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DESCRIBE <http://purl.uniprot.org/SHA-384/9C2E30C176E611A4E8FD5748481136CAD9240A9F310ADE89126262D7582934DA6DBB7A0C762C9F7B2637D7FA0C0E9B9D>
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http://purl.uniprot.org/SHA-384/9C2E30C176E611A4E8FD5748481136CAD9240A9F310ADE89126262D7582934DA6DBB7A0C762C9F7B2637D7FA0C0E9B9D
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/9C2E30C176E611A4E8FD5748481136CAD9240A9F310ADE89126262D7582934DA6DBB7A0C762C9F7B2637D7FA0C0E9B9D
http://www.w3.org/2000/01/rdf-schema#comment
"results argue that there must be a cellular mechanism that limits GCAP1 access to RetGC2 and makes RetGC1 isozyme a preferential target for the disease-causing GCAP1 mutants."
xsd:string
http://purl.uniprot.org/uniprot/#_076596E409952130FA7F4E776B71CCC5B5FD28E49B675A72EAFD50FB2BC55434EE8F01026306B4F3660BAC4609D13DD2
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/9C2E30C176E611A4E8FD5748481136CAD9240A9F310ADE89126262D7582934DA6DBB7A0C762C9F7B2637D7FA0C0E9B9D
http://purl.uniprot.org/uniprot/P43081
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/9C2E30C176E611A4E8FD5748481136CAD9240A9F310ADE89126262D7582934DA6DBB7A0C762C9F7B2637D7FA0C0E9B9D
http://purl.uniprot.org/uniprot/#_P43081-mappedCitation-22623665
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/9C2E30C176E611A4E8FD5748481136CAD9240A9F310ADE89126262D7582934DA6DBB7A0C762C9F7B2637D7FA0C0E9B9D