{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(6)"],"submitter":["Liu Z"],"pubmed_abstract":["The molecular mediators underlying the effects of inflammation on neural stem cells (NSCs) are not fully characterized. In this study, we identified <i>Ascl2</i> as a downstream basic helix-loop-helix (bHLH) transcription factor in NSCs following exposure to TNFα. Under normal conditions, <i>Ascl2</i> expression is inhibited at post-transcriptional levels by miR-26a, which targets the 3' untranslated region (UTR) of <i>Ascl2</i>. Upon exposure to TNFα, miR-26a expression is reduced, which leads to up-regulation of <i>Ascl2</i>. Overexpression of <i>Ascl2</i> promotes neuronal differentiation, reduces proliferation, and increases the level of cleaved CASPASE 3 in NSCs, as observed in the <i>in vitro</i> and <i>in ovo</i> experiments. <i>Ascl2</i> may serve in NSCs as a standby factor that readily responds to TNFα, which is often induced in inflammatory situations. In a chronic inflammatory condition with consistent up-regulation of TNFα, overexpression of <i>Ascl2</i> may inhibit neurogenesis as a net result."],"journal":["Aging and disease"],"pagination":["1207-1220"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6844591"],"repository":["biostudies-literature"],"pubmed_title":["TNFα-induced Up-regulation of <i>Ascl2</i> Affects the Differentiation and Proliferation of Neural Stem Cells."],"pmcid":["PMC6844591"],"pubmed_authors":["Liu Z","Jiang K","Ji X","Chen Z","Zhang YA","Wang X"],"additional_accession":[]},"is_claimable":false,"name":"TNFα-induced Up-regulation of <i>Ascl2</i> Affects the Differentiation and Proliferation of Neural Stem Cells.","description":"The molecular mediators underlying the effects of inflammation on neural stem cells (NSCs) are not fully characterized. In this study, we identified <i>Ascl2</i> as a downstream basic helix-loop-helix (bHLH) transcription factor in NSCs following exposure to TNFα. Under normal conditions, <i>Ascl2</i> expression is inhibited at post-transcriptional levels by miR-26a, which targets the 3' untranslated region (UTR) of <i>Ascl2</i>. Upon exposure to TNFα, miR-26a expression is reduced, which leads to up-regulation of <i>Ascl2</i>. Overexpression of <i>Ascl2</i> promotes neuronal differentiation, reduces proliferation, and increases the level of cleaved CASPASE 3 in NSCs, as observed in the <i>in vitro</i> and <i>in ovo</i> experiments. <i>Ascl2</i> may serve in NSCs as a standby factor that readily responds to TNFα, which is often induced in inflammatory situations. In a chronic inflammatory condition with consistent up-regulation of TNFα, overexpression of <i>Ascl2</i> may inhibit neurogenesis as a net result.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Dec","modification":"2025-06-01T12:40:59.164Z","creation":"2025-06-01T12:40:59.164Z"},"accession":"S-EPMC6844591","cross_references":{"pubmed":["31788333"],"doi":["10.14336/AD.2018.1028"]}}