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DESCRIBE <http://purl.uniprot.org/SHA-384/9AF735E886F055767494595DA6447C2217C2FFA70A5B034F00020DBD67E6E83521A8DEB0908880AF33C0D2745BC7E418>
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http://purl.uniprot.org/SHA-384/9AF735E886F055767494595DA6447C2217C2FFA70A5B034F00020DBD67E6E83521A8DEB0908880AF33C0D2745BC7E418
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/9AF735E886F055767494595DA6447C2217C2FFA70A5B034F00020DBD67E6E83521A8DEB0908880AF33C0D2745BC7E418
http://www.w3.org/2000/01/rdf-schema#comment
"loss of ALS2 function is not sufficient to cause motor neuron disease in a mouse model. However lack of ALS2 did predispose neurons to oxidative stress implying that ALS2 might serve as a risk factor for motor neuron disease."
xsd:string
http://purl.uniprot.org/uniprot/#_58BE504B2222EC1552B96CBA8D492E6B506E985370A44A8C15EEB0D32D69D9224BEBF7D67CEF33DED1FC5BC06565366B
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/9AF735E886F055767494595DA6447C2217C2FFA70A5B034F00020DBD67E6E83521A8DEB0908880AF33C0D2745BC7E418
http://purl.uniprot.org/uniprot/Q920R0
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/9AF735E886F055767494595DA6447C2217C2FFA70A5B034F00020DBD67E6E83521A8DEB0908880AF33C0D2745BC7E418
http://purl.uniprot.org/uniprot/#_Q920R0-mappedCitation-16107644
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/9AF735E886F055767494595DA6447C2217C2FFA70A5B034F00020DBD67E6E83521A8DEB0908880AF33C0D2745BC7E418