{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRTN4R (also known as the Nogo‐66 receptor or NgR1) is a glycosylphosphatidylinositol‑anchored neuronal receptor that engages with myelin‐associated inhibitory factors—including Nogo‑A (through its Nogo‑66 domain), oligodendrocyte‑myelin glycoprotein (OMgp) and myelin‑associated glycoprotein (MAG)—to restrict neurite outgrowth and impede axonal regeneration in the adult central nervous system. RTN4R functions as the binding partner through which these ligands elicit inhibitory signals, often in complex with co‑receptors such as p75^NTR and LINGO‑1, and its specific spatiotemporal expression in neurons and oligodendrocytes is consistent with its role in limiting axonal sprouting following injury."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical role in mediating myelin‐dependent inhibition of axonal growth, RTN4R signaling also influences synaptic structure and function. Studies have demonstrated that its activity modulates dendritic spine morphology and the efficacy of long‑term synaptic plasticity, thereby impacting cortical network function and working memory. Genetic variations in the RTN4R gene have been associated with susceptibility to neuropsychiatric disorders—including schizophrenia and certain forms of dementia—and the receptor has even been implicated as an entry receptor for neurotropic viruses such as reovirus."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence further reveals that RTN4R is implicated in diverse pathophysiological processes. In white matter stroke models, aberrant RTN4R signaling contributes to altered oligodendrocyte progenitor cell fate and impaired remyelination, while in various tumor settings—such as gliomas and astrocytomas—RTN4R expression influences cell adhesion, invasion, and apoptosis. Its interactions with additional ligands (for example, BLyS) and binding partners (including BAI adhesion‐GPCRs) underscore a complex regulatory network that is modulated by proteolytic shedding, post‑translational modifications and genetic/epigenetic variation. Such multifaceted roles highlight RTN4R as a critical nexus in neural repair, synaptic regulation and disease susceptibility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kevin C Wang, Vuk Koprivica, Jieun A Kim, et al. 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