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. 2017 Aug 7;7(3):624–634. doi: 10.1086/689908

Fig. 7.

Fig. 7.

Expression of insulin receptor isoforms and downstream insulin signaling molecules in cultured endothelial cells with and without BMPR2 mutation. (a) Insulin receptor isoform A was not differentially expressed according to mutation status. Isoform B expression varied by mutation status, but the ratio was not skewed significantly towards increased presence of IR-A. (b) The MAPK signaling molecule Erk1/2 had no statistically significant change in phosphorylation by mutation or insulin status. (c–e) Akt, however, had reduced expression with one of two mutations in BMPR2 but relative phosphorylation of the Ser473 site remained intact. *P < 0.05 compared with cells without mutation (two-way ANOVA); †P < 0.05 compared with Mutation1 (two-way ANOVA); ‡P < 0.05 compared with no insulin (two-way ANOVA).