YAP1 (Yes-associated protein 1) is a transcriptional co-activator that functions as a major downstream effector of the Hippo signaling pathway, integrating mechanical and cellular signals to regulate cell proliferation, tissue homeostasis, organ size control, and transcriptional programs mediated by TEAD transcription factors
[4]. When the Hippo kinase cascade is active, LATS1/2-mediated phosphorylation restricts YAP1 nuclear localization and suppresses expression of genes involved in proliferation, migration, and epithelial-mesenchymal transition (EMT)
[4]. Mechanistically, YAP1 lacks intrinsic DNA-binding activity and exerts most of its transcriptional output through TEAD family proteins, which recruit YAP1 to enhancer elements and drive target gene activation
[1]. Dysregulated YAP1 signaling has been associated with cancer initiation, tumor progression, metastasis, therapy resistance, and stem cell-related phenotypes, making the Hippo-YAP1-TEAD axis an important experimental model for studying oncogenic transcriptional regulation
[2][5]. Compared with its closely related paralog TAZ (WWTR1), YAP1 exhibits distinct alternatively spliced isoforms, and characterization of these isoforms has provided insight into structural and functional diversity within Hippo pathway signaling
[6]. For experimental applications, disruption of the YAP1-TEAD complex is widely used to investigate YAP-dependent transcription, and verteporfin has been reported to suppress YAP-TEAD activity and serves as a commonly employed pharmacological tool in preclinical studies
[3][7].