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http://purl.uniprot.org/citations/19556538http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19556538http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19556538http://www.w3.org/2000/01/rdf-schema#comment"Numerous studies focus on the tumor suppressor p53 as a protector of genomic stability, mediator of cell cycle arrest and apoptosis, and target of mutation in 50% of all human cancers. The vast majority of information on p53, its protein-interaction partners and regulation, comes from studies of tumor-derived, cultured cells where p53 and its regulatory controls may be mutated or dysfunctional. To address regulation of endogenous p53 in normal cells, we created a mouse and stem cell model by knock-in (KI) of a tandem-affinity-purification (TAP) epitope at the endogenous Trp-53 locus. Mass spectrometry of TAP-purified p53-complexes from embryonic stem cells revealed Tripartite-motif protein 24 (Trim24), a previously unknown partner of p53. Mutation of TRIM24 homolog, bonus, in Drosophila led to apoptosis, which could be rescued by p53-depletion. These in vivo analyses establish TRIM24/bonus as a pathway that negatively regulates p53 in Drosophila. The Trim24-p53 link is evolutionarily conserved, as TRIM24 depletion in human breast cancer cells caused p53-dependent, spontaneous apoptosis. We found that Trim24 ubiquitylates and negatively regulates p53 levels, suggesting Trim24 as a therapeutic target to restore tumor suppression by p53."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0813177106"xsd:string
http://purl.uniprot.org/citations/19556538http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0813177106"xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Qin J."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Qin J."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Johnson R.L."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Johnson R.L."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Jung S.Y."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Jung S.Y."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Herz H.M."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Herz H.M."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Bergmann A."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Bergmann A."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Barton M.C."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Barton M.C."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Jain A.K."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Jain A.K."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Allton K."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Allton K."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Tsai W.W."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/author"Tsai W.W."xsd:string
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19556538http://purl.uniprot.org/core/date"2009"xsd:gYear