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DESCRIBE <http://purl.uniprot.org/SHA-384/AB3A7618F47C6F217CA82A1FE26102C4E77A88A13E184E0E473145BD9EE89E20C9032FBD0B6904A3C266E0B8777D6DB0>
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http://purl.uniprot.org/SHA-384/AB3A7618F47C6F217CA82A1FE26102C4E77A88A13E184E0E473145BD9EE89E20C9032FBD0B6904A3C266E0B8777D6DB0
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/AB3A7618F47C6F217CA82A1FE26102C4E77A88A13E184E0E473145BD9EE89E20C9032FBD0B6904A3C266E0B8777D6DB0
http://www.w3.org/2000/01/rdf-schema#comment
"This study demonstrates that lack of GLYT1 leads to a distinct human neurological syndrome hallmarked by mildly elevated cerebrospinal fluid glycine and normal serum glycine."
xsd:string
http://purl.uniprot.org/uniprot/#_57AC96240DA60249712E05D4BC859C9C836FB4FFB946EA8F9B80AAE0E787B4BE20D270D6879FF4185726968BB7148501
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/AB3A7618F47C6F217CA82A1FE26102C4E77A88A13E184E0E473145BD9EE89E20C9032FBD0B6904A3C266E0B8777D6DB0
http://purl.uniprot.org/uniprot/B7Z8W5
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/AB3A7618F47C6F217CA82A1FE26102C4E77A88A13E184E0E473145BD9EE89E20C9032FBD0B6904A3C266E0B8777D6DB0
http://purl.uniprot.org/uniprot/#_B7Z8W5-mappedCitation-27773429
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/AB3A7618F47C6F217CA82A1FE26102C4E77A88A13E184E0E473145BD9EE89E20C9032FBD0B6904A3C266E0B8777D6DB0