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DESCRIBE <http://purl.uniprot.org/SHA-384/F84F7CE519689E88B2B85913BAF009DC8D1898DA1EF5A33945C7A8CDDDDE6656351C7E0C31B0B1E14CFA35C9FB111701>
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http://purl.uniprot.org/SHA-384/F84F7CE519689E88B2B85913BAF009DC8D1898DA1EF5A33945C7A8CDDDDE6656351C7E0C31B0B1E14CFA35C9FB111701
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/F84F7CE519689E88B2B85913BAF009DC8D1898DA1EF5A33945C7A8CDDDDE6656351C7E0C31B0B1E14CFA35C9FB111701
http://www.w3.org/2000/01/rdf-schema#comment
"Alk1 deletion leads to increased endothelial PI3K pathway activation that may be a novel target for the treatment of vascular lesions in hereditary haemorrhagic telangiectasia type 2."
xsd:string
http://purl.uniprot.org/uniprot/#_C4ADAABCE43F2496804D4073F7A64ED5D582BA786B48EB05BB2BA785591A10963023E9BEDBF9C3B40A64DA595F0B9B6C
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/F84F7CE519689E88B2B85913BAF009DC8D1898DA1EF5A33945C7A8CDDDDE6656351C7E0C31B0B1E14CFA35C9FB111701
http://purl.uniprot.org/uniprot/Q80UI5
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/F84F7CE519689E88B2B85913BAF009DC8D1898DA1EF5A33945C7A8CDDDDE6656351C7E0C31B0B1E14CFA35C9FB111701
http://purl.uniprot.org/uniprot/#_Q80UI5-mappedCitation-27897192
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/F84F7CE519689E88B2B85913BAF009DC8D1898DA1EF5A33945C7A8CDDDDE6656351C7E0C31B0B1E14CFA35C9FB111701