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DESCRIBE <http://purl.uniprot.org/SHA-384/7022847080F1BD188CD2BD5F4E75D63B5FD67A2830B6F247E035C563CD9B7FCFF87256CD005AD97E20B4A6254CA67A12>
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http://purl.uniprot.org/SHA-384/7022847080F1BD188CD2BD5F4E75D63B5FD67A2830B6F247E035C563CD9B7FCFF87256CD005AD97E20B4A6254CA67A12
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/7022847080F1BD188CD2BD5F4E75D63B5FD67A2830B6F247E035C563CD9B7FCFF87256CD005AD97E20B4A6254CA67A12
http://www.w3.org/2000/01/rdf-schema#comment
"An important mechanism underlying impaired activity of eNOS in injured sinusoidal endothelial cells is defective phosphorylation of Akt caused by overexpression of GRK2 after injury."
xsd:string
http://purl.uniprot.org/uniprot/#_EF9419A44D460C621D19FC6AB8D959D1DBD63B4D4CDD53CA9768750BB94DED685EE3FFE5BF9F30C13ED65C1A1CDA33A3
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/7022847080F1BD188CD2BD5F4E75D63B5FD67A2830B6F247E035C563CD9B7FCFF87256CD005AD97E20B4A6254CA67A12
http://purl.uniprot.org/uniprot/P26817
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/7022847080F1BD188CD2BD5F4E75D63B5FD67A2830B6F247E035C563CD9B7FCFF87256CD005AD97E20B4A6254CA67A12
http://purl.uniprot.org/uniprot/#_P26817-mappedCitation-16142243
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/7022847080F1BD188CD2BD5F4E75D63B5FD67A2830B6F247E035C563CD9B7FCFF87256CD005AD97E20B4A6254CA67A12