Insulin-stimulated trafficking of GLUT4 requires the myosin motor Myo1C and signaling adaptor 14-3-3β. Originally, it was thought that 14-3-3β promotes GLUT4 transport by binding the Myo1C lever arm and activating the Myo1C motor. New work by Ji and Ostap using in vitro assays reveals that 14-3-3β binding actually inhibits Myo1C motility, prompting reconsideration of the functional relationship between 14-3-3β and Myo1C and the regulatory potential of atypical light chains.
Bibliographical noteFunding Information:
This work is supported by National Institutes of Health Grants R01GM122917 and R01GM122917-01S1. The authors declare that they have no conflicts of interest with the contents of this article. The content is solely the respon-sibility of the authors and does not necessarily represent the official views of the National Institutes of Health.