GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE345nnn/GSE345280/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE345280GEOGSEfalseKaiso is a novel TAZ-interaction partner that promotes hepatic stellate cell activation and regulates the downstream lncRNA HIF1A-AS3Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), are key regulators of hepatic stellate cell (HSC) activation and liver fibrosis. While the canonical YAP/TAZ-TEAD axis is well-characterized, non-canonical interaction partners and downstream long non-coding RNAs (lncRNAs) that orchestrate fibrogenic programs in HSCs remain undefined. Using BioID and next-generation sequencing (NGS) in LX-2 cells, we identified YAP/TAZ-interactomes and YAP/TAZ-regulated lncRNAs. BioID results and proximity ligation assay (PLA) identified the transcription factor Kaiso as a TAZ interaction partner. Functionally, Kaiso knockdown suppressed key aspects of HSC activation in LX-2 cells. We next integrated our NGS results from YAP/TAZ-knockdown in LX-2 cells with publicly available Kaiso ChIP-seq data. This identified HIF1A-AS3 as a common downstream lncRNA. ChIP-qPCR confirmed direct binding of Kaiso to HIF1A-AS3 promoter. Furthermore, HIF1A-AS3 silencing mirrored the functional effects of Kaiso knockdown. Global proteomic profiling following knockdown of TAZ, Kaiso, or HIF1A-AS3 revealed a network of commonly regulated proteins enriched for pathways central to HSC activation. In conclusion, we establish Kaiso as a novel TAZ interaction partner and identify HIF1A-AS3 as a shared downstream target of TAZ and Kaiso, suggesting a potential profibrotic regulatory network that promotes HSC activation and may represent a therapeutic target for liver fibrosis.2026/09/14GSE345280GSM10000814GSM10000813GSM10000818GSM10000817GSM10000816GSM10000815GSM10000819GSM10000821GSM1000082023227345280Homo sapiens