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Partitioning defective 3 homolog (PARD3) is a master regulator of cell polarity, especially in the formation and maintenance of apical-basal polarity in epithelial cells[1][3]. It serves as a scaffolding protein enabling the assembly of large multi-protein complexes, such as the Par polarity complex (made up of PAR3 (PARD3), PAR6, and atypical protein kinase C/aPKC), and coordinates asymmetric cell division, differentiation, axonogenesis, and tight junction formation[1][3][5]. PARD3 exerts effects on signaling pathways involved in tissue homeostasis and growth control, particularly the Hippo pathway through regulation of YAP/TAZ transcriptional co-activators[2]. Genetic or functional disruption of PARD3 results in loss of cell polarity and tissue disorganization, phenomena important in cancer progression, where PARD3 can function as either a tumor suppressor or promoter depending on cell context and tumor type[3]. Thus, PARD3 is a critical non-enzymatic scaffolding protein required for epithelial tissue architecture and is not currently considered a direct therapeutic drug target in clinical practice[1][3][5].
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