<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chailangkarn T</submitter><funding>NIMH NIH HHS</funding><funding>NIDCD NIH HHS</funding><funding>NIH HHS</funding><funding>PHS HHS</funding><pagination>338-43</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4995142</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>536(7616)</volume><pubmed_abstract>Williams syndrome is a genetic neurodevelopmental disorder characterized by an uncommon hypersociability and a mosaic of retained and compromised linguistic and cognitive abilities. Nearly all clinically diagnosed individuals with Williams syndrome lack precisely the same set of genes, with breakpoints in chromosome band 7q11.23 (refs 1-5). The contribution of specific genes to the neuroanatomical and functional alterations, leading to behavioural pathologies in humans, remains largely unexplored. Here we investigate neural progenitor cells and cortical neurons derived from Williams syndrome and typically developing induced pluripotent stem cells. Neural progenitor cells in Williams syndrome have an increased doubling time and apoptosis compared with typically developing neural progenitor </pubmed_abstract><journal>Nature</journal><pubmed_title>A human neurodevelopmental model for Williams syndrome.</pubmed_title><pmcid>PMC4995142</pmcid><funding_grant_id>R56 MH109587</funding_grant_id><funding_grant_id>U19MH107367</funding_grant_id><funding_grant_id>1-DP2-OD006495-01</funding_grant_id><funding_grant_id>R01MH094753</funding_grant_id><funding_grant_id>U19MH106434</funding_grant_id><funding_grant_id>R01MH095741</funding_grant_id><funding_grant_id>DP2 OD006495</funding_grant_id><funding_grant_id>R01 MH094753</funding_grant_id><funding_grant_id>T32 MH020002</funding_grant_id><funding_grant_id>R01MH103134</funding_grant_id><funding_grant_id>U19 MH107367</funding_grant_id><funding_grant_id>T32 DC007361</funding_grant_id><funding_grant_id>P01 NICHD033113</funding_grant_id><funding_grant_id>R01 MH100175</funding_grant_id><funding_grant_id>R01 MH103134</funding_grant_id><pubmed_authors>Bellugi U</pubmed_authors><pubmed_authors>Halgren E</pubmed_authors><pubmed_authors>Searcy YM</pubmed_authors><pubmed_authors>Marchetto MC</pubmed_authors><pubmed_authors>Muotri AR</pubmed_authors><pubmed_authors>DeWitt M</pubmed_authors><pubmed_authors>Freitas BC</pubmed_authors><pubmed_authors>Romero S</pubmed_authors><pubmed_authors>Stefanacci L</pubmed_authors><pubmed_authors>Herai RH</pubmed_authors><pubmed_authors>Yu DX</pubmed_authors><pubmed_authors>Trujillo CA</pubmed_authors><pubmed_authors>Korenberg JR</pubmed_authors><pubmed_authors>McHenry L</pubmed_authors><pubmed_authors>Wong W</pubmed_authors><pubmed_authors>Hanson KL</pubmed_authors><pubmed_authors>Gage FH</pubmed_authors><pubmed_authors>Chailangkarn T</pubmed_authors><pubmed_authors>Jarvinen A</pubmed_authors><pubmed_authors>Dai L</pubmed_authors><pubmed_authors>Semendeferi K</pubmed_authors><pubmed_authors>Brown TT</pubmed_authors><pubmed_authors>Hrvoj-Mihic B</pubmed_authors><pubmed_authors>Lai P</pubmed_authors><pubmed_authors>Dale AM</pubmed_authors><pubmed_authors>Jacobs B</pubmed_authors><pubmed_authors>Bardy C</pubmed_authors><pubmed_authors>Ard MC</pubmed_authors></additional><is_claimable>false</is_claimable><name>A human neurodevelopmental model for Williams syndrome.</name><description>Williams syndrome is a genetic neurodevelopmental disorder characterized by an uncommon hypersociability and a mosaic of retained and compromised linguistic and cognitive abilities. Nearly all clinically diagnosed individuals with Williams syndrome lack precisely the same set of genes, with breakpoints in chromosome band 7q11.23 (refs 1-5). The contribution of specific genes to the neuroanatomical and functional alterations, leading to behavioural pathologies in humans, remains largely unexplored. Here we investigate neural progenitor cells and cortical neurons derived from Williams syndrome and typically developing induced pluripotent stem cells. Neural progenitor cells in Williams syndrome have an increased doubling time and apoptosis compared with typically developing neural progenitor </description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Aug</publication><modification>2026-05-01T03:56:42.497Z</modification><creation>2026-04-07T16:39:45.995Z</creation></dates><accession>S-EPMC4995142</accession><cross_references><pubmed>27509850</pubmed><doi>10.1038/nature19067</doi></cross_references></HashMap>