Channel Biology

Cardiac Action Potentials

Science's STKE  22 Jan 2002:
Vol. 2002, Issue 116, pp. tw35
DOI: 10.1126/stke.2002.116.tw35

Efficient intracellular signal transduction requires proper localization of signaling components. Neurotransmitters bind to β-adrenergic receptors in the heart and control action potential duration by altering ion current through K+ channels composed of hKCNQ1 and hKCNE1 subunits. Marx et al. show that the adenosine 3′,5′-monophosphate-(cAMP)-dependent protein kinase is physically yoked to these proteins by a targeting protein known as yotiao and is required for the enhancement of current through the K+ channel in response to adrenergic signaling. Furthermore, one of the genetic abnormalities associated with a potentially deadly hereditary form of cardiac arrhythmia in humans (long QT syndrome) turns out to be a mutation in a K+ channel subunit that disrupts interaction with yotiao.

S. O. Marx, J. Kurokawa, S. Reiken, H. Motoike, J. D'Armiento, A. R. Marks, R. S. Kass, Requirement of a macromolecular signaling complex for β adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel. Science 295, 496-499 (2002). [Abstract] [Full Text]