TY  - INPR
N2  - Insulin stimulates glucose transport by triggering regulated delivery of intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane. This process is defective in diseases such as type 2 diabetes (T2DM). While studies in rodent cells have been invaluable in understanding GLUT4 traffic, evolutionary plasticity must be considered when extrapolating these findings to humans. Recent work has identified species-specific distinctions in GLUT4 traffic, notably the participation of a novel clathrin isoform, CHC22, in humans but not rodents. Here, we discuss GLUT4 sorting in different species and how studies of CHC22 have identified new routes for GLUT4 trafficking. We further consider how different sorting-protein complexes relate to these routes and discuss other implications of these pathways in cell biology and disease.
PB  - Elsevier
Y1  - 2020/06/30/
A1  - Gould, GW
A1  - Brodsky, F
A1  - Bryant, NJ
ID  - discovery10099534
SN  - 0962-8924
N1  - © 2020 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
JF  - Trends in Cell Biology
AV  - public
UR  - https://doi.org/10.1016/j.tcb.2020.05.007
KW  - GLUT4
KW  -  insulin
KW  -  CHC22 clathrin
KW  -  ERGIC
KW  -  membrane trafficking
KW  -  diabetes
TI  - Building GLUT4 vesilces: CHC22 clathrin's human touch
ER  -