<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314079/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE314079</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>KAT6A is essential for developmental control gene expression in neural stem and progenitor cells</name><description>Heterozygous mutations in the MYST family histone acetyltransferase gene, KAT6A (MOZ, MYST3) cause the human congenital disorders characterised by intellectual disability, Arboleda-Tham syndrome (KAT6A syndrome). In this dataset, we used neural stem cells isolated from Kat6a+/+, Kat6a+/– and Kat6a–/– E12.5 mouse embryos cultured under proliferating and differentiating conditions to assess the effects of loss of one or both alleles of Kat6a on neural stem and progenitor proliferation and differentiation.</description><dates><publication>2026/04/20</publication></dates><accession>GSE314079</accession><cross_references><GSM>GSM9381223</GSM><GSM>GSM9381234</GSM><GSM>GSM9381222</GSM><GSM>GSM9381233</GSM><GSM>GSM9381244</GSM><GSM>GSM9381243</GSM><GSM>GSM9381232</GSM><GSM>GSM9381221</GSM><GSM>GSM9381231</GSM><GSM>GSM9381242</GSM><GSM>GSM9381230</GSM><GSM>GSM9381241</GSM><GSM>GSM9381240</GSM><GSM>GSM9381229</GSM><GSM>GSM9381228</GSM><GSM>GSM9381239</GSM><GSM>GSM9381227</GSM><GSM>GSM9381238</GSM><GSM>GSM9381237</GSM><GSM>GSM9381226</GSM><GSM>GSM9381225</GSM><GSM>GSM9381236</GSM><GSM>GSM9381235</GSM><GSM>GSM9381224</GSM><GPL>30172</GPL><GSE>314079</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>