Update on GLUT4 Vesicle Traffic: A Cornerstone of Insulin Action
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 rec...
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| Veröffentlicht in: | Trends in endocrinology and metabolism 2017-08, Vol.28 (8), p.597-611 |
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| creator | Jaldin-Fincati, Javier R Pavarotti, Martin Frendo-Cumbo, Scott Bilan, Philip J Klip, Amira |
| description | 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. |
| doi_str_mv | 10.1016/j.tem.2017.05.002 |
| format | Article |
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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.</description><identifier>ISSN: 1043-2760</identifier><identifier>EISSN: 1879-3061</identifier><identifier>DOI: 10.1016/j.tem.2017.05.002</identifier><identifier>PMID: 28602209</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>actin cytoskeleton ; Animals ; Cytoplasmic Vesicles - drug effects ; Cytoplasmic Vesicles - metabolism ; Endocrinology & Metabolism ; Glucose Transporter Type 4 - metabolism ; GLUT4 ; Humans ; Insulin - pharmacology ; Insulin - physiology ; insulin signaling ; membrane fusion ; Mice ; Protein Transport - drug effects ; Rab GTPases ; vesicle traffic</subject><ispartof>Trends in endocrinology and metabolism, 2017-08, Vol.28 (8), p.597-611</ispartof><rights>Elsevier Ltd</rights><rights>2017 Elsevier Ltd</rights><rights>Copyright © 2017 Elsevier Ltd. 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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). 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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). 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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | actin cytoskeleton Animals Cytoplasmic Vesicles - drug effects Cytoplasmic Vesicles - metabolism Endocrinology & Metabolism Glucose Transporter Type 4 - metabolism GLUT4 Humans Insulin - pharmacology Insulin - physiology insulin signaling membrane fusion Mice Protein Transport - drug effects Rab GTPases vesicle traffic |
| title | Update on GLUT4 Vesicle Traffic: A Cornerstone of Insulin Action |
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