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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2014 Aug 21;34(10):2301–2309. doi: 10.1161/ATVBAHA.114.304338

Fig. 1. P66Shc is required for canonical Wnt signaling in endothelial cells.

Fig. 1

a) siRNA-mediated knockdown of p66Shc in BAEC inhibits Wnt3a-stimulated dephosphorylation and increase of β-catenin. b) shRNA-mediated knockdown of p66Shc in HUVEC suppresses Wnt3a-stimulated increase of β-catenin. Adp66shcRNAi: adenovirus expressing p66shc shRNA; AdlacZ: control adenovirus encoding E. Coli LacZ. c) Wnt3a stimulates β-catenin-mediated transcription in BAEC measured by TOP-Flash (TOP) luciferase reporter plasmid. Mutated FOP-Flash (FOP) reporter was used as a negative control. Lithium chloride (LiCl) was used as a positive control (n=3). d) Wnt3a-stimulated TOP-Flash luciferase activity in HEK 293 cells is suppressed by knocking down p66Shc (n=3). e) Expression of p66Shc, but not the redox deficient p66Shc S36A, induces β-catenin-mediated transcription (TOP-Flash luciferase activity) in HEK 293 cells (n=3). All values are shown as mean ± SEM. *** P < 0.001 vs. indicated group. ns = not significant. Immunoblots are representative of three experiments.