{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Txt":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337629/suppl/GSE337629_gene_fpkm.txt.gz","ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337629/suppl/GSE337629_gene_count.txt.gz"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337629/"]},"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=GSE337629"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"OASL Regulates Endothelial Function via USP39-Mediated Deubiquitination of CDK1 to Promote Large Full-Thickness Skin Defect Healing","description":"Large full-thickness skin defects (LFSDs) remain a major clinical challenge due to insufficient vascular regeneration and impaired tissue repair. Emerging evidence suggests that oligoadenylate synthase-like protein (OASL), an interferon-stimulated protein, contributes to endothelial homeostasis and vascular function; however, its role in endothelial regeneration and wound healing has not been elucidated. Here, we investigated the molecular mechanism by which OASL regulates endothelial regeneration and explored its therapeutic potential for LFSD repair.","dates":{"publication":"2026/07/09"},"accession":"GSE337629","cross_references":{"GSM":["GSM9858899","GSM9858900","GSM9858901","GSM9858902","GSM9858903","GSM9858904"],"GPL":["24676"],"GSE":["337629"],"taxon":["Homo sapiens"]}}