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The Yes-associated protein and transcriptional co-activator with PDZ-binding motif (YAP/TAZ) signaling pathway, most commonly referred to as the YAP/TAZ signaling pathway, comprises two key transcriptional co-activator proteins—YAP and TAZ—that act as principal nuclear effectors of the Hippo signaling pathway[1][7][9]. YAP and TAZ translocate to the nucleus upon activation, where they interact with TEAD family transcription factors (TEAD1-4) to promote the expression of genes involved in cell proliferation, inhibition of apoptosis, stem cell maintenance, lineage specification, and tissue growth control[1][3][4]. While primarily regarded as essential factors for normal tissue regeneration and repair, dysregulation of YAP/TAZ activity is broadly implicated in a wide spectrum of cancers—driving tumor cell proliferation, therapy resistance, and stemness. The pathway is also linked to fibrotic and neurodevelopmental diseases[2][5][8]. YAP/TAZ activity is tightly controlled by the Hippo core kinase cascade, cell-cell junctions, mechanical signals, metabolic cues, and a range of upstream pathways (e.g., Wnt, GPCR, EGFR)[4][8][9]. Given their central role in oncogenesis and tissue biology, YAP/TAZ (often evaluated as their nuclear-to-cytoplasmic localization status or target gene signature) are being pursued as therapeutic targets, mainly through inhibition of the YAP/TAZ–TEAD transcriptional program[2][5][7].
Inhibition of YAP/TAZ–TEAD DNA-binding and transcriptional co-activation; Disruption of the Hippo pathway upstream kinase function, leading to altered YAP/TAZ regulation
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