{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Y"],"funding":["Johns Hopkins University","NINDS NIH HHS","National Institutes of Health","Shriners Hospitals for Children"],"pagination":["111842"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9875714"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(12)"],"pubmed_abstract":["Children with SOX2 deficiency develop ocular disorders and extra-ocular CNS anomalies. Animal data show that SOX2 is essential for retinal and neural stem cell development. In the CNS parenchyma, SOX2 is primarily expressed in astroglial and oligodendroglial cells. Here, we report a crucial role of astroglial SOX2 in postnatal brain development. Astroglial Sox2-deficient mice develop hyperactivity in locomotion and increased neuronal excitability in the corticostriatal circuit. Sox2 deficiency inhibits postnatal astrocyte maturation molecularly, morphologically, and electrophysiologically without affecting astroglia proliferation. Mechanistically, SOX2 directly binds to a cohort of astrocytic signature and functional genes, the expression of which is significantly reduced in Sox2-deficient"],"journal":["Cell reports"],"pubmed_title":["SOX2 is essential for astrocyte maturation and its deletion leads to hyperactive behavior in mice."],"pmcid":["PMC9875714"],"funding_grant_id":["R01 NS099073","R01NS094559","R01NS099073","R21 NS109790","R01 NS123080","R21 NS125464","R01NS123080","R21NS109790","R01 NS094559","R01 NS123165"],"pubmed_authors":["Zhu M","Hull VL","Kim B","Gray JA","Zhang CL","Guo F","Liu S","Wang Y","Zhang S","Doan V","Lan Z","Rihani S"],"additional_accession":[]},"is_claimable":false,"name":"SOX2 is essential for astrocyte maturation and its deletion leads to hyperactive behavior in mice.","description":"Children with SOX2 deficiency develop ocular disorders and extra-ocular CNS anomalies. Animal data show that SOX2 is essential for retinal and neural stem cell development. In the CNS parenchyma, SOX2 is primarily expressed in astroglial and oligodendroglial cells. Here, we report a crucial role of astroglial SOX2 in postnatal brain development. Astroglial Sox2-deficient mice develop hyperactivity in locomotion and increased neuronal excitability in the corticostriatal circuit. Sox2 deficiency inhibits postnatal astrocyte maturation molecularly, morphologically, and electrophysiologically without affecting astroglia proliferation. Mechanistically, SOX2 directly binds to a cohort of astrocytic signature and functional genes, the expression of which is significantly reduced in Sox2-deficient","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2026-05-28T11:32:18.64Z","creation":"2025-04-07T03:16:01.176Z"},"accession":"S-EPMC9875714","cross_references":{"pubmed":["36543123"],"doi":["10.1016/j.celrep.2022.111842"]}}