{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336865/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"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=GSE336865"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Nootkatone preferentially suppressed the AKT/mTOR signaling in activated fibroblasts","description":"Having established that nootkatone restores autophagic flux and that autophagy contributes functionally to its anti-fibrotic activity, we next sought to identify the upstream events associated with this response. Transcriptomic profiling was therefore performed in TGF-β1–activated lung fibroblasts treated with or without nootkatone. RNA-seq analysis revealed clear separation among control, TGF-β1-treated, and nootkatone + TGF-β1-treated fibroblasts by principal component analysis, indicating distinct transcriptional states across groups。Pathway enrichment analysis of genes downregulated by nootkatone revealed significant enrichment of PI3K-Akt signaling and focal adhesion–PI3K-Akt-mTOR signaling, together with matrix-adhesion and cytoskeletal programs, including ECM-receptor interaction, focal adhesion, and cytoskeleton in muscle cells","dates":{"publication":"2026/08/17"},"accession":"GSE336865","cross_references":{"GSM":["GSM9843892","GSM9843893","GSM9843894","GSM9843895","GSM9843896","GSM9843897","GSM9843898","GSM9843899","GSM9843900"],"GPL":["34284"],"GSE":["336865"],"taxon":["Homo sapiens"]}}