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• W1901420182 abstract "Abstract Canine hemangiosarcoma ( HSA ) is an endothelial cell malignancy driven, in part, by activating mutations in receptor and non‐receptor tyrosine kinases. Proteomics, Western blots and a tyrosine kinase inhibitor were used to elucidate activating mechanisms in HSA cell lines. Phosphotyrosine peptides from focal adhesion kinase ( FAK ) STAT 3, Lyn , Fyn and other signal transduction kinases were identified by mass spectrometry. FAK was constitutively activated at tyrosine 397, the autophosphorylation site, and this was reversible with high concentrations of a FAK inhibitor. FAK inhibitor‐14 suppressed migration and phosphorylation of FAK tyrosine 397 and tyrosines 576/577 and was cytotoxic to HSA cells suggesting FAK signalling may be an important contributor to canine HSA survival." @default.
• W1901420182 created "2016-06-24" @default.
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• W1901420182 creator A5029701926 @default.
• W1901420182 creator A5036389960 @default.
• W1901420182 date "2012-04-06" @default.
• W1901420182 modified "2023-10-18" @default.
• W1901420182 title "Phosphotyrosine enrichment identifies focal adhesion kinase and other tyrosine kinases for targeting in canine hemangiosarcoma" @default.
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• W1901420182 doi "https://doi.org/10.1111/j.1476-5829.2012.00325.x" @default.
• W1901420182 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22487216" @default.
• W1901420182 hasPublicationYear "2012" @default.
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