Figure 1. Comparison of potential mechanisms by which LKB1 controls monocarboxylate and GLUT4 glucose transporters. In contracting muscle, depletion of ATP leads to activation of AMPK, which phosphorylates and inhibits the Rab-GTPase–activating proteins termed AS160 and TBC1D1. This leads to an increase in the levels of active (GTP-bound) Rab8A that promotes relocalization of GLUT4 to the plasma membrane. AMPK or an AMPK-related kinase could phosphorylate an intermediate substrate to induce the translocation of MCT1/Sln to the plasma membrane.
Figure 1.

Comparison of potential mechanisms by which LKB1 controls monocarboxylate and GLUT4 glucose transporters. In contracting muscle, depletion of ATP leads to activation of AMPK, which phosphorylates and inhibits the Rab-GTPase–activating proteins termed AS160 and TBC1D1. This leads to an increase in the levels of active (GTP-bound) Rab8A that promotes relocalization of GLUT4 to the plasma membrane. AMPK or an AMPK-related kinase could phosphorylate an intermediate substrate to induce the translocation of MCT1/Sln to the plasma membrane.

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