Cargando…
PERTURBATION OF SODIUM CHANNEL STRUCTURE BY AN INHERITED LONG QT SYNDROME MUTATION
The cardiac voltage-gated sodium channel (Na(V)1.5) underlies impulse conduction in the heart and its depolarization-induced inactivation is essential in control of the duration of the QT interval of the electrocardiogram (ECG). Perturbation of Nav1.5 inactivation by drugs or inherited mutation can...
Autores principales: | Glaaser, Ian W., Osteen, Jeremiah D., Puckerin, Akil, Sampson, Kevin J., Jin, Xiangshu, Kass, Robert S. |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2012
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518026/ https://www.ncbi.nlm.nih.gov/pubmed/22426227 http://dx.doi.org/10.1038/ncomms1717 |
Ejemplares similares
-
Modeling Tissue- and Mutation- Specific Electrophysiological Effects in the Long QT Syndrome: Role of the Purkinje Fiber
por: Iyer, Vivek, et al.
Publicado: (2014) -
Exploring mutation specific beta blocker pharmacology of the pathogenic late sodium channel current from patient-specific pluripotent stem cell myocytes derived from long QT syndrome mutation carriers
por: Comollo, Thomas W., et al.
Publicado: (2022) -
Pharmacological rescue of specific long QT variants of KCNQ1/KCNE1 channels
por: Zou, Xinle, et al.
Publicado: (2022) -
Purkinje Cells as Sources of Arrhythmias in Long QT Syndrome Type 3
por: Iyer, Vivek, et al.
Publicado: (2015) -
Gating Properties of Mutant Sodium Channels and Responses to Sodium Current Inhibitors Predict Mexiletine-Sensitive Mutations of Long QT Syndrome 3
por: Li, Gang, et al.
Publicado: (2020)