Figure 8. Hypothetical model showing insulin-triggered formation of a PKCζ–80K-H–munc18c complex and how this may trigger GLUT4 translocation to the plasma membrane.

The model shows how the complex formation may decrease the clamping action of munc18c, thereby allowing VAMP-2 to bind syntaxin-4 and deliver GLUT4 to the plasma membrane. Displaced munc18c may also be involved in fusing the GLUT4 vesicle to the plasma membrane. Although PKCζ, 80K-H and munc18c are shown to bind each other, the precise interactions that result in the complex formation require elucidation. Other accessory proteins are omitted for simplicity.