Statements in which the resource exists.
SubjectPredicateObjectContext
http://www.reactome.org/bio...rdf:typebiopax3:Pathwaylld:biopax3
http://www.reactome.org/bio...biopax3:commentReviewed: Kunapuli, SP, 2010-06-07lld:biopax3
http://www.reactome.org/bio...biopax3:commentAuthored: Akkerman, JW, 2009-06-03lld:biopax3
http://www.reactome.org/bio...biopax3:commentEdited: Jupe, S, 2010-06-07lld:biopax3
http://www.reactome.org/bio...biopax3:commentNitric Oxide (NO) inhibits smooth muscle cell proliferation and migration, oxidation of low-density lipoproteins, and platelet aggregation and adhesion. It can stimulate vasodilatation of the endothelium, disaggregation of  preformed platelet aggregates and inhibits activated platelet recruitment to the aggregate. NO is synthesized from L-arginine by a family of isoformic enzymes known as nitric oxide synthase (NOS). Three isoforms, namely endothelial, neuronal, and inducible NOS (eNOS, nNOS, and iNOS, respectively), have been identified. The eNOS isoform is found in the endothelium and platelets. NO regulation of cyclic guanosine-3,5-monophosphate (cGMP), via activation of soluble guanylate cyclase, is the principal mechanism of negative control over platelet activity. Defects in this control mechanism have been associated with platelet hyperaggregability and associated thrombosis.lld:biopax3
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http://www.reactome.org/bio...biopax3:displayNameNitric oxide stimulates guanylate cyclaselld:biopax3
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