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Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 knock-down [RNA-seq2]

ABSTRACT: We report the identification of human genes that are differentially expressed upon growth factor deprivation of Huntington's disease neural stem cells, in a FOXO3-knockdown-dependent manner. To this end, we generated RNA-seq data in human Huntington's disease (HD) and CAG-corrected (C116) neural stem cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE126869 | GEO | 2021/01/30

REPOSITORIES: GEO

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Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 nuclear induction [ChIP-Seq]

Project description:We report the identification of F0X03 targets in human Huntington's disease neural stem cells. To this end, we generated FOXO3 ChIP-seq data upon FOXO3 nuclear induction in human Huntington's disease (HD) and CAG-corrected (C116) neural stem cells.

2021-01-30 | GSE109871 | GEO

Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 nuclear induction [RNA-Seq]

Project description:We report the identification of F0X03 targets in human Huntington's disease neural stem cells. To this end, we generated RNA-seq data upon FOXO3 nuclear induction in human Huntington's disease (HD) and CAG-corrected (C116) neural stem cells.

2021-01-30 | GSE109872 | GEO

GENETIC CORRECTION OF HUNTINGTON'S DISEASE PHENOTYPES IN INDUCED PLURIPOTENT STEM CELLS

Project description:Huntington's Disease (HD) is caused by a CAG expansion in the huntingtin gene. Expansion of the polyglutamine tract in the huntingtin protein results in massive cell death in the striatum of HD patients. We report that human induced pluripotent stem cells (iPSCs) derived from HD patient fibroblasts can be corrected by replacing the expanded CAG repeat with a normal repeat using homologous recombination, and that the correction persists in iPSC differentiation into DARPP-32 positive neurons in vitro and vivo. Further, correction of the HD-iPSCs normalized pathogenic HD signaling pathways (cadherin, TGF-?, BNDF, caspase activation), and reversed disease phenotypes such as susceptibility to cell death and altered mitochondrial bioenergetics in neural stem cells. The ability to make patient-specific, genetically corrected iPSCs from HD patients will provide relevant disease models in identical genetic backgrounds and is a critical step for the eventual use of these cells in cell replacement therapy. 16 experimental samples were used overall. There were 8 replicates per group, with one group being the control, and the other being the experimental. Comparison was carried out on the Nimblegen platform.

2012-06-14 | E-GEOD-37547 | biostudies-arrayexpress

GENETIC CORRECTION OF HUNTINGTON'S DISEASE PHENOTYPES IN INDUCED PLURIPOTENT STEM CELLS

Project description:Huntington's Disease (HD) is caused by a CAG expansion in the huntingtin gene. Expansion of the polyglutamine tract in the huntingtin protein results in massive cell death in the striatum of HD patients. We report that human induced pluripotent stem cells (iPSCs) derived from HD patient fibroblasts can be corrected by replacing the expanded CAG repeat with a normal repeat using homologous recombination, and that the correction persists in iPSC differentiation into DARPP-32 positive neurons in vitro and vivo. Further, correction of the HD-iPSCs normalized pathogenic HD signaling pathways (cadherin, TGF-β, BNDF, caspase activation), and reversed disease phenotypes such as susceptibility to cell death and altered mitochondrial bioenergetics in neural stem cells. The ability to make patient-specific, genetically corrected iPSCs from HD patients will provide relevant disease models in identical genetic backgrounds and is a critical step for the eventual use of these cells in cell replacement therapy.

2012-06-15 | GSE37547 | GEO

Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 knock-down [RNA-seq2]

Project description:Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 knock-down [RNA-seq2]

| PRJNA523628 | ENA

Analysis of FOXO3 human targets in Huntington's disease neural stem cells

Project description:Analysis of FOXO3 human targets in Huntington's disease neural stem cells

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Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 nuclear induction [ChIP-Seq]

Project description:Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 nuclear induction [ChIP-Seq]

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Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 nuclear induction [RNA-Seq]

Project description:Analysis of FOXO3 human targets in Huntington's disease neural stem cells: FOXO3 nuclear induction [RNA-Seq]

| PRJNA432226 | ENA

RNA-sequencing of brain microvascular endothelial cell dysfunction in an isogenic juvenile iPSC model of Huntington’s disease

Project description:Huntington's disease (HD) is associated with dysfunction of the blood-brain barrier, including brain microvasscular endothelial cells (BMECs). We report changes in gene expression of induced pluripotent stem cells (iPSCs) and iPSC-derived brain microvascular endothelial cell-like cells (iBMECs) derived from an isogenic pair of iPSCs with either 180 (HD-corrected) or 18 (HD180) CAG repeats in the HTT gene.

2022-02-01 | GSE194416 | GEO

Expression data from human induced pluripotent stem cell derived NSCs and striatal-like cells

Project description:Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expanded stretch of CAG trinucleotide repeats that results in neuronal dysfunction and death. We made induced pluripotent stem cell (iPSC) lines from HD patients and controls. Though no obvious effects of the CAG expansion on reprogramming or subsequent neural stem cell (NSC) production were seen, HD-NSCs showed CAG expansion-associated gene expression patterns and, upon differentiation, changes in electrophysiology, metabolism, cell adhesion, and ultimately an increased risk of cell death for both medium and longer CAG repeat expansions, with some deficits greater in cells from longer repeat HD NSCs. The HD180 lines were more vulnerable than control lines to cellular stressors and BDNF withdrawal using a range of assays across consortium laboratories. This HD iPSC collection represents a unique and well-characterized resource to elucidate disease mechanisms in HD and provides a novel human stem cell platform for screening new candidate therapeutics. 8 NSC samples (5 HD, 3 control), of which 3 were run as replicates (2HD, 1 control), and 5 striatal-like samples (3 HD, 2 control) Contributor: The HD iPS consortium

2012-04-24 | E-GEOD-37517 | biostudies-arrayexpress

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