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http://purl.uniprot.org/citations/26484536http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26484536http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26484536http://www.w3.org/2000/01/rdf-schema#comment"The ability of specific neurons to regenerate their axons after injury is governed by cell-intrinsic regeneration pathways. In Caenorhabditis elegans, the JNK and p38 MAPK pathways are important for axon regeneration. Axonal injury induces expression of the svh-2 gene encoding a receptor tyrosine kinase, stimulation of which by the SVH-1 growth factor leads to activation of the JNK pathway. Here, we identify ETS-4 and CEBP-1, related to mammalian Ets and C/EBP, respectively, as transcriptional activators of svh-2 expression following axon injury. ETS-4 and CEBP-1 function downstream of the cAMP and Ca2+-p38 MAPK pathways, respectively. We show that PKA-dependent phosphorylation of ETS-4 promotes its complex formation with CEBP-1. Furthermore, activation of both cAMP and Ca2+ signaling is required for activation of svh-2 expression. Thus, the cAMP/Ca2+ signaling pathways cooperatively activate the JNK pathway, which then promotes axon regeneration."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.org/dc/terms/identifier"doi:10.1371/journal.pgen.1005603"xsd:string
http://purl.uniprot.org/citations/26484536http://purl.org/dc/terms/identifier"doi:10.1371/journal.pgen.1005603"xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/author"Li C."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/author"Li C."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/author"Matsumoto K."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/author"Matsumoto K."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/author"Hisamoto N."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/author"Hisamoto N."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/name"PLoS Genet."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/name"PLoS Genet."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/pages"E1005603"xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/pages"E1005603"xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/title"Axon regeneration is regulated by Ets-C/EBP transcription complexes generated by activation of the cAMP/Ca2+ signaling pathways."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/title"Axon regeneration is regulated by Ets-C/EBP transcription complexes generated by activation of the cAMP/Ca2+ signaling pathways."xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/26484536http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/26484536http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26484536
http://purl.uniprot.org/citations/26484536http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26484536
http://purl.uniprot.org/citations/26484536http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26484536
http://purl.uniprot.org/citations/26484536http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26484536