Decomposition of slide helix contributions to ATP-dependent inhibition of Kir6.2 channels

Abstract

Background: Kir6.2 potassium channels are inhibited by intracellular ATP. Results: A rescue mechanism was applied to loss-of-function channel mutations. Asp-58 mutations in an interfacial helix (the "slide" helix) abolish ATP sensitivity. Conclusion: Residue Asp-58 is essential for coupling Kir6.2 channel cytoplasmic and transmembrane domains. Significance: We describe a novel rescue mechanism to characterize loss-of-function Kir6.2 channel mutants. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.