<HashMap><database>GEO</database><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=GSE305691</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Effect of PAX2 and PAX8 knockdown on gene expression in ADPKD-derived epithelial cells WT9-7 and WT9-12</name><description>PAX2 and PAX8 are transcription factors linked to autosomal dominant polycystic kidney disease (ADPKD). Based on observations in 3D in vitro models showing that knockdown of either PAX2 or PAX8 reduced cyst-like growth in ADPKD-derived epithelial cells, transcriptomic analysis was performed to investigate their downstream gene regulatory roles. RNA sequencing was conducted in two human ADPKD-derived cell lines, WT9-7 and WT9-12, following siRNA-mediated knockdown. In WT9-7 cells, PAX2, PAX8, or combined PAX2/PAX8 knockdowns were performed, whereas in WT9-12 cells only PAX8 knockdown was carried out due to minimal PAX2 expression. Differential expression and gene ontology enrichment analyses were conducted to identify distinct and overlapping biological pathways regulated by PAX2 and PAX8 in cystic epithelial cells.</description><dates><publication>2026/05/20</publication></dates><accession>GSE305691</accession><cross_references><GSM>GSM9181810</GSM><GSM>GSM9181821</GSM><GSM>GSM9181820</GSM><GSM>GSM9181823</GSM><GSM>GSM9181812</GSM><GSM>GSM9181822</GSM><GSM>GSM9181811</GSM><GSM>GSM9181818</GSM><GSM>GSM9181817</GSM><GSM>GSM9181809</GSM><GSM>GSM9181819</GSM><GSM>GSM9181808</GSM><GSM>GSM9181825</GSM><GSM>GSM9181814</GSM><GSM>GSM9181813</GSM><GSM>GSM9181824</GSM><GSM>GSM9181816</GSM><GSM>GSM9181815</GSM><GPL>34284</GPL><GSE>305691</GSE><taxon>Homo sapiens</taxon><PMID>[41501598]</PMID></cross_references></HashMap>