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The integrin antagonist cilengitide activates alphaVbeta3, disrupts VE-cadherin localization at cell junctions and enhances permeability in endothelial cells.

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Academic year: 2017

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Figure 5. Cilengitide induces Src-dependent phosphorylation of VE-cadherin cytoplasmic domain
Figure 6. Src inhibition prevents cilengitide-induced relocalization of aVb3 at the cell edge and disappearance of VE-cadherin from cellular junctions
Table 1. Relative cell death of HUVEC cultures exposed to cilengitide or EMD135981.
Figure 9. Proposed model of cilengitide effects on endothelial cells. Cilengitide acts on aVb3-expressing endothelial cells in three ways: 1, it suppresses aVb3-dependent adhesion by directly inhibiting aVb3-ligand-binding function; 2, it interferes with b

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