{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nWWTR1 (TAZ) is a versatile transcriptional co‐activator that functions as a key mechanosensor and mediator of extracellular cues. In response to physical signals—such as extracellular matrix rigidity, cell geometry and actomyosin tension—TAZ shuttles into the nucleus where it regulates gene expression to control stem cell fate, tissue regeneration, and differentiation. For example, TAZ modulates mesenchymal stem cell lineage decisions by co‐activating osteogenic transcription factors while repressing adipogenic signals, and it is essential for maintaining basal cell identity in epithelia and for proper wound repair. These findings demonstrate that TAZ interprets mechanical inputs into biochemical responses that guide normal development and homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer and other disease contexts, TAZ becomes pathologically activated and drives tumor progression, metastasis, and therapy resistance. By partnering predominantly with TEAD transcription factors and interfacing with signaling pathways such as TGF‑β, Wnt/β‐catenin and Hippo, TAZ promotes epithelial–mesenchymal transition, the acquisition of cancer stem cell properties, and even the modulation of drug responses (including evasion of taxane‐induced cytotoxicity and ferroptosis). In diverse malignancies ranging from breast and oral cancers to glioblastoma, aberrant TAZ activity reprograms gene expression programs that foster uncontrolled proliferation, invasive behavior and immune evasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "27"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, TAZ orchestrates transcription by localizing to specific enhancer and super‐enhancer regions, recruiting co‐activators (for example, BRD4 and Mediator) and even forming phase‑separated nuclear condensates that potentiate robust gene activation. Beyond its transcriptional co‐activation role, TAZ can also function as a co‐repressor – for instance, by engaging chromatin‐remodeling complexes to silence tumor‐suppressive genes. TAZ additionally integrates signals from metabolic and inflammatory pathways: it modulates nutrient uptake and mTORC1 activation via regulation of amino acid transporters, influences fibroblast activation in stiff, fibrotic matrices, and even dampens innate immune responses by inhibiting kinases such as TBK1. Collectively, these multifaceted functions underscore TAZ’s role as a central node linking mechanical, metabolic, and inflammatory cues to gene expression programs that govern cell identity, tissue homeostasis and disease pathogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "41"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jeong-Ho Hong, Eun Sook Hwang, Michael T McManus, et al. 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