William A. Coetzee

This study shows that loss of either SUR1 or Kir6.2 subunits in neurons increases dorsal root ganglion excitability and reduces morphine antinociception in mice.

This study shows that a CACNA1D variant causes electrophysiological abnormalities in hiPSC-CMs, which are reversed by AAV6-Cav1.3-C-terminus gene therapy.

This study identifies Kir6.1 as a key regulator of natural killer cell development in mice, showing its expression in mature NK cells and its role in NK-cell differentiation.