RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/16919435http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16919435http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16919435http://www.w3.org/2000/01/rdf-schema#comment"Integrins can alter cellular behavior through the recruitment and activation of signaling proteins such as non-receptor tyrosine kinases including focal adhesion kinase (FAK) and c-Src that form a dual kinase complex. The FAK-Src complex binds to and can phosphorylate various adaptor proteins such as p130Cas and paxillin. In normal cells, multiple integrin-regulated linkages exist to activate FAK or Src. Activated FAK-Src functions to promote cell motility, cell cycle progression and cell survival. Recent studies have found that the FAK-Src complex is activated in many tumor cells and generates signals leading to tumor growth and metastasis. As both FAK and Src catalytic activities are important in promoting VEGF-associated tumor angiogenesis and protease-associated tumor metastasis, support is growing that FAK and Src may be therapeutically relevant targets in the inhibition of tumor progression."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.org/dc/terms/identifier"doi:10.1016/j.ceb.2006.08.011"xsd:string
http://purl.uniprot.org/citations/16919435http://purl.org/dc/terms/identifier"doi:10.1016/j.ceb.2006.08.011"xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/author"Schlaepfer D.D."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/author"Schlaepfer D.D."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/author"Mitra S.K."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/author"Mitra S.K."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/name"Curr. Opin. Cell Biol."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/name"Curr. Opin. Cell Biol."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/pages"516-523"xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/pages"516-523"xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/title"Integrin-regulated FAK-Src signaling in normal and cancer cells."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/title"Integrin-regulated FAK-Src signaling in normal and cancer cells."xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/volume"18"xsd:string
http://purl.uniprot.org/citations/16919435http://purl.uniprot.org/core/volume"18"xsd:string
http://purl.uniprot.org/citations/16919435http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16919435
http://purl.uniprot.org/citations/16919435http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16919435
http://purl.uniprot.org/citations/16919435http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16919435
http://purl.uniprot.org/citations/16919435http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16919435
http://purl.uniprot.org/uniprot/Q05397http://purl.uniprot.org/core/citationhttp://purl.uniprot.org/citations/16919435
http://purl.uniprot.org/uniprot/Q05397#attribution-D0B24CBBF03E85CF8172B9B6C79BC5C3http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16919435