{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang T"],"funding":["Malaysian Ministry of Higher Education FRGS grant"],"pagination":["2818"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11754635"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Increasing shreds of evidence suggest that neurogenic-to-gliogenic shift may be critical to the abnormal neurodevelopment observed in individuals with Down syndrome (DS). REST, the Repressor Element-1 Silencing Transcription factor, regulates the differentiation and development of neural cells. Downregulation of REST may lead to defects in post-differentiation neuronal morphology in the brain of the DS fetal. This study aims to elucidate the role of REST in DS-derived NPCs using bioinformatics analyses and laboratory validations. We identified and validated vital REST-targeted DEGs: CD44, TGFB1, FN1, ITGB1, and COL1A1. Interestingly, these genes are involved in neurogenesis and gliogenesis in DS-derived NPCs. Furthermore, we identified nuclear REST loss and the neuroblast marker, DCX, was downregulated in DS human trisomic induced pluripotent stem cells (hiPSCs)-derived NPCs, whereas the glioblast marker, NFIA, was upregulated. Our findings indicate that the loss of REST is critical in the neurogenic-to-gliogenic shift observed in DS-derived NPCs. REST and its target genes may collectively regulate the NPC phenotype."],"journal":["Scientific reports"],"pubmed_title":["Dysregulation of REST and its target genes impacts the fate of neural progenitor cells in down syndrome."],"pmcid":["PMC11754635"],"funding_grant_id":["FRGS/1/2022/SKK10/UPM/02/4"],"pubmed_authors":["Huang T","Fakurazi S","Ling KH","Cheah PS"],"additional_accession":[]},"is_claimable":false,"name":"Dysregulation of REST and its target genes impacts the fate of neural progenitor cells in down syndrome.","description":"Increasing shreds of evidence suggest that neurogenic-to-gliogenic shift may be critical to the abnormal neurodevelopment observed in individuals with Down syndrome (DS). REST, the Repressor Element-1 Silencing Transcription factor, regulates the differentiation and development of neural cells. Downregulation of REST may lead to defects in post-differentiation neuronal morphology in the brain of the DS fetal. This study aims to elucidate the role of REST in DS-derived NPCs using bioinformatics analyses and laboratory validations. We identified and validated vital REST-targeted DEGs: CD44, TGFB1, FN1, ITGB1, and COL1A1. Interestingly, these genes are involved in neurogenesis and gliogenesis in DS-derived NPCs. Furthermore, we identified nuclear REST loss and the neuroblast marker, DCX, was downregulated in DS human trisomic induced pluripotent stem cells (hiPSCs)-derived NPCs, whereas the glioblast marker, NFIA, was upregulated. Our findings indicate that the loss of REST is critical in the neurogenic-to-gliogenic shift observed in DS-derived NPCs. REST and its target genes may collectively regulate the NPC phenotype.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-01T15:01:56.009Z","creation":"2025-04-05T00:26:10.312Z"},"accession":"S-EPMC11754635","cross_references":{"pubmed":["39843579"],"doi":["10.1038/s41598-025-87314-y"]}}