{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPAX7 is a pivotal paired‐box transcription factor that governs the specification, maintenance, and regenerative capacity of muscle progenitor and satellite cells. Its expression defines and regulates myogenic precursors during embryonic development and postnatal muscle homeostasis, as demonstrated in diverse models ranging from zebrafish to human induced pluripotent stem cell–derived myogenic progenitors. Aberrant PAX7 activity, such as its persistent expression in cachectic conditions and muscular dystrophies, has been linked to impaired myogenic differentiation and muscle wasting, underscoring its central role in sustaining muscle regenerative potential."}, {"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 the context of rhabdomyosarcoma, PAX7 plays multifaceted roles that vary according to tumor subtype and molecular context. In alveolar variants, chimeric fusion proteins such as PAX7‐FKHR emerge from chromosomal translocations and contribute to oncogenesis by altering transcriptional programs that block terminal myogenic differentiation. Conversely, in fusion‐negative tumors, the upregulation of wild‐type PAX7 may drive tumorigenesis by sustaining a satellite cell–like state. Furthermore, alternative splicing of PAX7 and its dynamic interactions with other myogenic regulators—including MyoD, microRNAs (for example, miR‑206) and other signaling cascades—modulate its transcriptional activity, with implications for tumor diagnosis, prognosis, and the development of differentiation‐based therapies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic studies have also implicated PAX7 in craniofacial development. Variants and rare mutations within or surrounding the PAX7 locus have been associated with an increased risk for non‐syndromic cleft lip with or without cleft palate, suggesting that—beyond its myogenic functions—PAX7 may influence broader aspects of tissue morphogenesis and developmental patterning in the craniofacial region."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence further highlights additional regulatory layers that modulate PAX7 function in both normal and disease states. In other soft tissue tumors such as Ewing sarcoma, PAX7 immunoreactivity has proven useful as a diagnostic marker, while post‐translational modifications (for example, SUMOylation) and non‐coding RNAs (including circular RNAs that modulate miR‑133/PAX7 axes) have been shown to fine‑tune its activity. 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