{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE311nnn/GSE311195/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311195"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"NUCB2/Nesfatin-1 promotes keratinocyte re-epithelialization by activating the mTORC1–SREBP2–HMGCR cholesterol biosynthesis axis","description":"Cutaneous re-epithelialization is a rate-limiting step of wound healing and depends on the proliferation and migration of keratinocytes. NUCB2/Nesfatin-1 is a multifunctional peptide widely expressed in mammalian tissues, but its regulatory role in keratinocyte biology remains unclear. To investigate transcriptomic programs controlled by NUCB2, we performed bulk RNA sequencing of HaCaT keratinocytes after NUCB2 knockdown. NUCB2 silencing significantly altered global gene expression patterns, most notably down-regulating sterol and cholesterol biosynthesis pathways including the SREBP2–HMGCR axis. This dataset provides a transcriptomic resource for exploring molecular mechanisms underlying NUCB2/Nesfatin-1-mediated epithelial regeneration.","dates":{"publication":"2026/09/10"},"accession":"GSE311195","cross_references":{"GSM":["GSM9320899","GSM9320902","GSM9320903","GSM9320900","GSM9320901","GSM9320904"],"GPL":["24676"],"GSE":["311195"],"taxon":["Homo sapiens"],"PMID":["[42684001]"]}}