{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPlexin‐B1 (PLXNB1) acts as a transmembrane receptor for several semaphorins—most notably Semaphorin 4D—and is a key mediator of diverse signaling events. In both developing neural tissues and endothelial cells, PLXNB1 transduces semaphorin cues to regulate axon guidance as well as angiogenesis. Its activation by semaphorins triggers repulsive responses in neuronal growth cones while simultaneously promoting proangiogenic events in vascular endothelium."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, PLXNB1 orchestrates intracellular signaling through direct interactions with small GTPases and Rho guanine nucleotide exchange factors. Binding of active Rac, Rho, R-Ras, and M-Ras to distinct regions of its cytoplasmic domain drives cytoskeletal reorganization, integrin‐dependent adhesion, and growth cone collapse. Moreover, coupling with receptor tyrosine kinases—such as Met, Ron, and ErbB‐2—further modulates downstream cascades including the PI3K–Akt and MAPK pathways, ultimately balancing bidirectional signals that can promote or inhibit cell migration and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDysregulation of PLXNB1 signaling has been widely implicated in tumor biology. In several cancer types—including melanoma, prostate, pancreatic, and glioma—alterations in PLXNB1 expression, mutational status, or its association with partner proteins (for example, through proteolytic processing or microRNA regulation) contribute to either oncogenic or tumor‐suppressive outcomes. Depending on the cellular context, PLXNB1 can inhibit oncogenic receptor activation (such as c‐Met) and reduce integrin–FAK signaling, thereby suppressing proliferation and invasion, or it can facilitate tumor cell migration, invasion and angiogenesis by activating RhoA and other downstream effectors. Thus, PLXNB1 plays a pivotal role in mediating invasive growth, metastasis and the tumor microenvironment, with its expression levels correlating with clinical prognosis in various cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPLXNB1 function is further refined by post‐translational mechanisms—including proteolytic conversion and interactions with specific Rho proteins—and by its integration within broader tissue-specific signaling networks. Mutation in PLXNB1’s regulatory domains can alter its binding to Rac and Rnd family proteins, impacting the assembly of signaling complexes that control cell motility, differentiation, endometrial adhesiveness, and even stem cell conversion. 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