Sci. STKE, 22 January 2002
Channel Biology Cardiac Action Potentials
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]
Citation: Cardiac Action Potentials. Sci. STKE 2002, tw35 (2002).
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