<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cao G</submitter><funding>the National Key Research and Development Program of China</funding><funding>National Natural Science Foundation of China</funding><funding>National Key Research and Development Program of China</funding><funding>the National Natural Science Foundation of China</funding><pagination>13921</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10530892</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(18)</volume><pubmed_abstract>&lt;i>FOXG1&lt;/i> (forkhead box G1) syndrome is a neurodevelopmental disorder caused by variants in the &lt;i>Foxg1&lt;/i> gene that affect brain structure and function. Individuals affected by &lt;i>FOXG1&lt;/i> syndrome frequently exhibit delayed myelination in neuroimaging studies, which may impair the rapid conduction of nerve impulses. To date, the specific effects of FOXG1 on oligodendrocyte lineage progression and myelination during early postnatal development remain unclear. Here, we investigated the effects of &lt;i>Foxg1&lt;/i> deficiency on myelin development in the mouse brain by conditional deletion of &lt;i>Foxg1&lt;/i> in neural progenitors using &lt;i>NestinCreER;Foxg1&lt;sup>fl/fl&lt;/sup>&lt;/i> mice and tamoxifen induction at postnatal day 0 (P0). We found that &lt;i>Foxg1&lt;/i> deficiency resulted in a transient de</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Conditional Deletion of &lt;i>Foxg1&lt;/i> Delayed Myelination during Early Postnatal Brain Development.</pubmed_title><pmcid>PMC10530892</pmcid><funding_grant_id>2018YFF0215202</funding_grant_id><funding_grant_id>31200823</funding_grant_id><pubmed_authors>Cao G</pubmed_authors><pubmed_authors>Lu H</pubmed_authors><pubmed_authors>Sun C</pubmed_authors><pubmed_authors>Shen C</pubmed_authors><pubmed_authors>Shen H</pubmed_authors><pubmed_authors>Qu D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Conditional Deletion of &lt;i>Foxg1&lt;/i> Delayed Myelination during Early Postnatal Brain Development.</name><description>&lt;i>FOXG1&lt;/i> (forkhead box G1) syndrome is a neurodevelopmental disorder caused by variants in the &lt;i>Foxg1&lt;/i> gene that affect brain structure and function. Individuals affected by &lt;i>FOXG1&lt;/i> syndrome frequently exhibit delayed myelination in neuroimaging studies, which may impair the rapid conduction of nerve impulses. To date, the specific effects of FOXG1 on oligodendrocyte lineage progression and myelination during early postnatal development remain unclear. Here, we investigated the effects of &lt;i>Foxg1&lt;/i> deficiency on myelin development in the mouse brain by conditional deletion of &lt;i>Foxg1&lt;/i> in neural progenitors using &lt;i>NestinCreER;Foxg1&lt;sup>fl/fl&lt;/sup>&lt;/i> mice and tamoxifen induction at postnatal day 0 (P0). We found that &lt;i>Foxg1&lt;/i> deficiency resulted in a transient de</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Sep</publication><modification>2025-06-25T03:04:20.652Z</modification><creation>2025-04-05T09:43:18.052Z</creation></dates><accession>S-EPMC10530892</accession><cross_references><pubmed>37762220</pubmed><doi>10.3390/ijms241813921</doi></cross_references></HashMap>