作者: Bernardo Tavora , Silvia Batista , Louise E. Reynolds , Shalini Jadeja , Stephen Robinson
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摘要: Focal adhesion kinase (FAK) is a cytoplasmic tyrosine that plays fundamental role in integrin and growth factor mediated signalling an important player cell migration proliferation, processes vital for angiogenesis. However, the of FAK adult pathological angiogenesis unknown. We have generated endothelial-specific tamoxifen-inducible knockout mice by crossing FAK-floxed (FAKfl/fl) with platelet derived b (Pdgfb)-iCreER mice. Tamoxifen-treatment Pdgfb-iCreER;FAKfl/fl results deletion endothelial cells (ECs) without any adverse effects. Importantly however, FAK-deletion inhibited tumour reduced Furthermore, vivo angiogenic assays impairs vascular (VEGF)-induced neovascularization. In addition, vitro ECs resulted VEGF-stimulated Akt phosphorylation correlating cellular proliferation as well increased death. Our data suggest required validates possible target anti-angiogenic therapies.