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. Author manuscript; available in PMC: 2014 May 7.
Published in final edited form as: Cell Metab. 2013 Apr 25;17(5):745–755. doi: 10.1016/j.cmet.2013.03.017

Figure 6. WNT3A stimulates glucose consumption via LRP5 and RAC1.

Figure 6

(A–B) Effects of DKK1 on WNT3A-induced phosphorylation and glycolytic enzymes. P-LRP6, P-AKT, P-S6 normalized to respective total protein. Other proteins normalized to β-ACTIN. (C) Effect of DKK1 on WNT3A-induced glucose consumption. (D–F) Effect of LRP5 or LRP6 knockdown (D) on WNT3A-induced glucose consumption (E), and on signaling events after 1 hour of treatment (F). β-CAT* denotes β-CATENIN unphosphorylated at N-terminus. (G) Effect of RAC1 knockdown on mTORC2 and LDHA induction by 24-hour WNT3A treatment. (H) Effect of RAC1 knockdown on WNT3A-induced glucose consumption. (I) Representative confocal images of RAC1 immunofluorescence. ST2 cells were serum-starved overnight before being treated for 2 hours with vehicle (Ctrl) or Wnt3a. Arrows denote RAC1 membrane localization. All glucose consumption measured after 24 hours of WNT3A or vehicle treatment. V: vehicle; W: WNT3A. *: n=3, p<0.05. Error bars: STDEV.