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http://purl.uniprot.org/citations/21795712http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21795712http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21795712http://www.w3.org/2000/01/rdf-schema#comment"Transforming growth factor-β (TGF-β) signaling is controlled by a variety of regulators, of which Smad7, c-Ski, and SnoN play a pivotal role in its negative regulation. Arkadia is a RING-type E3 ubiquitin ligase that targets these negative regulators for degradation to enhance TGF-β signaling. In the present study we identified a candidate human tumor suppressor gene product RB1CC1/FIP200 as a novel positive regulator of TGF-β signaling that functions as a substrate-selective cofactor of Arkadia. Overexpression of RB1CC1 enhanced TGF-β signaling, and knockdown of endogenous RB1CC1 attenuated TGF-β-induced expression of target genes as well as TGF-β-induced cytostasis. RB1CC1 down-regulated the protein levels of c-Ski but not SnoN by enhancing the activity of Arkadia E3 ligase toward c-Ski. Substrate selectivity is primarily attributable to the physical interaction of RB1CC1 with substrates, suggesting its role as a scaffold protein. RB1CC1 thus appears to play a unique role as a modulator of TGF-β signaling by restricting substrate specificity of Arkadia."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m111.227561"xsd:string
http://purl.uniprot.org/citations/21795712http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m111.227561"xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Goto K."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Goto K."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Nagano Y."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Nagano Y."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Imamura T."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Imamura T."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Miyazono K."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Miyazono K."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Saitoh M."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Saitoh M."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Miyazawa K."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Miyazawa K."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Shinozaki M."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Shinozaki M."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Ikushima H."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Ikushima H."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Chano T."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Chano T."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Koinuma D."xsd:string
http://purl.uniprot.org/citations/21795712http://purl.uniprot.org/core/author"Koinuma D."xsd:string