http://purl.uniprot.org/citations/24380865 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/24380865 | http://www.w3.org/2000/01/rdf-schema#comment | "YAP is a transcriptional co-activator that acts downstream of the Hippo signaling pathway and regulates multiple cellular processes, including proliferation. Hippo pathway-dependent phosphorylation of YAP negatively regulates its function. Conversely, attenuation of Hippo-mediated phosphorylation of YAP increases its ability to stimulate proliferation and eventually induces oncogenic transformation. The C-terminus of YAP contains a highly conserved PDZ-binding motif that regulates YAP's functions in multiple ways. However, to date, the importance of the PDZ-binding motif to the oncogenic cell transforming activity of YAP has not been determined. In this study, we disrupted the PDZ-binding motif in the YAP (5SA) protein, in which the sites normally targeted by Hippo pathway-dependent phosphorylation are mutated. We found that loss of the PDZ-binding motif significantly inhibited the oncogenic transformation of cultured cells induced by YAP (5SA). In addition, the increased nuclear localization of YAP (5SA) and its enhanced activation of TEAD-dependent transcription of the cell proliferation gene CTGF were strongly reduced when the PDZ-binding motif was deleted. Similarly, in mouse liver, deletion of the PDZ-binding motif suppressed nuclear localization of YAP (5SA) and YAP (5SA)-induced CTGF expression. Taken together, our results indicate that the PDZ-binding motif of YAP is critical for YAP-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF transcription."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2013.12.100"xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/author | "Hirayama J."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/author | "Miura R."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/author | "Hata S."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/author | "Nishina H."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/author | "Miyamura N."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/author | "Shimomura T."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/pages | "917-923"xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/title | "The PDZ-binding motif of Yes-associated protein is required for its co-activation of TEAD-mediated CTGF transcription and oncogenic cell transforming activity."xsd:string |
http://purl.uniprot.org/citations/24380865 | http://purl.uniprot.org/core/volume | "443"xsd:string |
http://purl.uniprot.org/citations/24380865 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24380865 |
http://purl.uniprot.org/citations/24380865 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24380865 |
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