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DESCRIBE <http://purl.uniprot.org/SHA-384/352FCECC85A2C4DC735B3732D501017F5F12EC436F82DB09ABB0DDA3057F1BBB948B5CD033FB6A282A1BB23CF18C9AAA>
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http://purl.uniprot.org/SHA-384/352FCECC85A2C4DC735B3732D501017F5F12EC436F82DB09ABB0DDA3057F1BBB948B5CD033FB6A282A1BB23CF18C9AAA
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/352FCECC85A2C4DC735B3732D501017F5F12EC436F82DB09ABB0DDA3057F1BBB948B5CD033FB6A282A1BB23CF18C9AAA
http://www.w3.org/2000/01/rdf-schema#comment
"LKB1 deficiency induces an autocrine INSL4 signaling that critically supports the growth and survival of lung cancer cells. Therefore aberrant INSL4 signaling is a promising therapeutic target for LKB1-deficient lung cancers."
xsd:string
http://purl.uniprot.org/uniprot/#_9FEC0741094525E335C07F7CE976481F9ECEE435096C0F37631E6EFFAE95B6CFFE995E8FB6791E541F84A29F43F3738B
http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
http://purl.uniprot.org/SHA-384/352FCECC85A2C4DC735B3732D501017F5F12EC436F82DB09ABB0DDA3057F1BBB948B5CD033FB6A282A1BB23CF18C9AAA
http://purl.uniprot.org/uniprot/Q14641
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/352FCECC85A2C4DC735B3732D501017F5F12EC436F82DB09ABB0DDA3057F1BBB948B5CD033FB6A282A1BB23CF18C9AAA
http://purl.uniprot.org/uniprot/#_Q14641-mappedCitation-30423141
http://purl.uniprot.org/core/mappedAnnotation
http://purl.uniprot.org/SHA-384/352FCECC85A2C4DC735B3732D501017F5F12EC436F82DB09ABB0DDA3057F1BBB948B5CD033FB6A282A1BB23CF18C9AAA