S. Perez-Feliz

Transgenic short-QT syndrome 1 rabbits mimic the human disease phenotype with QT/action potential duration shortening in the atria and ventricles and increased ventricular tachycardia/ventricular fibrillation inducibility

J. Behrends, R. Peyronnet, C. Bode, 2018, European heart journal.

Docosahexaenoic acid normalizes QT interval in long QT type 2 transgenic rabbit models in a genotype-specific fashion.

C. Bode, Z. Bősze, M. Zehender, 2021, Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.

A novel LMNA nonsense mutation causes two distinct phenotypes of cardiomyopathy with high risk of sudden cardiac death in a large five-generation family

A. Köttgen, C. Bode, P. Rainer, 2018, Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.

Postpartum hormones oxytocin and prolactin cause pro-arrhythmic prolongation of cardiac repolarization in long QT syndrome type 2.

G. Seemann, C. Bode, John Sorge, 2019, Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.

Differential Effects of the β‐Adrenoceptor Blockers Carvedilol and Metoprolol on SQT1‐ and SQT2‐Mutant Channels

C. Bode, M. Zehender, M. Brunner, 2013, Journal of cardiovascular electrophysiology.

Transgenic LQT2, LQT5, and LQT2‐5 rabbit models with decreased repolarisation reserve for prediction of drug‐induced ventricular arrhythmias

C. Bode, Z. Bősze, M. Zehender, 2020, British journal of pharmacology.