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DESCRIBE <http://purl.uniprot.org/SHA-384/23F9C9E67A04A2D7003BA136A40FA0FF86643BC9B7E5D467A00AC9A43C6A9AD0C5ED0D5FF1E0FC535C8AA984DA337B3C>
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http://purl.uniprot.org/SHA-384/23F9C9E67A04A2D7003BA136A40FA0FF86643BC9B7E5D467A00AC9A43C6A9AD0C5ED0D5FF1E0FC535C8AA984DA337B3C
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/23F9C9E67A04A2D7003BA136A40FA0FF86643BC9B7E5D467A00AC9A43C6A9AD0C5ED0D5FF1E0FC535C8AA984DA337B3C
http://www.w3.org/2000/01/rdf-schema#comment
"This study demonstrated that S1P significantly promotes angiogenesis inflammation and barrier integrity which was attenuated by inhibition of S1P2 or S1P3 suggesting that regulation of S1P2 and S1P3 is a novel therapeutic target for CNV."
xsd:string
http://purl.uniprot.org/uniprot/#_3C3B620995AAB423CD690ED79935D06862DA7F9D15ED7E6EF9C6552B03C387954CC48A70A36F907F6443329A24F104EB
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/23F9C9E67A04A2D7003BA136A40FA0FF86643BC9B7E5D467A00AC9A43C6A9AD0C5ED0D5FF1E0FC535C8AA984DA337B3C
http://purl.uniprot.org/uniprot/Q9Z0U9
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/23F9C9E67A04A2D7003BA136A40FA0FF86643BC9B7E5D467A00AC9A43C6A9AD0C5ED0D5FF1E0FC535C8AA984DA337B3C
http://purl.uniprot.org/uniprot/#_Q9Z0U9-mappedCitation-31415870
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/23F9C9E67A04A2D7003BA136A40FA0FF86643BC9B7E5D467A00AC9A43C6A9AD0C5ED0D5FF1E0FC535C8AA984DA337B3C