<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/GSE336nnn/GSE336865/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</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=GSE336865</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Nootkatone preferentially suppressed the AKT/mTOR signaling in activated fibroblasts</name><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</description><dates><publication>2026/08/17</publication></dates><accession>GSE336865</accession><cross_references><GSM>GSM9843892</GSM><GSM>GSM9843893</GSM><GSM>GSM9843894</GSM><GSM>GSM9843895</GSM><GSM>GSM9843896</GSM><GSM>GSM9843897</GSM><GSM>GSM9843898</GSM><GSM>GSM9843899</GSM><GSM>GSM9843900</GSM><GPL>34284</GPL><GSE>336865</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>