{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRBFOX1 (also known as A2BP1 or Fox‐1) is a highly conserved, neuron‐ and tissue‐specific RNA binding protein that plays a pivotal role in regulating alternative splicing. By selectively recognizing the short UGCAUG motif through its RNA recognition motif (RRM), RBFOX1 modulates exon inclusion or exclusion in a position‐dependent manner. Structural and biochemical studies have revealed its unusual molecular mechanism of high‐affinity RNA binding, which not only governs splicing decisions in neural, muscle, and heart tissues but also integrates with broader splicing networks. In addition, detailed molecular dynamics analyses have demonstrated that hydration of its RRM domain can further stabilize its interaction with target sequences, underlining its finely tuned specificity for short regulatory elements."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its fundamental role in splicing regulation, genetic studies have implicated RBFOX1 as a critical risk factor and disease modifier across a diverse spectrum of neurodevelopmental and psychiatric disorders. Structural variants such as CNVs, exonic deletions, and point mutations in RBFOX1 have been associated with attention-deficit/hyperactivity disorder, autism spectrum disorder, epilepsy, and anxiety-related traits. These genetic alterations compromise its splicing network in human neural stem cells and developing neurons, leading to misregulated splicing of transcripts that control synaptic function, cortical development, and neuronal excitability. Moreover, RBFOX1’s involvement in regulating both nuclear splicing and cytoplasmic mRNA stability—as revealed by studies showing distinct nuclear versus cytoplasmic isoforms—is underscored by its overlapping associations with conditions such as glioblastoma, mood disorders, and even aspects of metabolic regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRBFOX1 also participates in specialized regulatory networks beyond the nervous system. Within cardiac and skeletal muscle, diminished RBFOX1 expression is associated with pathological conditions such as heart failure, where its reintroduction modulates the alternative splicing of key transcription factors (for example, members of the MEF2 family) that govern hypertrophic signalling. Similarly, studies in erythroid cells and zebrafish have demonstrated that precise RBFOX1-mediated splicing is essential for the proper differentiation and contractile function of muscle tissues. In addition, RBFOX1 function is dynamically modulated by interactions with other splicing regulators, such as the CELF protein family, underscoring an antagonistic balance that shapes tissue-specific exon usage and maintains cellular homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Chaolin Zhang, Zuo Zhang, John Castle, et al. 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