{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nA large body of genetic and clinical studies has implicated PHACTR1 as an important factor in vascular disease. Genome‐wide association studies have repeatedly linked non‐coding variants in the PHACTR1 locus to early‐onset myocardial infarction, coronary artery disease, cervical artery dissection, fibromuscular dysplasia, spontaneous coronary artery dissection, and other vascular traits. In these studies, risk alleles (for example, rs9349379) have been associated not only with disease susceptibility but also with measures of vascular tone, carotid geometry, pulse pressure, and atherosclerotic plaque formation. These observations suggest that PHACTR1 is centrally involved in modulating vascular homeostasis, potentially through distal regulation of vasoactive factors such as endothelin‑1 as well as other cellular mechanisms that influence endothelial function and vessel remodeling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the cellular and molecular level, PHACTR1 encodes a protein that binds actin and regulates protein phosphatase 1 (PP1) activity, thereby modulating actin cytoskeletal dynamics. In endothelial cells, PHACTR1 is up‑regulated by VEGF signaling and is required for tube formation, cell migration, and survival. Moreover, in other cell types such as breast cancer cells, TGF‑β–induced down‑regulation of specific microRNAs leads to enhanced PHACTR1 expression, which in turn promotes actin reorganization and cell migration. These findings highlight PHACTR1’s role as a key mediator of cytoskeletal remodeling—a process that is essential for both vessel formation and vascular stability."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its vascular functions, emerging evidence indicates that PHACTR1 is critical for proper brain development. De novo missense mutations in PHACTR1 that impair its actin‐binding or phosphatase regulatory functions have been linked to neurodevelopmental disorders such as West syndrome and epileptic encephalopathies. In neuronal cells, disruption of PHACTR1 activity interferes with cortical neuron migration and synaptic function, suggesting that precise control of actin dynamics by PHACTR1 is essential for normal cortical organization and neuronal activity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "32", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Sekar Kathiresan, Benjamin F Voight, Shaun Purcell, et al. 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