作者: K. Marley , C. S. Maier , S. C. Helfand
DOI: 10.1111/J.1476-5829.2012.00325.X
关键词:
摘要: Canine hemangiosarcoma (HSA) is an endothelial cell malignancy driven, in part, by activating mutations receptor and non-receptor tyrosine kinases. Proteomics, Western blots a kinase inhibitor were used to elucidate mechanisms HSA lines. Phosphotyrosine peptides from focal adhesion (FAK) STAT3, Lyn, Fyn other signal transduction kinases identified mass spectrometry. FAK was constitutively activated at 397, the autophosphorylation site, this reversible with high concentrations of inhibitor. inhibitor-14 suppressed migration phosphorylation 397 tyrosines 576/577 cytotoxic cells suggesting signalling may be important contributor canine survival.