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http://purl.uniprot.org/citations/10523301http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10523301http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10523301http://www.w3.org/2000/01/rdf-schema#comment"In Rat-1 fibroblasts epidermal growth factor (EGF), but not platelet-derived growth factor (PDGF) stimulates the activity of the c-Jun N-terminal kinase (JNK). Moreover, PDGF induced suppression of EGF-mediated JNK activation, apparently through protein kinase C (PKC) activation. Further analysis revealed that PKD was specifically activated by PDGF but not EGF in Rat-1 cells. In SF126 glioblastoma cells, however, EGF and PDGF synergistically activated JNK, while neither PDGF nor EGF stimulated PKD activity. In this cell line, overexpression of PKD blocked EGF- and PDGF-induced JNK activation. Mutational analysis further revealed that the EGFR mutant (T654/669E) was incapable of activating JNK and provided evidence that PKD-mediated dual phosphorylation of these critical threonine residues leads to suppression of EGF-induced JNK activation. Our results establish a novel crosstalk mechanism which allows signal integration and definition in cells with many different RTKs."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.org/dc/terms/identifier"doi:10.1093/emboj/18.20.5567"xsd:string
http://purl.uniprot.org/citations/10523301http://purl.org/dc/terms/identifier"doi:10.1093/emboj/18.20.5567"xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Ullrich A."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Ullrich A."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Choidas A."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Choidas A."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Bagowski C.P."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Bagowski C.P."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Stein-Gerlach M."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/author"Stein-Gerlach M."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/name"EMBO J."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/name"EMBO J."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/pages"5567-5576"xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/pages"5567-5576"xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/title"Cell-type specific phosphorylation of threonines T654 and T669 by PKD defines the signal capacity of the EGF receptor."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/title"Cell-type specific phosphorylation of threonines T654 and T669 by PKD defines the signal capacity of the EGF receptor."xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/volume"18"xsd:string
http://purl.uniprot.org/citations/10523301http://purl.uniprot.org/core/volume"18"xsd:string
http://purl.uniprot.org/citations/10523301http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10523301
http://purl.uniprot.org/citations/10523301http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10523301