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http://purl.uniprot.org/citations/16188233http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16188233http://www.w3.org/2000/01/rdf-schema#comment"We investigated the expression of KIT (product of c-kit oncogene), gain-of-function mutations, and activation of its downstream signal transduction in human testicular cancers. KIT was expressed in 88% (22/25) of seminomas and in 44.4% (4/9) of non-seminomas compared to adjacent normal testicular tissue. Nine of the KIT-expressing seminomas had mutations (40.9%; 9/22) in the c-kit gene; two cases in exon 11 and 7 cases in exon 17. Two of these mutations in exon 17 were novel, and the other seven mutations were identical to the already known gain-of-function mutations which cause activation of KIT without ligand stem cell factor. All of the mutant KIT and 53.8% (7/13) of wild-type KIT were phosphorylated (activated) and associated with phosphorylated phosphatidylinositol 3-kinase (PI3K). Akt was also phosphorylated in these seminomas, suggesting that the KIT-PI3K-Akt pathway is activated in seminoma. These findings suggest that the KIT-PI3K-Akt pathway is constitutively activated in testicular germ cell tumors, due to overexpression of KIT protein and/or gain-of-function mutations in the c-kit gene."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.org/dc/terms/identifier"doi:10.1016/j.bbrc.2005.09.042"xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Arai Y."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Inoue H."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Miki T."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Nakai Y."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Nakayama M."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Nishimura K."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Mizutani Y."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Okuyama A."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Nonomura N."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Shiba M."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Aozasa K."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/author"Oka D."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/name"Biochem Biophys Res Commun"xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/pages"289-296"xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/title"KIT (c-kit oncogene product) pathway is constitutively activated in human testicular germ cell tumors."xsd:string
http://purl.uniprot.org/citations/16188233http://purl.uniprot.org/core/volume"337"xsd:string
http://purl.uniprot.org/citations/16188233http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16188233
http://purl.uniprot.org/citations/16188233http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16188233
http://purl.uniprot.org/uniprot/#_A0A0U2N547-mappedCitation-16188233http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16188233
http://purl.uniprot.org/uniprot/#_A0A8I5KR87-mappedCitation-16188233http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16188233
http://purl.uniprot.org/uniprot/#_E2I6G0-mappedCitation-16188233http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16188233