This SuperSeries is composed of the SubSeries listed below.
Autophagy maintains the metabolism and function of young and old stem cells.
Specimen part
View SamplesAutophagy is critical for protecting HSCs from metabolic stress. Here, we used a genetic approach to inactivate autophagy in adult HSCs by deleting the Atg12 gene. We show that loss of autophagy causes accumulation of mitochondria and an oxidative phosphorylation (OXPHOS)-activated metabolic state, which drives accelerated myeloid differentiation likely through epigenetic deregulations rather than transcriptional changes, and impairs HSC self-renewal activity and regenerative potential.
Autophagy maintains the metabolism and function of young and old stem cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Neural-specific Sox2 input and differential Gli-binding affinity provide context and positional information in Shh-directed neural patterning.
Specimen part, Treatment
View SamplesThe objective of this study was to identify genes regulated by Sonic Hedgehog pathway stimulation in neural progenitors.
Neural-specific Sox2 input and differential Gli-binding affinity provide context and positional information in Shh-directed neural patterning.
Specimen part, Treatment
View SamplesVarious pluripotent stem (PS) cells can be isolated from early developing embryos in mouse. Among these, two kinds of PS cells were isolated from mouse blastocysts: conventional embryonic stem (ES) cells with domed morphology that are maintained with LIF and BMP for self-renewal, and FAB-ES cells with flat morphology that need bFGF, activinA and BIO for self-renewal. Here, we report a novel PS cell line from rat blastocysts, which is distinguishable from conventional ES cells but is morphologically similar to mouse epiblast stem cell (EpiSC) lines. We used microarrays to detail the global program of gene expression of rES and rPS.
The heterogeneity and dynamic equilibrium of rat embryonic stem cells.
Specimen part
View SamplesSkeletal stem and progenitor cells from vertebrate species
No associated publication
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 SamplesXEN 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 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 Samples