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Requirement of a Macromolecular Signaling Complex for Adrenergic Receptor Modulation of the KCNQ1-KCNE1 Potassium Channel
Steven O. Marx,*Junko Kurokawa,*Steven Reiken,Howard Motoike,Jeanine D'Armiento,Andrew R. Marks,Robert S. Kass
Sympathetic nervous system (SNS) regulation of cardiac action
potential duration (APD) is mediated by adrenergic receptor(AR)
activation, which increases the slow outward potassium ioncurrent
(IKS). Mutations in two human
IKS channel subunits, hKCNQ1and hKCNE1, prolong
APD and cause inherited cardiac arrhythmiasknown as LQTS (long QT
syndrome). We show that AR modulationof IKS
requires targeting of adenosine 3',5'-monophosphate
(cAMP)-dependentprotein kinase (PKA) and protein phosphatase 1 (PP1) to hKCNQ1through the targeting protein yotiao. Yotiao binds to
hKCNQ1 bya leucine zipper motif, which is disrupted by an LQTS
mutation(hKCNQ1-G589D). Identification of the hKCNQ1 macromolecular
complexprovides a mechanism for SNS modulation of cardiac APD throughIKS.
Department of Pharmacology, Center for Molecular Cardiology,
Department of Medicine, College of Physicians and Surgeons of Columbia
University, New York, NY 10032, USA.
*
These authors contributed equally to this report.
To whom correspondence should be addressed.
E-mail: rsk20{at}columbia.edu
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