Arrhythmia susceptibility and premature death in transgenic mice overexpressing both SUR1 and Kir6.2[DeltaN30,K185Q] in the heart.

Sarcolemmal ATP-sensitive potassium (K(ATP)) channels are activated after pathological depletion of intracellular ATP, unlike their pancreatic beta-cell counterparts, which dynamically regulate membrane excitability in response to changes in blood glucose. We recently engineered a series of transgenic (TG) mice overexpressing an ATP-insensitive inward rectifying K(+) channel protein (Kir)6.2 mutant (Kir6.