Using a stromal cell free system, we described the gene expression and two genome wide epigenetic profiles of a unique population of undifferentiated bone marrow cells selectively driven towards the T cell differentiation pathway
An epigenetic profile of early T-cell development from multipotent progenitors to committed T-cell descendants.
Specimen part, Treatment
View SamplesDifferencies between groups between pre and post haematopoietic stem cell transplantation children
Genetic Background of Immune Complications after Allogeneic Hematopoietic Stem Cell Transplantation in Children.
Specimen part, Disease stage
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Modeling of epigenome dynamics identifies transcription factors that mediate Polycomb targeting.
Specimen part
View SamplesWhile changes in chromatin are integral to transcriptional reprogramming during cellular differentiation, it is currently unclear how chromatin modifications are targeted to specific loci. We developed a computational model on the premise that transcription factors (TFs) direct dynamic chromatin changes during cell fate decisions. When applied to a neurogenesis paradigm, this approach predicted the TF REST as a determinant of gain of Polycomb-mediated H3K27me3 in neuronal progenitor cells. We prove this prediction experimentally by showing that the absence of REST causes loss of H3K27me3 at target promoters in trans at the same cellular state. Moreover, promoter fragments containing a REST binding site are sufficient to recruit H3K27me3 in cis, while deletion of their REST site results in loss of H3K27me3. These findings illustrate that computational modeling can systematically identify TFs that regulate chromatin dynamics genome-wide. Local determination of Polycomb activity by REST exemplifies such TF based regulation of chromatin.
Modeling of epigenome dynamics identifies transcription factors that mediate Polycomb targeting.
Specimen part
View SamplesDifferences between groups of children with obesity and healthy controls.
Looking for new diagnostic tools and biomarkers of hypertension in obese pediatric patients.
Specimen part, Disease
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Parity induces differentiation and reduces Wnt/Notch signaling ratio and proliferation potential of basal stem/progenitor cells isolated from mouse mammary epithelium.
Specimen part
View SamplesIn the present study we have studied the mechanistic and functional aspects of NCoR1 function in mouse skeletal muscle. NCoR1 muscle-specific knockout mice exhibited an increased oxidative metabolism. Global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha) overexpression on oxidative metabolism in skeletal muscle. The repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1alpha-mediated coactivation of ERRalpha. We therefore delineated the molecular mechanism by which a transcriptional network controlled by corepressor and coactivator proteins determines the metabolic properties of skeletal muscle, thus representing a potential therapeutic target for metabolic diseases.
The corepressor NCoR1 antagonizes PGC-1α and estrogen-related receptor α in the regulation of skeletal muscle function and oxidative metabolism.
Sex, Disease
View SamplesThis study examined the effect of early pregnancy on the gene expression profile of total isolated mammary epithelial cells in mice.
Parity induces differentiation and reduces Wnt/Notch signaling ratio and proliferation potential of basal stem/progenitor cells isolated from mouse mammary epithelium.
Specimen part
View SamplesExpression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated.
Sox4 is a master regulator of epithelial-mesenchymal transition by controlling Ezh2 expression and epigenetic reprogramming.
Cell line, Treatment
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Tyrosine phosphatase SHP2 promotes breast cancer progression and maintains tumor-initiating cells via activation of key transcription factors and a positive feedback signaling loop.
Cell line
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