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. 2013 Nov;33(21):4181–4197. doi: 10.1128/MCB.00650-13

Fig 12.

Fig 12

TAPI inhibited ADAM17-mediated VEGFR2 shedding and EC apoptosis induced by the inactivation of Cdc42. (A) HUVECs transfected with Cdc42 siRNA were either left untreated or treated with TAPI-1 (50 μM) for 4 h, and internalized VEGFR2 was then analyzed by Western blotting. Samples were also blotted with antibodies against Cdc42 and vinculin. (B) Quantitative analysis results show that TAPI treatment significantly decreased the level of production of 75-kDa VEGFR2 fragments. (C through N) Cultured Cdc42flox/flox ECs were infected either with Ad-LacZ (C through F), with Ad-Cre without further treatment (G through J), or with Ad-Cre plus TAPI-1 (50 μM) (K through N). TUNEL assays, PECAM-1 staining, and Hoechst staining for nuclei were then performed. Bars, 25 μm.