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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Kir6.2 is required for adaptation to stress.

Reaction to stress requires feedback adaptation of cellular functions to secure a response without distress, but the molecular order of this process is only partially understood. Here, we report a previously unrecognized regulatory element in the general adaptation syndrome. Kir6.2, the ion-conducting subunit of the metabolically responsive ATP-sensitive potassium (K(ATP)) channel, was mandatory for optimal adaptation capacity under stress. Genetic deletion of Kir6.2 disrupted K(ATP) channel-dependent adjustment of membrane excitability and calcium handling, compromising the enhancement of cardiac performance driven by sympathetic stimulation, a key mediator of the adaptation response. In the absence of Kir6.2, vigorous sympathetic challenge caused arrhythmia and sudden death, preventable by calcium-channel blockade. Thus, this vital function identifies a physiological role for K(ATP) channels in the heart.[1]


  1. Kir6.2 is required for adaptation to stress. Zingman, L.V., Hodgson, D.M., Bast, P.H., Kane, G.C., Perez-Terzic, C., Gumina, R.J., Pucar, D., Bienengraeber, M., Dzeja, P.P., Miki, T., Seino, S., Alekseev, A.E., Terzic, A. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
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