LQTS mutation N1325S in cardiac sodium channel gene SCN5A causes cardiomyocyte apoptosis, cardiac fibrosis and contractile dysfunction in mice
- 1 March 2011
- journal article
- research article
- Published by Elsevier in International Journal of Cardiology
- Vol. 147 (2) , 239-245
Abstract
No abstract availableKeywords
This publication has 26 references indexed in Scilit:
- Ethical authorship and publishingInternational Journal of Cardiology, 2009
- The cardiac sodium channel mutation delQKP 1507-1509 is associated with the expanding phenotypic spectrum of LQT3, conduction disorder, dilated cardiomyopathy, and high incidence of youth sudden deathEP Europace, 2008
- Divergent Biophysical Defects Caused by Mutant Sodium Channels in Dilated Cardiomyopathy With ArrhythmiaCirculation Research, 2008
- Induction of high STAT1 expression in transgenic mice with LQTS and heart failureBiochemical and Biophysical Research Communications, 2007
- Cardiac-specific overexpression of SCN5A gene leads to shorter P wave duration and PR interval in transgenic miceBiochemical and Biophysical Research Communications, 2007
- Optical mapping of ventricular arrhythmias in LQTS mice with SCN5A mutation N1325SBiochemical and Biophysical Research Communications, 2007
- Mechanisms by which SCN5A mutation N1325S causes cardiac arrhythmias and sudden death in vivoCardiovascular Research, 2004
- Regulation of cell death: the calcium–apoptosis linkNature Reviews Molecular Cell Biology, 2003
- Prolongation of the QT interval in heart failure occurs at low but not at high heart ratesClinical Science, 2000
- Ischemia-induced STAT-1 Expression and Activation Play a Critical Role in Cardiomyocyte ApoptosisJournal of Biological Chemistry, 2000