXO1-Positive Alveolar Rhabdomyosarcoma.
Sample Metadata Fields
Disease, Cell line, Treatment
View Samples- Drosophila melanogaster
- 48 Downloadable Samples
Illumina HiSeq 2000
Description
Organisms need to assess their nutritional state and adapt their digestive capacity to the demands for various nutrients. Modulation of digestive enzyme production represents a rational step to regulate nutriment uptake. However, the role of digestion in nutrient homeostasis has been largely neglected. In this study, we analyzed the mechanism underlying glucose repression of digestive enzymes in the adult Drosophila midgut. We demonstrate that glucose represses the expression of many carbohydrases and lipases. Our data reveal that the consumption of nutritious sugars stimulates the secretion of the transforming growth factor ß (TGF-ß) ligand, Dawdle, from the fat body. Dawdle then acts via circulation to activate TGF-ß/Activin signaling in the midgut, culminating in the repression of digestive enzymes that are highly expressed during starvation. Thus, our study not only identifies a mechanism that couples sugar sensing with digestive enzyme expression but points to an important role of TGF-ß/Activin signaling in sugar metabolism. Overall design: RNA-sequencing of whole guts from Drosophila melannogaster OregonR adult females was performed under three feeding conditions: Standard medium, glucose, and agar. Three biological repeats were performed for each condition.
Publication Title
Transforming growth factor β/activin signaling functions as a sugar-sensing feedback loop to regulate digestive enzyme expression.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples
GSE17993- Danio rerio
- 15 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Ischemic cardiopathy is the leading cause of death in the world, for which efficient regenerative therapy is not currently available. In mammals, after a myocardial infarction episode, the damaged myocardium is replaced by scar tissue featuring collagen deposition and tissue remodelling with negligible cardiomyocyte proliferation. Zebrafish, in contrast, display an extensive regenerative capacity as they are able to restore completely lost cardiac tissue after partial ventricular amputation. Due to the lack of genetic lineage tracing evidence, it is not yet clear if new cardiomyocytes arise from existing contractile cells or from an uncharacterised set of progenitors cells. Nonetheless, several genes and molecules have been shown to participate in this process, some of them being cardiomyocyte mitogens in vitro. Though questions as what are the early signals that drive the regenerative response and what is the relative role of each cardiac cell in this process still need to be answered, the zebrafish is emerging as a very valuable tool to understand heart regeneration and devise strategies that may be of potential value to treat human cardiac disease. Here, we performed a genome-wide transcriptome profile analysis focusing on the early time points of zebrafish heart regeneration and compared our results with those of previously published data. Our analyses confirmed the differential expression of several transcripts, and identified additional genes the expression of which is differentially regulated during zebrafish heart regeneration. We validated the microarray data by conventional and/or quantitative RT-PCR. For a subset of these genes, their expression pattern was analyzed by in situ hybridization and shown to be upregulated in the regenerating area of the heart. The specific role of these new transcripts during zebrafish heart regeneration was further investigated ex vivo using primary cultures of zebrafish cardiomyocytes and/or epicardial cells. Our results offer new insights into the biology of heart regeneration in the zebrafish and, together with future experiments in mammals, may be of potential interest for clinical applications.
Publication Title
Transcriptomics approach to investigate zebrafish heart regeneration.
Sample Metadata Fields
Specimen part, Time
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The objective of this set of samples is to identify genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by ionizing radiation in wild-type murine pre-B cells. The data generated in this project will be compared to the data generated in GSE9024, in which genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by the Rag proteins in murine pre-B cells were examined. In order to understand the differences between the physiologic and genotoxic responses to DSB DNA damage, we need to compare cells that are all in the same compartment of the cell cycle. We are therefore examining the response to IR-induced damage in cells that are arrested in G1, which would correspond to our previous study of G1 arrested cells with Rag-induced breaks. This will illuminate the difference directly, allowing us to better understand the signaling responses to the different types of DNA damage.
Publication Title
DNA damage activates a complex transcriptional response in murine lymphocytes that includes both physiological and cancer-predisposition programs.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The objective is to identify genes that are differentially expressed following the introduction of DNA double-strand breaks (DSBs) by the Rag proteins in murine pre-B cells. Cells lacking Artemis are used since the Rag-induced DSBs will not be repaired, and thus, will provide a continuous stimulus to the cell.
Publication Title
DNA damage activates a complex transcriptional response in murine lymphocytes that includes both physiological and cancer-predisposition programs.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples SRP044619- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
To identify isoform differential expression underlying peripheral nerve regeneration we performed RNA-Sequencing on DRG neurons after axotomy. Overall design: RNA was sequenced from peripheral Dorsal Root Ganglia (DRG) neurons from adult male mice 7 days after a conditioning lesion at the level of the sciatic nerve (Crushed samples) or after a sham surgery (Controls surgery).
Publication Title
Identification of miRNAs involved in DRG neurite outgrowth and their putative targets.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 16 Downloadable Samples
- Illumina HiSeq 2500
Description
G9a mediates a transcriptional switch, and activates the Notch pathway to coordinate endothelial cell and trophoblast proliferation to promote vascular maturation in the placenta. Overall design: Examination of global transcriptional profiles in control and mutant placenta labyrinth at 2 developmental stages (E12.5 and 13.5).
Publication Title
G9a controls placental vascular maturation by activating the Notch Pathway.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The aim of the study was to identify markers for the early diagnosis of endoprosthesis loosening, for the differentiation between wear-particle induced and septic loosening, as well as to gather new insights into the pathogenesis.
Publication Title
Gene expression in endoprosthesis loosening: chitinase activity for early diagnosis?
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
AIMS/HYPOTHESIS: Manoeuvres aimed at increasing beta cell mass have been proposed as regenerative medicine strategies for diabetes treatment. Raf-1 kinase inhibitor protein 1 (RKIP1) is a common regulatory node of the mitogen-activated protein kinase (MAPK) and nuclear factor B (NF-B) pathways and therefore may be involved in regulation of beta cell homeostasis. The aim of this study was to investigate the involvement of RKIP1 in the control of beta cell mass and function.
Publication Title
The role of Raf-1 kinase inhibitor protein in the regulation of pancreatic beta cell proliferation in mice.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 108 Downloadable Samples
- Illumina mouse-6 v1.1 expression beadchip
Description
In summary, we characterized genomic signatures of response to drugs of abuse and we found positive correlations between the drug-induced expression and various behavioral effects. These signatures are formed by two dynamically inducible transcriptional networks: (1) CREB/SRF-dependent gene pattern that appears to be related to drug-induced neuronal activity, (2) the pattern of genes controlled at least in part via release of glucocorticoids and androgens that are associated with rewarding and harmful drug effects. The discovery of co-expressed networks of genes allowed for the identification of master-switch controlling factors involved in molecular response to the drugs. Finally, using the pharmacological tools we were able to dissect and inhibit particular gene expression patterns from genomic profile.
Publication Title
The dissection of transcriptional modules regulated by various drugs of abuse in the mouse striatum.
Sample Metadata Fields
Compound, Time
View Samples