AI Article Synopsis
- Glucose transport is crucial for how muscles and fat use dietary glucose, with the GLUT4 transporter playing a key role by being relocated to the cell surface in response to insulin.
- Recent advancements in techniques like total internal reflection fluorescence microscopy (TIRFM) are enhancing our understanding of how GLUT4 moves to the plasma membrane, focusing on the processes of vesicle tethering and fusion.
- New research highlights the roles of various molecular players, including Rab GTPases and myosins, in the complex insulin-regulated trafficking of GLUT4, revealing important new insights into this cellular mechanism.
Article Abstract
Glucose transport is rate limiting for dietary glucose utilization by muscle and fat. The glucose transporter GLUT4 is dynamically sorted and retained intracellularly and redistributes to the plasma membrane (PM) by insulin-regulated vesicular traffic, or 'GLUT4 translocation'. Here we emphasize recent findings in GLUT4 translocation research. The application of total internal reflection fluorescence microscopy (TIRFM) has increased our understanding of insulin-regulated events beneath the PM, such as vesicle tethering and membrane fusion. We describe recent findings on Akt-targeted Rab GTPase-activating proteins (GAPs) (TBC1D1, TBC1D4, TBC1D13) and downstream Rab GTPases (Rab8a, Rab10, Rab13, Rab14, and their effectors) along with the input of Rac1 and actin filaments, molecular motors [myosinVa (MyoVa), myosin1c (Myo1c), myosinIIA (MyoIIA)], and membrane fusion regulators (syntaxin4, munc18c, Doc2b). Collectively these findings reveal novel events in insulin-regulated GLUT4 traffic.
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| http://dx.doi.org/10.1016/j.tem.2017.05.002 | DOI Listing |
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