ABSTRACT: Expression data from dexamethasone treated mouse embryonic neural progenitor/stem cells isolated from wild type C57Bl/6 or caveolin-1 knockout mice
Project description:Expression data from dexamethasone treated mouse embryonic neural progenitor/stem cells isolated from wild type C57Bl/6 or caveolin-1 knockout mice
Project description:Neurosphere cultures prepared from E14.5 mouse cerebral cortex at passage 3 were treated for 4 hours with 100 nM dexamethasone We used microarrays to detail the global program of dexamethasone regulated gene expression in embryonic neural progenitor/stem cells. Cerebral cortex was isolated from E14.5 mouse fetuses and cultured as neurospheres for 3 passages prior to treatment with 100 nM dexamethasone or ethanol vehicle for 4 hours.
Project description:Expression data from dexamethasone treated mouse embryonic hypothalamic progenitor/stem cells isolated from wild type C57Bl/6 male or female mice
Project description:We used RNA-Seq to detail the global program of sexually dimorphic dexamethasone regulated gene expression in embryonic hypothalamic neural progenitor/stem cells.
Project description:The goal of this study was to measure genome-wide expression in primary mouse neural stem/progenitor cell (NSPC) cultures to determine if SOX2 ablation alters the transcriptomic response which occurs following glucocorticoid receptor activation by the synthetic glucocorticoid, Dexamethasone. Neurosphere cultures of SOX2 knock out (KO) NSPCs and control non-deleted wild-type (WT) NSPCs (C57BL/6) derived from the fetal telencephalon were established at postnatal day zero (P0).
Project description:Neurosphere cultures prepared from E14.5 mouse cerebral cortex at passage 3 were treated for 4 hours with 100 nM dexamethasone We used microarrays to detail the global program of dexamethasone regulated gene expression in embryonic neural progenitor/stem cells
Project description:Background: E2A, encoded by the TCF3 gene locus, belongs to the E protein transcription factor family, which also includes HEB (TCF12) and E2-2 (TCF4), has been suggested to play an important role in leukemogenesis. However, far less is known about the function of E2A in cell-fate regulation of hESCs. Therefore, further understanding of E2A in self-renewal and differentiation of embryonic stem cells may be influenced. In the study, we demonstrated E2A knockout exhibited blocked neural differentiation, which is tightly related to histone modification H3K4me3 and H3K27me3. Methods: The genomic DNA of H3K4me3 and H3K27me3 binding peaks in wild type and E2A knockout neural progenitor cells were generated by ChIP-seq technique using IIIumina Hiseq 2500. Results: A comprehensive human chromatin state of H3K4me3 and H3K27me3 in wild type and E2A knockout neural progenitor cells was provided. Function enrichment, network characteristics and disease association of the binding peaks were analyzed. Conclusion: The dataset could serve as a baseline resource for investigating the potential effects and mechanism of H3K4me3/H3K27me3/E2A complex in neural differentiation period of embryonic stem cells
Project description:We have showed that cancer cells (or tumorigenic cells) resemble neural stem/progenitor cells in regulatory network, tumorigenicity and differentiation potential. We have shown PRMT1 is a protein that is upreguated in and promotes vaious cancers. The expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis. The project is to identify the interaction partners of PRMT1, by which PRMT1 regulates neural stemness in both cancer cells and neural stem cells.
Project description:Metabolism is vital to cellular function and tissue homeostasis during human lung development. In utero, embryonic pluripotent stem cells undergo endodermal differentiation towards a lung progenitor cell fate that can be mimicked in vitro using induced human pluripotent stem cells (hiPSCs) to study genetic mutations. To identify differences between wild type and surfactant protein B (SFTPB)-deficient cell lines during endoderm specification towards lung, we used an untargeted metabolomics approach to evaluate the developmental changes in metabolites. We found that the metabolites most enriched during the differentiation from pluripotent stem cell to lung progenitor cell, regardless of cell line, were sphingomyelins and phosphatidylcholines, two important lipid classes in fetal lung development. The SFTPB mutation had no metabolic impact on early endodermal lung development. The identified metabolite signatures during lung progenitor cell differentiation may be utilized as biomarkers for normal embryonic lung development.