These data include RNA Seq data generated from Ring1b wild type and Ring1b KO Ring1a-/- Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa. Overall design: Total RNA extracted from Ring1b wild type and Ring1b KO Ring1a-/- Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa.
Maintenance of leukemic cell identity by the activity of the Polycomb complex PRC1 in mice.
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View SamplesThese data include RNA Seq data generated from wild type and Ring1a Ring1b dKO Cdkn2a-/- MLL-AF9 Leukemic cells Overall design: mRNA library preparation from Ring1a-/-;Ring1bf/f Cdkn2a-/- MLL-AF9 leukemic cells treated with OHT or EtOH
Maintenance of leukemic cell identity by the activity of the Polycomb complex PRC1 in mice.
Cell line, Treatment, Subject
View SamplesPolycomb proteins control proliferation and cellular transformation regulating DNA replication independently of cell cycle checkpoints
Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication.
Specimen part
View SamplesBackground: Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification. Results: We identified 5 miRNAs and 272 genes as significantly differentially expressed. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion related biological processes. Functional similarity and protein interaction based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling. Conclusions: We determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs to ACM pathogenesis or phenotype maintenance. Besides known pathways, we identified also deregulation of genes encoding ephrin receptors and ephrins, thus suggesting a potential involvement of Eph-ephrin signaling in CStCs from ACM hearts. Overall design: Expression profiles of cardiac stromal cells from 3 ACM patients were compared against those of cardiac stromal cells from 3 healthy individuals.
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells.
Sex, Disease, Subject
View SamplesExpression Profiling of a Genetic Animal Model of Depression Reveals Novel Molecular Pathways Underlying Depressive-like Behaviours
Expression profiling of a genetic animal model of depression reveals novel molecular pathways underlying depressive-like behaviours.
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