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http://purl.uniprot.org/citations/12037567http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12037567http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12037567http://www.w3.org/2000/01/rdf-schema#comment"Myelin-derived axon outgrowth inhibitors, such as Nogo, may account for the lack of axonal regeneration in the central nervous system (CNS) after trauma in adult mammals. A 66-residue domain of Nogo (Nogo-66) is expressed on the surface of oligodendrocytes and can inhibit axonal outgrowth through an axonal Nogo-66 receptor (NgR). The IN-1 monoclonal antibody recognizes Nogo-A and promotes corticospinal tract regeneration and locomotor recovery; however, the undefined nature of the IN-1 epitope in Nogo, the limited specificity of IN-1 for Nogo, and nonspecific anti-myelin effects have prevented a firm conclusion about the role of Nogo-66 or NgR. Here, we identify competitive antagonists of NgR derived from amino-terminal peptide fragments of Nogo-66. The Nogo-66(1 40) antagonist peptide (NEP1 40) blocks Nogo-66 or CNS myelin inhibition of axonal outgrowth in vitro, demonstrating that NgR mediates a significant portion of axonal outgrowth inhibition by myelin. Intrathecal administration of NEP1 40 to rats with mid-thoracic spinal cord hemisection results in significant axon growth of the corticospinal tract, and improves functional recovery. Thus, Nogo-66 and NgR have central roles in limiting axonal regeneration after CNS injury, and NEP1-40 provides a potential therapeutic agent."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.org/dc/terms/identifier"doi:10.1038/417547a"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.org/dc/terms/identifier"doi:10.1038/417547a"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/author"Strittmatter S.M."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/author"Strittmatter S.M."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/author"GrandPre T."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/author"GrandPre T."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/name"Nature"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/name"Nature"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/pages"547-551"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/pages"547-551"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/title"Nogo-66 receptor antagonist peptide promotes axonal regeneration."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/title"Nogo-66 receptor antagonist peptide promotes axonal regeneration."xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/volume"417"xsd:string
http://purl.uniprot.org/citations/12037567http://purl.uniprot.org/core/volume"417"xsd:string
http://purl.uniprot.org/citations/12037567http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12037567
http://purl.uniprot.org/citations/12037567http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12037567
http://purl.uniprot.org/citations/12037567http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12037567
http://purl.uniprot.org/citations/12037567http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12037567