Proarrhythmic Consequences of a KCNQ1 AKAP-Binding Domain Mutation-Reference-Cited by-同舟云学术

Proarrhythmic Consequences of a KCNQ1 AKAP-Binding Domain Mutation

Published:2004-12-10 Issue:12 Volume:95 Page:1216-1224
ISSN:0009-7330
Container-title:Circulation Research
language:en
Short-container-title:Circulation Research

Author:

Saucerman Jeffrey J.¹,Healy Sarah N.¹,Belik Mary E.¹,Puglisi Jose L.¹,McCulloch Andrew D.¹

Affiliation:

1. From the Department of Bioengineering (J.J.S., S.N.H., M.E.B., A.D.M), Whitaker Institute of Biomedical Engineering, University of California San Diego, La Jolla; and the Department of Physiology (J.L.P.), Loyola University Chicago, Maywood, Ill.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

Reference53 articles.

1. Genotype-Phenotype Correlation in the Long-QT Syndrome

2. Epinephrine-Induced QT Interval Prolongation: A Gene-Specific Paradoxical Response in Congenital Long QT Syndrome

3. Requirement of a Macromolecular Signaling Complex for β Adrenergic Receptor Modulation of the KCNQ1-KCNE1 Potassium Channel

4. Four potassium channel mutations account for 73% of the genetic spectrum underlying long‐QT syndrome (LQTS) and provide evidence for a strong founder effect in Finland

5. A founder mutation of the potassium channel KCNQ1 in long QT syndrome

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