XEN cells are derived from the primitive endoderm of mouse blastocysts. In culture and in chimeras they exhibit properties of parietal endoderm. However, BMP signaling promotes XEN cells to form an epithelium and differentiate into visceral endoderm (VE). Of the several different subtypes of VE described, BMP induces a subtype that is most similar to the VE adjacent to the trophoblast-derived extraembryonic ectoderm.
BMP signaling induces visceral endoderm differentiation of XEN cells and parietal endoderm.
Treatment
View SamplesComparison of mouse ES cells and three different XEN cell cultures.
Imprinted X-inactivation in extra-embryonic endoderm cell lines from mouse blastocysts.
No sample metadata fields
View SamplesWe used a mouse strain in which one Tbx3 gene was replaced with the yellow fluorescent protein variant Venus. Luminal cells had either very high Tbx3 promoter activity or not at all.
Transcriptional repressor Tbx3 is required for the hormone-sensing cell lineage in mammary epithelium.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Parkinson's disease induced pluripotent stem cells with triplication of the α-synuclein locus.
Specimen part
View SamplesA major barrier to research on Parkinsons disease (PD) is inaccessibility of diseased tissue for study. One solution is to derive induced pluripotent stem cells (iPSCs) from patients with PD and differentiate them into neurons affected by disease. We created an iPSC model of PD caused by triplication of SNCA encoding -synuclein. -Synuclein dysfunction is common to all forms of PD, and SNCA triplication leads to fully penetrant familial PD with accelerated pathogenesis. After differentiation of iPSCs into neurons enriched for midbrain dopaminergic subtypes, those from the patient contain double -synuclein protein compared to those from an unaffected relative, precisely recapitulating the cause of PD in these individuals. A measurable biomarker makes this model ideal for drug screening for compounds that reduce levels of -synuclein, and for mechanistic experiments to study PD pathogenesis.
Parkinson's disease induced pluripotent stem cells with triplication of the α-synuclein locus.
Specimen part
View SamplesKlf5 has essential functions during early embryogenesis and in the derivation of ES cells from inner-cell mass of blastocyst. Among Kruppel-like factor (Klf) family members, only Klf5 shows peri-implantation lethal phenotype, but the precise mechanisms still remain unknown. To understand and identify molecular mechanisms, we performed microarray analysis by using E3.0 WT and Klf5 KO embryos when first phenotype of Klf5 deficiency appears.
<i>Klf5</i> maintains the balance of primitive endoderm versus epiblast specification during mouse embryonic development by suppression of <i>Fgf4</i>.
Specimen part
View SamplesA major barrier to research on Parkinsons disease (PD) is inaccessibility of diseased tissue for study. One solution is to derive induced pluripotent stem cells (iPSCs) from patients with PD and differentiate them into neurons affected by disease. We created an iPSC model of PD caused by triplication of SNCA encoding -synuclein. -Synuclein dysfunction is common to all forms of PD, and SNCA triplication leads to fully penetrant familial PD with accelerated pathogenesis. After differentiation of iPSCs into neurons enriched for midbrain dopaminergic subtypes, those from the patient contain double -synuclein protein compared to those from an unaffected relative, precisely recapitulating the cause of PD in these individuals. A measurable biomarker makes this model ideal for drug screening for compounds that reduce levels of -synuclein, and for mechanistic experiments to study PD pathogenesis.
Parkinson's disease induced pluripotent stem cells with triplication of the α-synuclein locus.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Coassembly of REST and its cofactors at sites of gene repression in embryonic stem cells.
Cell line, Treatment
View SamplesAnalysis of gene expression profiling upon REST shRNA knockdown in mouse ES cells for 72 hours,
Coassembly of REST and its cofactors at sites of gene repression in embryonic stem cells.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transposable elements have rewired the core regulatory network of human embryonic stem cells.
Specimen part, Disease, Cell line, Time
View Samples