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http://purl.uniprot.org/citations/21840486http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21840486http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21840486http://www.w3.org/2000/01/rdf-schema#comment"Tumor hypoxia is associated with disease progression and treatment failure, but the hypoxia signaling mechanism is not fully understood. Here, we show that KLHL20, a Cullin3 (Cul3) substrate adaptor induced by HIF-1, coordinates with the actions of CDK1/2 and Pin1 to mediate hypoxia-induced PML proteasomal degradation. Furthermore, this PML destruction pathway participates in a feedback mechanism to maximize HIF-1α induction, thereby potentiating multiple tumor hypoxia responses, including metabolic reprogramming, epithelial-mesenchymal transition, migration, tumor growth, angiogenesis, and chemoresistance. In human prostate cancer, overexpression of HIF-1α, KLHL20, and Pin1 correlates with PML down-regulation, and hyperactivation of the PML destruction pathway is associated with disease progression. Our study indicates that the KLHL20-mediated PML degradation and HIF-1α autoregulation play key roles in tumor progression."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.org/dc/terms/identifier"doi:10.1016/j.ccr.2011.07.008"xsd:string
http://purl.uniprot.org/citations/21840486http://purl.org/dc/terms/identifier"doi:10.1016/j.ccr.2011.07.008"xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen C.H."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen C.H."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen H.Y."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen H.Y."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Tsai C.H."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Tsai C.H."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Lin Y.M."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Lin Y.M."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Shih H.M."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Shih H.M."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Lu K.P."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Lu K.P."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen T.Y."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen T.Y."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Lee Y.R."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Lee Y.R."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chiang C.T."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chiang C.T."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen R.H."xsd:string
http://purl.uniprot.org/citations/21840486http://purl.uniprot.org/core/author"Chen R.H."xsd:string