Skip to main content
. 2015 Jan 9;6:5951. doi: 10.1038/ncomms6951

Figure 2. Tmod3 functions downstream of Akt2 signalling and is required for ISGT and glucose uptake.

Figure 2

(a) Normal proximal insulin signalling in Tmod3-KD 3T3-L1 adipocytes. After 2-h serum starvation, the cells received mock or insulin treatment for 20 min. The specificity of anti-PAS antibody to pull-down phosphorylated Tmod3 was confirmed in Tmod3-KD cells, bottom panel. (b) Impaired glucose uptake in Tmod3-KD 3T3-L1 adipocytes. After 3-h serum starvation, the cells received mock or insulin treatment for 20 min for measurement of 2-DG uptake. Data are expressed as mean±s.e.m. (n=4; analysis of variance (ANOVA) with Dunnett’s multiple comparison test). **P<0.01 versus Scr Insulin groups. (c) GLUT4 fusion protein for detection of GLUT4 translocation and PM surface exposure. (d,e) Impaired insulin-stimulated GLUT4 surface exposure in Tmod3-KD 3T3-L1 adipocytes. The cells received mock or insulin treatment for 20 min after 2-h serum starvation. The ratio of surface to total GLUT4 was quantified by detecting surface GLUT4 through anti-Myc fluorescence immunolabelling and total GLUT4 through mCherry fluorescence in non-permeabilized cells. Data in each group were normalized and expressed as a percentage of insulin-treated control cells. Data presented are representative confocal microscopic images and means±s.e.m. of about 100 cells in each group from three independent experiments (ANOVA with Dunnett’s multiple comparison test). **P<0.01 versus Scr Insulin groups. Scale bars in e, 20 μm.