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http://purl.uniprot.org/SHA-384/E7F56F3A420EEEEFAE9CA831E0E007126241E7D4B6F42CDB2D46ECE3EA9A2DF4646B94259143E2B5EC4A282EC39EF57Ahttp://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/E7F56F3A420EEEEFAE9CA831E0E007126241E7D4B6F42CDB2D46ECE3EA9A2DF4646B94259143E2B5EC4A282EC39EF57Ahttp://www.w3.org/2000/01/rdf-schema#comment"The apoptosis phenotype was partly dependent on HRK upregulation as HRK knockdown significantly abrogated the sensitization. KDM2B-silenced tumors exhibited slower growth in vivo. Taken together our findings suggest a novel mechanism where the key apoptosis components are under epigenetic control of KDM2B in glioblastoma multiforme cells."xsd:string
http://purl.uniprot.org/uniprot/#_9AE212513EA51A1C4EECB637B843988058F150FA424686452E7DF7E0485017C47EAC2658FB74D271AAD7DD72A1A92731http://www.w3.org/1999/02/22-rdf-syntax-ns#subjecthttp://purl.uniprot.org/SHA-384/E7F56F3A420EEEEFAE9CA831E0E007126241E7D4B6F42CDB2D46ECE3EA9A2DF4646B94259143E2B5EC4A282EC39EF57A
http://purl.uniprot.org/uniprot/A0A0C4DGG3http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/E7F56F3A420EEEEFAE9CA831E0E007126241E7D4B6F42CDB2D46ECE3EA9A2DF4646B94259143E2B5EC4A282EC39EF57A
http://purl.uniprot.org/uniprot/#_A0A0C4DGG3-mappedCitation-28661478http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/E7F56F3A420EEEEFAE9CA831E0E007126241E7D4B6F42CDB2D46ECE3EA9A2DF4646B94259143E2B5EC4A282EC39EF57A