Stem cell biology has garnered much attention due to its potential to impact human health through disease modeling and cell replacement therapy. This is especially pertinent to myelin-related disorders such as multiple sclerosis and leukodystrophies where restoration of normal oligodendrocyte function could provide an effective treatment. Progress in myelin repair has been constrained by the difficulty in generating pure populations of oligodendrocyte progenitor cells (OPCs) in sufficient quantities. Pluripotent stem cells theoretically provide an unlimited source of OPCs but significant advances are currently hindered by heterogeneous differentiation strategies that lack reproducibility. Here we provide a platform for the directed differentiation of pluripotent mouse epiblast stem cells (EpiSCs) through a defined series of developmental transitions into a pure population of highly expandable OPCs in ten days. These OPCs robustly differentiate into myelinating oligodendrocytes both in vitro and in vivo. Our results demonstrate that pluripotent stem cells can provide a pure population of clinically-relevant, myelinogenic oligodendrocytes and offer a tractable platform for defining the molecular regulation of oligodendrocyte development, drug screening, and potential cell-based remyelinating therapies.
Rapid and robust generation of functional oligodendrocyte progenitor cells from epiblast stem cells.
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View SamplesNine accessions of Arabidopsis were sampled before and after 14d of cold acclimation at 4°C. Transcript data were combined with metabolite data and related to quantitative measurement of plant freezing tolerance as determined by leaf electrolyte leakage assays.
Natural genetic variation of freezing tolerance in Arabidopsis.
Specimen part
View SamplesA-to-I RNA editing levels differ across tissues and cell types, but regulators of the editing process are largely unknown. We used RNA-seq on whole fly brains with different RNA binding proteins knocked down to test for A-to-I RNA editing level differences between controls and knockdowns. Overall design: To screen for editing regulators in the Drosophila brain, we crossed a pan-neuronal Gal4 driver, C155-Gal4, to different UAS-shRNA lines targeting individual RNA binding proteins, extracted RNA and made RNA-seq libraries. We sequenced four total replicates of shGFP controls and two replicates of all RNA binding protein knockdowns.
Zinc Finger RNA-Binding Protein Zn72D Regulates ADAR-Mediated RNA Editing in Neurons.
Sex, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Differentiation-Defective Human Induced Pluripotent Stem Cells Reveal Strengths and Limitations of the Teratoma Assay and In Vitro Pluripotency Assays.
Specimen part
View SamplesHere we perfomed the Teratoma assay for a normal human embryonic stem cell line (H9(+Dox)), a human embryonic stem cell line with a mesendodermal differentiation bias (H9Hyb), a normal human induced pluripotent stem cell line (LU07), a human induced pluripotent stem cell line with reactivated transgenes (LU07+Dox) and a human embryonal carcinoma cell line (EC) and anayzed their gene expression.
Differentiation-Defective Human Induced Pluripotent Stem Cells Reveal Strengths and Limitations of the Teratoma Assay and In Vitro Pluripotency Assays.
No sample metadata fields
View SamplesThis dataset describe the transcriptomic profiling of cecum, stomach and ileum from wild type, cdx2 conditional knock out and cdx2 ; apc deficient mice, by mRNA-seq. Each condition was analyzed in triplicated experiment to analyze the role of cdx2 in colorectal cancer susceptibilities Overall design: Biological samples from dissected tissue were tested by RNASeq in triplicates resulting into a total of 24 samples.
The Cdx2 homeobox gene suppresses intestinal tumorigenesis through non-cell-autonomous mechanisms.
Specimen part, Treatment, Subject
View SamplesCyclin D3 is critical hematopoiesis and loss of cyclin D3 leads to resistance to transformation of bone marrow progenitors by Notch1-IC.
Therapeutic targeting of the cyclin D3:CDK4/6 complex in T cell leukemia.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Notch pathway activation targets AML-initiating cell homeostasis and differentiation.
Sex, Specimen part, Cell line, Treatment
View SamplesExpression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation.
Notch pathway activation targets AML-initiating cell homeostasis and differentiation.
Specimen part, Cell line, Treatment
View SamplesTo determine role of Notch signaling in AML leukemia initiating cells we used a conditional mouse knock-in model of Notch1-IC to induce Notch1-IC expression in MLL-AF9 transformed LGMP. WT and Notch1-IC+ LGMP were analyzed to determined genes controlled by Notch signaling.
Notch pathway activation targets AML-initiating cell homeostasis and differentiation.
Sex, Specimen part
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