{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327779/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327779"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"miR-151-5p Regulates Neural Stem Cell Fate by Targeting Aph1a to Modulate Notch Signaling Gradients","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.","dates":{"publication":"2026/04/16"},"accession":"GSE327779","cross_references":{"GSM":["GSM9665808","GSM9665807","GSM9665806","GSM9665805","GSM9665804","GSM9665803"],"GPL":["9185"],"GSE":["327779"],"taxon":["Mus musculus"]}}