{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Moore JM"],"funding":["Medical Research Council","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["e105933"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4146563"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(8)"],"pubmed_abstract":["Members of the AFF (AF4/FMR2) family of putative transcription factors are involved in infant acute leukaemia and intellectual disability (ID), although very little is known about their transcriptional targets. For example, deletion of human lymphoid nuclear protein related to AF4/AFF member 3 (LAF4/AFF3) is known to cause severe neurodevelopmental defects, and silencing of the gene is also associated with ID at the folate-sensitive fragile site (FSFS) FRA2A; yet the normal function of this gene in the nervous system is unclear. The aim of this study was to further investigate the function of Laf4 in the brain by focusing on its role in the cortex. By manipulating expression levels in organotypic slices, we demonstrate here that Laf4 is required for normal cellular migration in the develop"],"journal":["PloS one"],"pubmed_title":["Laf4/Aff3, a gene involved in intellectual disability, is required for cellular migration in the mouse cerebral cortex."],"pmcid":["PMC4146563"],"funding_grant_id":["G0900901","BB/I021833/1","MC_UU_12021/2","084655","MC_U137761449"],"pubmed_authors":["Lee S","Lickiss T","Davies KE","Finelli MJ","Molnar Z","Moore JM","Oliver PL"],"additional_accession":[]},"is_claimable":false,"name":"Laf4/Aff3, a gene involved in intellectual disability, is required for cellular migration in the mouse cerebral cortex.","description":"Members of the AFF (AF4/FMR2) family of putative transcription factors are involved in infant acute leukaemia and intellectual disability (ID), although very little is known about their transcriptional targets. For example, deletion of human lymphoid nuclear protein related to AF4/AFF member 3 (LAF4/AFF3) is known to cause severe neurodevelopmental defects, and silencing of the gene is also associated with ID at the folate-sensitive fragile site (FSFS) FRA2A; yet the normal function of this gene in the nervous system is unclear. The aim of this study was to further investigate the function of Laf4 in the brain by focusing on its role in the cortex. By manipulating expression levels in organotypic slices, we demonstrate here that Laf4 is required for normal cellular migration in the develop","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014","modification":"2026-04-17T19:32:41.398Z","creation":"2019-03-26T23:27:00Z"},"accession":"S-EPMC4146563","cross_references":{"pubmed":["25162227"],"doi":["10.1371/journal.pone.0105933"]}}