RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/22869143http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22869143http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22869143http://www.w3.org/2000/01/rdf-schema#comment"Promyelocytic leukemia protein (PML) modulates the p53 tumor suppressor through its interaction with p53 and MDM2. We found that activated big MAP kinase 1 (BMK1) preferentially associates with PML isoform IV and disrupts PML-MDM2 interaction. Doxorubicin, a common chemotherapeutic agent, is known to promote PML-mediated p53 activation in part by promoting PML-dependent MDM2 nucleolar sequestration. We discovered that BMK1 deactivation coupled with doxorubicin synergistically enhanced MDM2 nucleolar sequestration and, consequently, promoted PML-mediated p53 upregulation leading to tumor cell apoptosis in vitro and tumor regression in vivo. Collectively, these results not only suggest that BMK1 activity has a role in suppressing p53 by blocking the interaction between PML and MDM2, but also implicate that pharmacological BMK1 inhibitor should significantly enhance the anticancer capacity of doxorubicin-based chemotherapy."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.org/dc/terms/identifier"doi:10.1038/onc.2012.332"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.org/dc/terms/identifier"doi:10.1038/onc.2012.332"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Chen R."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Chen R."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Deng X."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Deng X."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Yang Q."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Yang Q."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Yates J.R. III"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Yates J.R. III"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Liao L."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Liao L."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Gray N.S."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Gray N.S."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Lee J.D."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/author"Lee J.D."xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/name"Oncogene"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/name"Oncogene"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/pages"3156-3164"xsd:string
http://purl.uniprot.org/citations/22869143http://purl.uniprot.org/core/pages"3156-3164"xsd:string