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http://purl.uniprot.org/SHA-384/BA96BA0525031397F638C40B0A5A1D5C2E0C1114BF4D5D43BCC047D7D16995DF497864F6529114E4D782DAE3EAFC3614http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/BA96BA0525031397F638C40B0A5A1D5C2E0C1114BF4D5D43BCC047D7D16995DF497864F6529114E4D782DAE3EAFC3614http://www.w3.org/2000/01/rdf-schema#comment"PTPROt thus functions as an obligate haploinsufficient TS in CLL where its expression levels determine its role as a promoter or inhibitor of the tumorigenic process in mice. Partial loss of PTPROt generates the strongest disease phenotype suggesting that its intermediate expression levels in CLL are selected for."xsd:string
http://purl.uniprot.org/uniprot/#_3E58EEF307E20E1A9834AD6E0C3C542A8DC712CFDAC4BA4D8F0B1D0AEF28A6FCCD709DA05BFDB1C8CA8EEA4A1AD40C70http://www.w3.org/1999/02/22-rdf-syntax-ns#subjecthttp://purl.uniprot.org/SHA-384/BA96BA0525031397F638C40B0A5A1D5C2E0C1114BF4D5D43BCC047D7D16995DF497864F6529114E4D782DAE3EAFC3614
http://purl.uniprot.org/uniprot/Q4U213http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/BA96BA0525031397F638C40B0A5A1D5C2E0C1114BF4D5D43BCC047D7D16995DF497864F6529114E4D782DAE3EAFC3614
http://purl.uniprot.org/uniprot/#_Q4U213-mappedCitation-28166196http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/BA96BA0525031397F638C40B0A5A1D5C2E0C1114BF4D5D43BCC047D7D16995DF497864F6529114E4D782DAE3EAFC3614