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. 2009 Sep 1;20(17):3918–3929. doi: 10.1091/mbc.E09-03-0187

Figure 5.

Figure 5.

Cortical actin remodeling is not required for insulin-induced transport of GLUT4 vesicles into the evanescent field. 3T3-L1 adipocytes expressing GLUT4-eGFP were serum starved for 120 min and treated with DMSO ± 10 μM Lat-B for 60 min. Time course of insulin-induced GLUT4-eGFP fluorescence increase in the evanescent field for DMSO and Lat-B treatments (A) and the area under the curve (B) are shown. Data are mean ± SEM (n = 3 experiments); time-course of insulin-induced GLUT4-eGFP fluorescence increase in the evanescent field for DMSO control and 50 μM BAPTA-AM (C), 100 nM wortmannin (E), or 10 μM Akti-1/2 inhibitor (G) treatments. Data are mean ± SEM of 2–3 independent experiments; HA-GLUT4–expressing adipocytes grown in 96-well plates were serum-starved for 2 h and treated with DMSO control and 50 μM BAPTA-AM (D), 100 nM wortmannin (F), or 10 μM Akti-1/2 inhibitor (H) treatments. Cells were then either unstimulated (Bas) or stimulated with 100 nM insulin (Ins) for 20 min at 37°C. The amount of HA-GLUT4 on the cell surface (nonpermeabilized cells) was expressed as a percentage of total HA-GLUT4 determined under permeabilizing conditions. * p < 0.05 versus DMSO control insulin (n = 3 experiments).