{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPlastin 3 (PLS3) is a critical actin‐bundling protein that plays a central role in neuromuscular function. In the context of spinal muscular atrophy (SMA), several studies have shown that increased PLS3 expression can counteract motor neuron defects by enhancing axonogenesis, stabilizing axonal growth, and restoring endocytotic capacity at neuromuscular junctions. For example, unaffected SMN1‐deleted individuals and SMA animal models display improved motor neuron connectivity when PLS3 levels are elevated, suggesting that PLS3 acts as a protective modifier by modulating the underlying actin cytoskeleton dynamics and calcium‐regulated processes in motor axons and synapses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its neuromuscular roles, PLS3 is pivotal for bone homeostasis. Genetic studies have identified loss‐of‐function mutations and deleterious variants in PLS3 as the causes of early‐onset, X‐linked osteoporosis and osteoporotic fractures. In these contexts, impaired PLS3 function disrupts osteoclast differentiation and bone remodeling—likely via alterations in NF‐κB signaling and defective bone matrix mineralization—and may compromise osteocyte dendritic function and skeletal mechanosensing. Together, these findings highlight that balanced PLS3 levels are essential for maintaining the structural integrity and metabolic function of bone."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPLS3 also has important functions in cancer biology and cell migration. Its aberrant expression has been exploited as a biomarker for circulating tumor cells in colorectal and breast cancers, where high PLS3 levels correlate with enhanced epithelial–mesenchymal transition, increased invasive potential, and even chemoresistance. Furthermore, studies in hematologic malignancies such as Sezary syndrome reveal that ectopic expression of T‐plastin (a form of PLS3) marks malignant lymphocytes and contributes to increased cell motility and survival. Complementary work in cell‐based assays has demonstrated that PLS3 modulates actin remodeling to facilitate processes such as keratinocyte migration, while biochemical investigations have clarified its calcium‐regulated binding to F‐actin through its EF‐hand domains—mechanisms that underlie its diverse roles across tumor biology, metastasis, and tissue development (e.g., in placental trophoblasts)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Gabriela E Oprea, Sandra Kröber, Michelle L McWhorter, et al. 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