β-catenin regulates muscle glucose transport via actin remodelling and M-cadherin binding.

ABSTRACT:

Objective

Skeletal muscle glucose disposal following a meal is mediated through insulin-stimulated movement of the GLUT4-containing vesicles to the cell surface. The highly conserved scaffold-protein β-catenin is an emerging regulator of vesicle trafficking in other tissues. Here, we investigated the involvement of β-catenin in skeletal muscle insulin-stimulated glucose transport.

Methods

Glucose homeostasis and transport was investigated in inducible muscle specific β-catenin knockout (BCAT-mKO) mice. The effect of β-catenin deletion and mutation of β-catenin serine 552 on signal transduction, glucose uptake and protein-protein interactions were determined in L6-G4-myc cells, and β-catenin insulin-responsive binding partners were identified via immunoprecipitation coupled t

SUBMITTER: Masson SWC 

PROVIDER: S-EPMC7568189 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature