Research summary
Past research was focused on mammalian CLC proteins, and we discovered that several mammalian family members are 2Cl-/H+ antiporters rather than chloride channels, and identified key residues for proton transport as well as the basis for nitrate selectivity of some plant CLC proteins.

Current research is looking at the pathophysiological consequences of mutations in KCNJ10, an inwardly rectifying potassium channel. Loss of function in both homomeric mutant and heteromeric mutant KCNJ10/16 potassium channels results in EAST syndrome, characterized by Epilepsy, Ataxia, Sensorineural hearing loss and mild renal salt wasting (Tubulopathy). We identified altered open probability, impaired PIP2 binding and altered pH dependence in some mutations.