René Barro-Soria

This study shows that the Panx11-89 mutant forms a functional ATP release channel independently of wild-type Panx1, with conserved structure-function features and sensitivity to inhibitors.

This study identifies phosphorylation as a switch that stabilizes Pannexin1 in an ATP-releasing conformation, important for developing disease modulators.

The paper investigates how two KCNQ3 mutations impair channel function and shows that polyunsaturated fatty acids can restore wild-type function in these mutations.