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http://purl.uniprot.org/citations/28731405http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28731405http://www.w3.org/2000/01/rdf-schema#comment"Aberrant NMDA receptor (NMDAR) activity contributes to several neurological disorders, but direct antagonism is poorly tolerated therapeutically. The GluN2B cytoplasmic C-terminal domain (CTD) represents an alternative therapeutic target since it potentiates excitotoxic signaling. The key GluN2B CTD-centred event in excitotoxicity is proposed to involve its phosphorylation at Ser-1303 by Dapk1, that is blocked by a neuroprotective cell-permeable peptide mimetic of the region. Contrary to this model, we find that excitotoxicity can proceed without increased Ser-1303 phosphorylation, and is unaffected by Dapk1 deficiency in vitro or following ischemia in vivo. Pharmacological analysis of the aforementioned neuroprotective peptide revealed that it acts in a sequence-independent manner as an open-channel NMDAR antagonist at or near the Mg2+ site, due to its high net positive charge. Thus, GluN2B-driven excitotoxic signaling can proceed independently of Dapk1 or altered Ser-1303 phosphorylation."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.org/dc/terms/identifier"doi:10.7554/elife.17161"xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Grant S.G.N."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Baxter P."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"McKay S."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Gillingwater T.H."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Wishart T.M."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Ryan T.J."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Komiyama N.H."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Hardingham G.E."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"McColl B.W."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Manson J.C."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Carpanini S.M."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"McQueen J."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Marwick K."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/author"Wyllie D.J.A."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/name"Elife"xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/pages"e17161"xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/title"Pro-death NMDA receptor signaling is promoted by the GluN2B C-terminus independently of Dapk1."xsd:string
http://purl.uniprot.org/citations/28731405http://purl.uniprot.org/core/volume"6"xsd:string
http://purl.uniprot.org/citations/28731405http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28731405
http://purl.uniprot.org/citations/28731405http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28731405
http://purl.uniprot.org/uniprot/#_A0A286YDD8-mappedCitation-28731405http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28731405