Control of human pancreatic beta cell kinome by GLP-1R biased agonism.

Results from this study suggest that differentially biased exendin-phe1 and exendin-asp3 can modulate distinct kinase interaction networks. Further understanding of these mechanisms will have important implications for the selection of appropriate anti-T2D therapies with optimised downstream kinomic profiles. This article is protected by copyright. All rights reserved.