<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/GSE327nnn/GSE327779/</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=GSE327779</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>miR-151-5p Regulates Neural Stem Cell Fate by Targeting Aph1a to Modulate Notch Signaling Gradients</name><description>To investigate the role of miR-151-5p in regulating neural stem cell (NSC) fate during neocortical development, we performed RNA-seq profiling of NSCs isolated from the developing mouse cerebral cortex. Conditional knockout of miR-151-5p led to increased Sox2 expression and enhanced NSC proliferation. Mechanistically, Aph1a, a core subunit of the γ-secretase complex, was identified as a direct target of miR-151-5p. Overexpression of Aph1a phenocopied the knockout phenotype, promoting NSC proliferation via elevated NICD levels. Our results demonstrate that miR-151-5p biases NSC fate specification by targeting Aph1a to modulate Notch signaling, thereby fine-tuning the balance between NSC maintenance and differentiation. This study reveals a novel miR-151-5p/Aph1a/Notch signaling axis governing NSC fate, providing a critical post-transcriptional regulatory layer in mammalian neocortical development.</description><dates><publication>2026/04/16</publication></dates><accession>GSE327779</accession><cross_references><GSM>GSM9665808</GSM><GSM>GSM9665807</GSM><GSM>GSM9665806</GSM><GSM>GSM9665805</GSM><GSM>GSM9665804</GSM><GSM>GSM9665803</GSM><GPL>9185</GPL><GSE>327779</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>