Uncoupling sodium channel dimers rescues phenotype of pain-linked Nav1.7 mutation
Annika H. Rühlmann, Jannis Körner, Ralf Hausmann, Nikolay Bebrivenski, Christian Neuhof, Silvia Detro‐Dassen, Petra A. I. Hautvast, Carène Benasolo, Jannis Meents, Jan‐Philipp Machtens, Günther Schmalzing, Angelika Lampert
The paper shows that uncoupling dimerized Nav1.7 channels reduces persistent current caused by a pain mutation, suggesting dimerization plays a role in pain syndromes.
British Journal of Pharmacology · Jul 14, 2020Peer-reviewedNeuroscience