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. 2010 Apr 15;21(8):1375–1386. doi: 10.1091/mbc.E09-08-0751

Figure 1.

Figure 1.

GLUT4 retention machinery driven by the FQQI and TELE motifs. (A) GLUT4 retention model. The TR recycling pathway (fast in both basal and insulin-stimulated states) and the GLUT4 specialized pathway (slow in basal and fast in the presence of insulin) contribute to PM GLUT4 distribution. GLUT4 is sorted from the endosomal recycling compartment (ERC) to the GLUT4 specialized vesicles (GSV; retention pathway 2) and an unidentified perinuclear compartment (retention pathway 1) in basal adipocytes. These two retention pathways are controlled by the TELE-based and FQQI motifs, respectively. Mutation of these motifs results in redistribution of GLUT4 to the endosomal compartments and increases PM GLUT4 (Blot and McGraw, 2008). (B) Schematic of the HA-GLUT4-GFP with mutated residues noted in bold type. (C) Surface-to-total distributions in basal adipocytes. WT, wild-type HA-GLUT4-GFP; FA, F5A mutation; EE, EE499,501AA mutation; FA/EE, F5A/EE499,501AA mutation in HA-GLUT4-GFP. The data are averages ± SEM of eight to nine independent experiments normalized to the WT GLUT4 surface-to-total ratio of each experiment. *p < 0.001 compared with WT; #p < 0.001 compared with the FA mutant.