<http://model.geneontology.org/SYNGO_849>	<http://purl.org/dc/elements/1.1/title>	"Nptxr_BP_849" .
<http://model.geneontology.org/SYNGO_849>	<http://purl.org/dc/elements/1.1/date>	"2017-11-06" .
<http://model.geneontology.org/SYNGO_849>	<http://purl.org/dc/elements/1.1/contributor>	"http://orcid.org/0000-0003-0912-1514" .
<http://model.geneontology.org/SYNGO_849>	<http://purl.org/pav/providedBy>	"https://syngo.vu.nl" .
<http://model.geneontology.org/SYNGO_849>	<http://geneontology.org/lego/modelstate>	"production" .
<http://model.geneontology.org/SYNGO_849>	<http://www.w3.org/2000/01/rdf-schema#comment>	"Rationale: Presynaptic NPR directly binds to the GluA1-N terminal extracellular domain and stimulates assembly of both excitatory and inhibitory postsynaptic sites. Loss of NPR suppressed surface GluA1 levels, and impaired excitatory synaptic transmission, without affecting synapse numbers.\n\nFigs.1 and 5 support that NPR is involved in formation of postsynaptic specializations.\nFig.2 shows that NPR binds the GluA1-NTD.\nFigs.10 and 11 show that global NPR knockdown in pre- and post-synaptic neurons impairs excitatory postsynaptic scaffold assembly and the strength of excitatory transmission.. Experimental description: Mouse hippocampal neurons were prepared.\n\n23/6/2017 Pim\n-All overexpression constructs are of human species: \"The constructs encoding cDNAs of hNPR (HsCD00083063), hNP1 (HsCD00296108), and hNARP (HsCD00040444) were obtained from PlasmID (http://plasmid.med.harvard.edu/PLASMID/).\"\n- Species of GluA1-NTD overexpressed protein is not mentioned." .
<http://model.geneontology.org/SYNGO_849>	<http://www.w3.org/1999/02/22-rdf-syntax-ns#type>	<http://www.w3.org/2002/07/owl#Ontology> .
<http://model.geneontology.org/SYNGO_849>	<http://www.w3.org/2002/07/owl#imports>	<http://purl.obolibrary.org/obo/go/extensions/go-lego.owl> .
<http://model.geneontology.org/SYNGO_849>	<http://purl.org/dc/elements/1.1/contributor>	"http://orcid.org/0000-0002-3670-7863" .