{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nYWHAZ, which encodes the 14-3-3ζ protein, functions as a versatile adaptor that regulates an extensive network of cellular processes by binding phosphorylated partners. Structural and biochemical studies have revealed that 14-3-3ζ interacts with a variety of targets—including kinases, transcription factors, and other signaling proteins—to modulate their stability, subcellular localization, and activity. For example, investigations have demonstrated its involvement in chaperone‐like activities, nuclear export of β‑catenin, and regulation of mRNA decay processes, thereby orchestrating diverse signaling cascades and cytoskeletal dynamics."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer contexts, overexpression and aberrant regulation of 14-3-3ζ contribute to tumor progression and metastasis in a variety of malignancies—including breast, gastric, lung, prostate, and hematologic cancers. Enhanced 14-3-3ζ expression has been linked to increased cell migration, invasion, and resistance to apoptosis by promoting epithelial–mesenchymal transition, stabilizing β‑catenin through reduced ubiquitination, and augmenting the activity of key signaling cascades such as PI3K/Akt and TGF‑β/Smads. Additionally, 14-3-3ζ has been implicated in modulating kinase activity (for example, via association with PKCε and p85 of PI3K), interactions with hormone receptors, and even interference with viral oncoprotein functions—collectively leading to chemoresistance and poorer clinical outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "27"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, 14-3-3ζ plays pivotal roles in neural development, neurodegeneration, and immune regulation. Studies using knockout models have linked loss of 14-3-3ζ to neurodevelopmental anomalies associated with disorders such as schizophrenia, autism spectrum disorder, and bipolar disorder. Moreover, 14-3-3ζ fosters the pathological aggregation of tau protein—a hallmark of Alzheimer’s disease—by promoting conformational transitions and filament formation. In parallel, it regulates autophagy through interactions with key components like Atg9A and modulates T cell activation and differentiation via its exosomal transfer, thereby influencing innate and adaptive immune responses. Additional findings also highlight its participation in metabolic regulation via modulation of transcription factors and in post‑transcriptional control mechanisms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "39"}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "N Ostrerova, L Petrucelli, M Farrer, et al. 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