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Homo sapiens

ABSTRACT: RNA-Seq Analysis in hES/ iPS cell-derived neuronal samples

PROVIDER: PRJNA266234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1639070.fastq.gz	Fastqsanger.gz
	SRR1639080.fastq.gz	Fastqsanger.gz
	SRR1639071.fastq.gz	Fastqsanger.gz
	SRR1639072.fastq.gz	Fastqsanger.gz
	SRR1639073.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:RNA-Seq Analysis in purified iPS cell-derived neuronal samples

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Transcription profiling of human embryonic stem cell-derived fibroblasts, primary human fetal cells, and diverse cells of neonatal and adult human origin derived pluripotent stem cells (iPS) - reprogramming of human somatic cells to pluripotency with defined factors

Project description:Pluripotency, the capacity of embryo-derived stem cells to generate all tissues in the organism, can be induced in somatic cells by nuclear transfer into oocyte, fusion with embryonic stem cells, and for male germ cells by cell culture alone. Recently, murine fibroblasts have been reprogrammed directly to pluripotency by ectopic expression of four transcription factors (Oct4, Sox2, Klf4, and Myc) to yield induced Pluripotent Stem (iPS) cells. Using the same four factors, we have derived iPS cells from human embryonic stem cell-derived fibroblasts, primary human fetal cells, and diverse cells of neonatal and adult human origin. The human iPS cells manifest the colony morphology, gene expression patterns, and epigenetic characteristics of human Embryonic Stem (hES) cells, and form well-differentiated teratomas in immune-deficient mice. These data demonstrate that defined factors can reprogram human cells to pluripotency, and establish a method whereby patient-specific cells might be established in culture. Biological replicates:; GSM248201 and GSM248202; GSM248205 and GSM248206; GSM248207 and GSM248208; GSM248209 and GSM248210; GSM248211 and GSM248212; GSM248213 and GSM248214. Sample descriptions:; H1-OGN: ES cells expressing GFP-NEO marker under OCT4 promoter; dH1f: differentiated H1-OGN fibroblasts; dHcf16: differentiated H1-OGN cloned fibroblasts; MRC5: fetal lung fibroblasts; BJ1: neonatal fibroblasts Experiment Overall Design: RNA samples from hES cells, differentiated hES cells, human fibroblasts, iPS cells from differentiated hES cells, and iPS cells from human fibroblasts. Gene expression of those cells were analyzed.

2008-06-17 | E-GEOD-9832 | biostudies-arrayexpress

ATAC-seq of human (Homo sapiens) and cynomolgus macaque (Macaca fascicularis) iPSC and iPSC-derived NPC cell lines

Project description:ATAC-seq samples from 2 species and 2 cell types were generated to study cis-regulatory element evolution. Briefly, previously generated urinary stem cell derived iPS-cells (Homo sapiens) of 2 human individuals and fibroblast derived cynomolgus macaque iPSCs (Macaca fascicularis) of 2 individuals (Geuder et al. 2021) were differentiated to neural progenitor cells via dual-SMAD inhibition as three-dimensional aggregation culture (Chambers et al. 2009; Ohnuki et al. 2014). The NPC lines were cultured in NPC proliferation medium and passaged 2 - 4 times until they were dissociated and subjected to ATAC-seq together with the respective iPSC clones. ATAC-seq libraries were generated using the Omni-ATAC protocol (Corces et al. 2017) with minor modifications.

2023-10-25 | E-MTAB-13373 | biostudies-arrayexpress

Functional changes of AMPA responses in human induced pluripotent stem cell-derived neural progenitors in fragile X syndrome

Project description:Transcriptome analysis of RNA samples collected from human control and FXS iPS cell-derived neural progenitors at day 1 of differentiation.

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Allele-specific open chromatin in human neurons elucidates functional noncoding disease variants

Project description:ASoC variants are prevalent and cell type-specific ASoC variants were over-represented in intergenic regions and active enhancers. The collection includes ATAC-Seq and RNA-Seq data that were taken from human iPS cells and their derived neuronal cells (neural progenitor cells, cortical glutamatergic neurons, GABAergic neurons, and dopaminergic neurons).

