{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPARD6A functions as a central scaffold protein that orchestrates the establishment and maintenance of cell polarity by assembling multiprotein complexes with atypical protein kinase C (aPKC) and other polarity determinants. It directly interacts with partners such as Par3, PLC‐β, and components of cell–cell junctions to regulate cytoskeletal organization, apical membrane targeting, and centrosomal protein recruitment. In epithelial, endothelial, and kidney podocyte models, PARD6A contributes to the formation and stability of tight junctions and slit diaphragms, and even localizes to specialized compartments such as nuclear speckles—thereby influencing both structural organization and signal transduction processes."}, {"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 the context of tumorigenesis and epithelial‐to‐mesenchymal transition (EMT), aberrant expression or regulation of PARD6A has been shown to drive oncogenic signaling, promote cell proliferation, and enhance invasive and migratory capabilities. By modulating the localization and activity of downstream effectors including Rho family GTPases, Rac1, and through sustained activation of the MEK/ERK cascade, PARD6A contributes to disrupted cell–cell adhesion and increased actomyosin contractility. These perturbations in polarity and cytoskeletal dynamics are linked to cancer progression in diverse tissues—including lung, breast, and bladder—and also influence insulin signaling pathways in muscle, underscoring its broad impact on pathological as well as metabolic processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional specialized roles for PARD6A emerge in the regulation of neuronal differentiation, synaptogenesis, and other developmental processes. In neuronal and placental models, PARD6A (sometimes referred to as Par6C) is upregulated in response to trophic factors such as BDNF and modulates the activity of RhoA inhibitors to influence dendritic spine formation. Moreover, by engaging with small GTPases (for example, Rit and Chp) and other effectors, it contributes to proper centrosomal positioning and the formation of a singular apical domain in polarized cells. Such interactions underline the importance of PARD6A in bridging extracellular signals to precise spatial organization during both normal development and in pathological conditions where migration and invasion become deregulated."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yoshinori Hirano, Sosuke Yoshinaga, Ryu Takeya, et al. 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