{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nYes‐associated protein 1 (YAP1) is a highly conserved transcriptional coactivator that functions as the nuclear effector of the Hippo pathway, integrating diverse upstream signals to control organ size, tissue regeneration, and stem/progenitor cell fate. In response to mechanical and physical cues—including extracellular matrix stiffness, cell shape and tension, and even direct force transmission on the nucleus that alters nuclear pore gating—YAP1 shuttles from the cytoplasm to the nucleus, where it coordinates gene‐expression programs that drive cell proliferation and inhibit apoptosis. Phosphorylation by core Hippo kinases (for example, LATS1/2) is a key regulatory event that sequesters YAP1 in the cytoplasm or targets it for degradation, thereby limiting its activity during normal development and regeneration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn numerous cancers YAP1 is aberrantly activated and acts as a potent oncogene. Elevated YAP1 activity promotes cell transformation, epithelial-to-mesenchymal transition, cancer stem cell attributes, chemoresistance, and metastasis by partnering with transcription factors (such as TEADs, TBX5, and others) and by cross-talking with signaling pathways including Wnt/β-catenin, Notch, and Ras. Moreover, altered regulation of YAP1—whether through loss of upstream inhibitory signals (for example, by mutation or misexpression of Hippo pathway components), through gene amplification, or via oncogenic fusion events—leads to unchecked proliferation and tumor progression in a wide range of epithelial and non-epithelial malignancies, including breast, colon, lung, mesothelioma, medulloblastoma, and even distinctive vascular tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its regulation by classic Hippo-mediated phosphorylation, YAP1 activity is further fine-tuned by multiple mechanisms that include post-transcriptional modifications, interactions with membrane receptors (for instance, binding to ErbB4 fragments), and modulation by metabolic cues (such as energy stress via AMPK). These additional layers of regulation not only shape its transcriptional output at distal enhancers but also influence its role in processes such as ferroptosis, alternative Wnt signaling, and even the emergence of fusion proteins in rare tumor types. In turn, these diverse regulatory inputs render YAP1 an attractive therapeutic target, as its modulation can impact drug resistance and tumor–stromal interactions across a spectrum of malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jixin Dong, Georg Feldmann, Jianbin Huang, et al. 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