<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Geben LC</submitter><funding>NEI NIH HHS</funding><funding>NICHD NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pubmed_abstract>A limiting factor in the regenerative capacity of the adult brain is the abundance and proliferative ability of neural stem cells (NSCs). Adult NSCs are derived from a subpopulation of embryonic NSCs that temporarily enter quiescence during mid-gestation and remain quiescent until postnatal reactivation. Here we present evidence that the mechanistic/mammalian target of rapamycin (mTOR) pathway regulates quiescence entry in embryonic NSCs of the developing forebrain. Throughout embryogenesis, two downstream effectors of mTOR, p-4EBP1/2 T37/46 and p-S6 S240/244, were mutually exclusive in NSCs, rarely occurring in the same cell. While 4EBP1/2 was phosphorylated in stem cells undergoing mitosis at the ventricular surface, S6 was phosphorylated in more differentiated cells migrating away from </pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.02.14.528513</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9948964</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Dephosphorylation of 4EBP1/2 Induces Prenatal Neural Stem Cell Quiescence.</pubmed_title><pmcid>PMC9948964</pmcid><funding_grant_id>T32 GM007628</funding_grant_id><funding_grant_id>F31 NS120608</funding_grant_id><funding_grant_id>F31 HD106890</funding_grant_id><funding_grant_id>U24 DK059637</funding_grant_id><funding_grant_id>P30 DK058404</funding_grant_id><funding_grant_id>T32 HD007502</funding_grant_id><funding_grant_id>P30 EY008126</funding_grant_id><funding_grant_id>U54 CA217450</funding_grant_id><funding_grant_id>P30 DK020593</funding_grant_id><funding_grant_id>R01 DK106476</funding_grant_id><funding_grant_id>P30 CA068485</funding_grant_id><funding_grant_id>R01 NS118580</funding_grant_id><funding_grant_id>R01 NS096238</funding_grant_id><funding_grant_id>R01 CA226833</funding_grant_id><pubmed_authors>Gallagher JE</pubmed_authors><pubmed_authors>Brockman AA</pubmed_authors><pubmed_authors>Scheuing AL</pubmed_authors><pubmed_authors>Irish JM</pubmed_authors><pubmed_authors>Ess KC</pubmed_authors><pubmed_authors>Chalkley MBL</pubmed_authors><pubmed_authors>Simerly RB</pubmed_authors><pubmed_authors>Sweet SR</pubmed_authors><pubmed_authors>Ihrie RA</pubmed_authors><pubmed_authors>Geben LC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dephosphorylation of 4EBP1/2 Induces Prenatal Neural Stem Cell Quiescence.</name><description>A limiting factor in the regenerative capacity of the adult brain is the abundance and proliferative ability of neural stem cells (NSCs). Adult NSCs are derived from a subpopulation of embryonic NSCs that temporarily enter quiescence during mid-gestation and remain quiescent until postnatal reactivation. Here we present evidence that the mechanistic/mammalian target of rapamycin (mTOR) pathway regulates quiescence entry in embryonic NSCs of the developing forebrain. Throughout embryogenesis, two downstream effectors of mTOR, p-4EBP1/2 T37/46 and p-S6 S240/244, were mutually exclusive in NSCs, rarely occurring in the same cell. While 4EBP1/2 was phosphorylated in stem cells undergoing mitosis at the ventricular surface, S6 was phosphorylated in more differentiated cells migrating away from </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2025-04-19T13:32:55.602Z</modification><creation>2025-04-19T13:32:55.602Z</creation></dates><accession>S-EPMC9948964</accession><cross_references><pubmed>36824760</pubmed><doi>10.1101/2023.02.14.528513</doi></cross_references></HashMap>