Thanks to a collaborative effort involving split intein-mediated protein engineering and MD simulations (credit to the group of Prof Lucie Delemotte), we were able to show how some Nav1.5 patient mutations are functionally benign – until they get phosphorylated and wreak havoc on inactivation. We were also able to provide insight on the basic mechanism of inactivation and how phosphorylation can affect Nav1.5 pharmacology. Big kudos to Keith Khoo for providing the foundation for the project. Get the full story here.
