{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRBFOX2, also known as Fox‐2, is a highly conserved RNA‐binding splicing factor that recognizes the UGCAUG element in a position‐dependent manner and orchestrates alternative splicing decisions during normal development. In human embryonic stem cells, neurons and muscle, RBFOX2 regulates the inclusion or skipping of critical exons, thereby controlling cell survival, differentiation and neuromuscular function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its developmental role, RBFOX2 is central to cell‐fate reprogramming and tissue-specific differentiation programs. Its splicing activity modulates transcript isoforms during cellular reprogramming and myogenesis––for example, by directing alternative splicing switches in transcripts involved in muscle cell fusion and in brain/muscle/heart microexon inclusion. Genetic studies have also linked RBFOX2 to reading and language performance, supporting its contribution to neural transcript diversity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRBFOX2 also contributes to the splicing programs that underlie the epithelial–mesenchymal transition and are frequently altered in cancer. Its regulated activity is essential to maintain mesenchymal splicing signatures, and loss or dysregulation of RBFOX2 leads to dramatic shifts in the splicing of genes involved in cell adhesion, cytoskeletal remodeling and apoptosis. Such mis‐regulation has been observed in ovarian, Ewing sarcoma, glioblastoma, lymphoid, gastric and pancreatic cancers, where altered RBFOX2‐dependent splicing is linked to enhanced cell migration, invasion and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the cardiovascular system, precise RBFOX2 splicing regulation is imperative for proper cardiac conduction and vascular function. Mutations or aberrant production of non‐muscle/dominant‐negative RBFOX2 isoforms disrupt the splicing of key substrates—including those controlling calcium channel function and myocyte fusion—thereby contributing to congenital heart defects such as hypoplastic left heart syndrome as well as diabetic cardiomyopathy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical role in exon definition, RBFOX2 integrates into broader layers of RNA metabolism. It can bind to miRNA precursor terminal loops to modulate microRNA biogenesis, associates with chromatin in a nascent RNA–dependent fashion to impact Polycomb complex recruitment, and interacts with additional splicing regulators (such as hnRNPs and SR proteins) using distinct binding configurations. 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