Fig. 4From: VEGF111b, a C-terminal splice variant of VEGF-A and induced by mitomycin C, inhibits ovarian cancer growthVEGF111b overexpression reduces VEGF-R2 phosphorylation and its downstream signaling. Total and phosphorylated VEGF-R2 were measured by western blot. Downstream signaling proteins of p- PI3K, p-Akt, and p-ERK1/2 were reduced by VEGF111b and VEGF165b overexpression, correspondingly. Actin served as loading controlBack to article page