@prefix dc: <
http://purl.org/dc/terms/
> .
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http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel
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http://www.w3.org/2000/01/rdf-schema#
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@prefix rdf: <
http://www.w3.org/1999/02/22-rdf-syntax-ns#
> .
@prefix xsd: <
http://www.w3.org/2001/XMLSchema#
> .
@prefix dce: <
http://purl.org/dc/elements/1.1/
> .
@prefix pav: <
http://purl.org/pav/
> .
@prefix np: <
http://www.nanopub.org/nschema#
> .
@prefix belv: <
http://www.selventa.com/vocabulary/
> .
@prefix prov: <
http://www.w3.org/ns/prov#
> .
@prefix chebi: <
http://www.ebi.ac.uk/chebi/searchId.do?chebiId=
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http://amigo.geneontology.org/amigo/term/GO:
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http://purl.bioontology.org/ontology/MSH/
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http://www.lgcstandards-atcc.org/Products/All/
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http://www.ncbi.nlm.nih.gov/pubmed/
> .
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http://orcid.org/
> .
sub:Head
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this:
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np:hasProvenance
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np:hasPublicationInfo
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sub:_2
dc:subject
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rdf:value
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"""These data suggest that CSE prevents VEGF-induced endothelial cell migration and tube
formation by increasing oxidative stress. The importance of NO in that physiopathology
was demonstrated by showing that NO donors (SNAP 75 μM, SNP 0.1 mM)
or a cGMP analog (8-Br-cGMP 2 mM) rescued integrin expression (Fig. 5A), cellular
migration (Fig. 5B) and tube formation (Fig. 5C) in endothelial cells exposed
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