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http://purl.uniprot.org/citations/10656683http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10656683http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10656683http://www.w3.org/2000/01/rdf-schema#comment"The adenomatous polyposis coli (APC) gene is mutated in familial adenomatous polyposis and in many sporadic colorectal tumors. The carboxyl-terminal S/TXV motif of the APC gene product interacts with the PDZ domain of hDLG, the human homolog of the Drosophila lethal (1) discs larige-1 (dlg) tumor suppressor. In the present study, we found that overexpression of hDLG suppresses cell proliferation by blocking cell cycle progression from the G0/G1 to S phase. This inhibition of cell cycle progression was abolished when the PDZ, SH3 or guanylate kinase-like domain of hDLG was mutated. Moreover, overexpression of these mutant hDLGs partially interfered with the cell cycle blocking activity of APC. Consistent with this result, mutant APC lacking the S/TXV motif exhibited weaker cell cycle blocking activity than the intact APC. These results suggest that APC-hDLG complex formation plays an important role in transducing the APC cell cycle blocking signal."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.org/dc/terms/identifier"doi:10.1038/sj.onc.1203309"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.org/dc/terms/identifier"doi:10.1038/sj.onc.1203309"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Akiyama T."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Akiyama T."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Toyoshima K."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Toyoshima K."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Ishidate T."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Ishidate T."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Matsumine A."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/author"Matsumine A."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/date"2000"xsd:gYear
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/date"2000"xsd:gYear
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/name"Oncogene"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/name"Oncogene"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/pages"365-372"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/pages"365-372"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/title"The APC-hDLG complex negatively regulates cell cycle progression from the G0/G1 to S phase."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/title"The APC-hDLG complex negatively regulates cell cycle progression from the G0/G1 to S phase."xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/volume"19"xsd:string
http://purl.uniprot.org/citations/10656683http://purl.uniprot.org/core/volume"19"xsd:string
http://purl.uniprot.org/citations/10656683http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10656683
http://purl.uniprot.org/citations/10656683http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10656683