{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRTN4—a gene encoding the Nogo proteins (including isoforms Nogo‐A, Nogo‐B, and Nogo‐C)—plays a multifaceted role in the nervous system. In the central nervous system, Nogo‐A is a well‐established inhibitor of neurite outgrowth and axonal regeneration. It exerts its effects by binding to receptors (such as NgR1 and, as more recently demonstrated, PirB or BAI–GPCR partners) and interfering with integrin‐mediated signaling and cytoskeletal rearrangements. Altered expression and splicing patterns of RTN4 isoforms are associated with several neurodegenerative and neuropsychiatric disorders, including amyotrophic lateral sclerosis, Alzheimer’s disease, multiple sclerosis, temporal lobe epilepsy, and schizophrenia; moreover, specific genetic polymorphisms and aberrant expression levels of Nogo in muscle and glial cells are emerging as potential diagnostic or prognostic markers in these conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRTN4 isoforms—especially Nogo‐B—also regulate vascular and inflammatory processes through effects on endothelial and smooth muscle cells. In blood vessels, Nogo‐B modulates cell migration, controls vascular remodeling, and contributes to the homeostatic response following injury by influencing leukocyte transmigration and intercellular adhesion molecule–1 signaling. In addition, Nogo‐related proteins shape the endoplasmic reticulum by defining tubular architecture and nanodomain organization, and phosphorylation events in Nogo‐B (mediated by kinases such as MAPKAP–K2) appear to participate in the adaptation to hypoxic and inflammatory stress in vascular smooth muscle and other cell types. These mechanisms are crucial in conditions such as pulmonary arterial hypertension, vein graft remodeling, and even aspects of heart failure."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in the nervous and vascular systems, aberrant RTN4 expression is implicated in oncogenesis and metabolic disease. In various cancers—from colorectal carcinoma to hepatocellular carcinoma and pancreatic adenocarcinoma—RTN4 (and particularly Nogo‐B) appears to be involved in the regulation of cell survival, apoptosis, and metabolic reprogramming. In certain tumor cell lines, RTN4 products have been reported to influence the balance between pro‐ and anti‐apoptotic signals (for example, via interactions with c‐FLIP and modulation of growth factor–signaling cascades), although the data are sometimes conflicting. These studies, along with observations linking RTN4 to altered lipid homeostasis and AKT signaling, support the notion that RTN4 could represent a promising therapeutic target in cancers linked to metabolic syndrome."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Luc Dupuis, Jose-Luis Gonzalez de Aguilar, Franck di Scala, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Schizophrenia and Nogo: elevated mRNA in cortex, and high prevalence of a homozygous CAA insert."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Brain Res Mol Brain Res (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/s0169-328x(02)00492-8"}], "href": "https://doi.org/10.1016/s0169-328x(02"}, {"type": "t", "text": "00492-8) PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12425946"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12425946"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Thomas Oertle, Chantal Huber, Herman van der Putten, et al. 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