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Focal Adhesion Kinase (FAK) tyrosine 397E mutation restores the vascular leakage defect in endothelium‐specific FAK‐kinase dead mice
Focal adhesion kinase (FAK) inhibitors have been developed as potential anticancer agents and are undergoing clinical trials. In vitro activation of the FAK kinase domain triggers autophosphorylation of Y397, Src activation, and subsequent phosphorylation of other FAK tyrosine residues. However, how...
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| Pubblicato in: | J Pathol |
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| Autori principali: | , , , , , , , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
John Wiley & Sons, Ltd
2017
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5518444/ https://ncbi.nlm.nih.gov/pubmed/28444899 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1002/path.4911 |
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