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DESCRIBE <http://purl.uniprot.org/SHA-384/255EFC8B6CE19E0DE0EAE7AB6F0CFE1B915F140655D42A2E74979F48A9CAF0B9F2C8B9C82A78A4F5EFDDD3E988F845DB>
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http://purl.uniprot.org/SHA-384/255EFC8B6CE19E0DE0EAE7AB6F0CFE1B915F140655D42A2E74979F48A9CAF0B9F2C8B9C82A78A4F5EFDDD3E988F845DB
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/255EFC8B6CE19E0DE0EAE7AB6F0CFE1B915F140655D42A2E74979F48A9CAF0B9F2C8B9C82A78A4F5EFDDD3E988F845DB
http://www.w3.org/2000/01/rdf-schema#comment
"Study shows that miR-215 regulates the Act1/IL-17RA pathway and represses the expression of Act1 protein in oxygen glucose deprivation/reperfusion-treated N2a cells and an middle cerebral artery occlusion mouse model of ischemic stroke."
xsd:string
http://purl.uniprot.org/uniprot/#_3BBE113EC03ECBA2723D2C34C8A75D1357E69DF16C64828BD2DF7E73C502B0A1EF93D57EBE13647294A569E01BAC6779
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/255EFC8B6CE19E0DE0EAE7AB6F0CFE1B915F140655D42A2E74979F48A9CAF0B9F2C8B9C82A78A4F5EFDDD3E988F845DB
http://purl.uniprot.org/uniprot/I7GPR1
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/255EFC8B6CE19E0DE0EAE7AB6F0CFE1B915F140655D42A2E74979F48A9CAF0B9F2C8B9C82A78A4F5EFDDD3E988F845DB
http://purl.uniprot.org/uniprot/#_I7GPR1-mappedCitation-29080697
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/255EFC8B6CE19E0DE0EAE7AB6F0CFE1B915F140655D42A2E74979F48A9CAF0B9F2C8B9C82A78A4F5EFDDD3E988F845DB