RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/16337594http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16337594http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16337594http://www.w3.org/2000/01/rdf-schema#comment"Inactivation of retinoblastoma protein (Rb) plays a critical role in the development of human malignancies. It has been shown that Rb is degraded through a proteasome-dependent pathway, yet the mechanism is largely unclear. MDM2 is frequently found amplified and overexpressed in a variety of human tumors. In this study, we find that MDM2 promotes Rb degradation in a proteasome-dependent and ubiquitin-independent manner. We show that Rb, MDM2, and the C8 subunit of the 20S proteasome interact in vitro and in vivo and that MDM2 promotes Rb-C8 interaction. Expression of wild-type MDM2, but not the mutant MDM2 defective either in Rb interaction or in RING finger domain, promotes cell cycle S phase entry independent of p53. Furthermore, MDM2 ablation results in Rb accumulation and inhibition of DNA synthesis. Taken together, these findings demonstrate that MDM2 is a critical negative regulator for Rb and suggest that MDM2 overexpression contributes to cancer development by destabilizing Rb."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2005.10.017"xsd:string
http://purl.uniprot.org/citations/16337594http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2005.10.017"xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Zheng H."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Zheng H."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Qiu W."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Qiu W."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Allday M.J."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Allday M.J."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Touitou R."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Touitou R."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Ying H."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Ying H."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Xiao Z.X."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Xiao Z.X."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Chang D.L."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Chang D.L."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Sdek P."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/author"Sdek P."xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/name"Mol. Cell"xsd:string
http://purl.uniprot.org/citations/16337594http://purl.uniprot.org/core/name"Mol. Cell"xsd:string