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A CRISPR-engineered Isogenic Model Reveals Altered Neuronal Phenotypes of the 22q11.2 A-B Syndromic Deletion

Project description:The 22q11.2 deletion syndrome (22q11.2DS) is the most common copy number variant (CNV)-associated syndrome, leading to congenital and neuropsychiatric anomalies. Patient-derived, induced pluripotent stem cell (iPS) models have provided important insight into the mechanisms of phenotypic features of this condition. However, patient-derived iPSC models may harbor underlying genetic heterogeneity that can confound analysis of pathogenic CNV effects. Furthermore, the ~1.5 Mb “A-B” deletion at this locus is inherited at higher frequency than the more common ~2.7 Mb “A-D” deletion, but remains under-studied due to lack of relevant models. To address these issues, here we leveraged a CRISPR-based strategy in Cas9-expressing iPS cells to engineer novel isogenic models of the 22q11.2 “A-B” deletion. After in vitro differentiation to excitatory neurons, integrated transcriptomic and cell surface proteomics identified deletion-associated alterations in surface adhesion markers. Furthermore, implantation of iPS-derived neuronal progenitor cells into the cortex of neonatal mice found decreased proliferation and accelerated neuronal maturation within a relevant microenvironment. Taken together, our results suggest potential pathogenic mechanisms of the 22q11.2 “A-B” deletion in driving neuronal and neurodevelopmental phenotypes. We further propose that the isogenic models generated here will provide a unique resource to study this less-common variant of the 22q11.2 microdeletion syndrome.

2023-05-11 | PXD032075 | Pride

Pompe disease induced pluripotent stem cells for pathogenesis modeling, drug testing and disease marker identification

Project description:Pompe disease is caused by autosomal recessive mutations in the GAA gene, which encodes acid alpha-glucosidase. Although enzyme replacement therapy has recently improved patient survival greatly, the results in skeletal muscles and for advanced disease are still not satisfactory. Here, we report the derivation of Pompe disease induced pluripotent stem cells (PomD-iPSCs) and their potential for pathogenesis modeling, drug testing and disease marker identification. PomD-iPSCs maintained pluripotent features, and had low GAA activity and high glycogen content. Cardiomyocyte-like cells (CMLCs) differentiated from PomD-iPSCs recapitulated the hallmark Pompe disease pathophysiological phenotypes, including high levels of glycogen, abundant intracellular LAMP-1- or LC3-positive granules, and multiple ultrastructural aberrances. Drug rescue assessment showed that exposure of PomD-iPSC-derived CMLCs to rhGAA reversed the major pathologic phenotypes. Further, L-carnitine and 3- methyladenine treatment reduced defective cellular respiration and buildup of phagolysosomes, respectively, in the diseased cells. By comparative transcriptome analysis, we identified glycogen metabolism, lysosome and mitochondria related marker genes whose expression robustly correlated with the therapeutic effect of drug treatment in PomD-iPSC-derived CMLCs. Collectively, these results demonstrate that PomD-iPSCs are a promising in vitro disease model for development of novel therapeutic strategies for Pompe disease. Total RNA were isolated from HESC, HF(Pompe disease), PomD-iPSC, HES-CMLC, and PomD-iPS-CMLC. The series included two HESC lines, two HF(Pompe disease) cell lines, four PomD-iPS cell lines, and HES-CMLC were differentiated from one HESC line(HESC2), PomD-iPS-CMLC were differentiated from 3 PomD-iPS cell lines(PomD-iPSC A10, PomD-iPSC A17, PomD-iPSC B03). Each condition was repeated twice and used HESC as control.

2011-02-17 | E-GEOD-27280 | biostudies-arrayexpress

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Project description:RNA sequence analysis of HBV genome inserted iPS cells derived hepatocyte

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Project description:Single-cell RNA sequence analysis of iPS cell-derived cardiomyocytes treated with S-RBD-sfGFP or GFP

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Project description:RNA-Seq of iPS cell-derived MN axons established from ALS patients with TARDBP mutation

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