YAP/TAZ

YAP (Yes-associated protein) and TAZ (WWTR1, transcriptional co-activator with PDZ-binding motif) are the principal transcriptional co-activators downstream of the Hippo signaling pathway and mediate major transcriptional outputs that regulate cell proliferation, survival, differentiation, and tissue growth^[1][2]. Mechanistically, Hippo pathway activation induces phosphorylation of YAP/TAZ through the MST1/2-LATS1/2 kinase cascade, resulting in their cytoplasmic retention and functional inhibition, whereas pathway inactivation promotes nuclear translocation of YAP/TAZ and activation of TEAD-dependent gene transcription^[3][4][5]. By integrating mechanical cues, cell density signals, polarity inputs, extracellular matrix interactions, and soluble factors, YAP/TAZ function as central effectors that coordinate cell-fate decisions and tissue homeostasis^[3][6][5]. In physiological systems, YAP/TAZ contribute to organ development, regeneration, wound repair, and stem-cell-associated processes through transcriptional programs controlling growth and differentiation^[3][6][7]. Aberrant YAP/TAZ activation is strongly associated with tumorigenesis and cancer progression, where elevated YAP/TAZ-TEAD activity promotes proliferative and survival programs that support malignant transformation and tissue overgrowth^[2][8][7]. Compared with related upstream Hippo pathway components, YAP and TAZ represent the major downstream transcriptional effectors and share substantial functional overlap, although TAZ is the paralogue of YAP and both proteins primarily exert their biological effects through interaction with TEAD transcription factors^[1][4][9]. For experimental applications, pharmacological modulation of YAP/TAZ signaling, particularly disruption of YAP/TAZ-TEAD activity, has emerged as a widely used strategy for investigating Hippo pathway function in cancer and regenerative biology models^[8][7].