Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death

By P. Mohler, J. Schott, A. Gramolini, K. Dilly, S. Guatimosim, W. DuBell, Long‐Sheng Song, K. Haurogné, F. Kyndt, M. E. Ali and 5 more. Nature, 2003

1,014 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/a24dfe22cabfc926b46a29bae2575cb9cb0b5135

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. Bernard R. Chaitman
2. Rick A. Nishimura
3. J. Halperin
4. Jose Luis Zamorano
5. R. Kass
6. J. Nerbonne
7. Douglas P. Zipes

In Molecular Biology

1. R. Kass
2. J. Nerbonne
3. Douglas P. Zipes

Citations in the corpus

• Molecular physiology of cardiac repolarization. (2005, background): “Consistent with this hypothesis, molecular genetic studies subsequently revealed a loss-of-function mutation in ankyrin B (E1425G) that is causally linked to variant 4 of familial long QT syndrome, LQT4 (351).”
• ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (2006, background): “Mutations in 8 genes have been identified: 7 of them encode cardiac ion channel subunits and 1 encodes an anchoring protein that has been implicated in controlling ion channel targeting specific membrane sites.(791) The distinguishing features of some of the genetic variants of the disease have been”