- A Novel Approach for In Vitro Testing and Hazard Evaluation of Nanoformulated RyR2-Targeting siRNA Drugs Using Human PBMCs
- Genetics, manifestations, and management of catecholaminergic polymorphic ventricular tachycardia
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Generation of an isogenic CRISPR/Cas9-corrected control induced pluripotent stem cell line from a patient with autosomal dominant catecholaminergic polymorphic ventricular tachycardia with a heterozygous variant in cardiac calsequestrin-2
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing Ca2+/Ba2+ Current Is Present
- Extracorporeal membrane oxygenation for catecholaminergic polymorphic ventricular tachycardia: a case report and literature review
- Disparate molecular mechanisms in cardiac ryanodine receptor channelopathies
- Development of a new solar system integrating photovoltaic and thermoelectric modules with paraffin-based nanomaterials
- Case Report: The unrelenting journey-successful resolution of catecholaminergic polymorphic ventricular tachycardia (CPVT) through right cardiac sympathetic denervation in a teenager after left cardiac sympathetic denervation
- Treatment Outcomes in Children With Catecholaminergic Polymorphic Ventricular Tachycardia: A Single Institutional Experience
- Catecholaminergic Polymorphic Ventricular Tachycardia in Children: Insights and Challenges From the Current Study
- International Multicenter Cohort Study on Beta-Blocker-Free Treatment Strategies for Catecholaminergic Polymorphic Ventricular Tachycardia Patients
- Dual calcium-voltage optical mapping of regional voltage and calcium signals in intact murine RyR2-R2474S hearts
- Conditional ablation of MCU exacerbated cardiac pathology in a genetic arrhythmic model of CPVT
- A case report of familial catecholaminergic polymorphic ventricular tachycardia with a novel mutation in the ryanodine receptor 2
- CPVT, PVCs, and Ambulatory Monitoring: Can Old Technology Be Used in New Ways?
- The Role of Human-Induced Pluripotent Stem Cells in Studying Cardiac Channelopathies
- Gain-of-Function and Loss-of-Function Mutations in the RyR2-Expressing Gene Are Responsible for the CPVT1-Related Arrhythmogenic Activities in the Heart
- Long-term clinical course of patients with catecholaminergic polymorphic ventricular tachycardia: A more than 10-year follow-up cohort study
- Electrical storms induced by multiple shocks in catecholaminergic polymorphic ventricular tachycardia, spotlight
- Generation of a heterozygous Calsequestrin 2 F189L iPSC line (UMGi158-B) by CRISPR/Cas9 genome editing to investigate the cardiac pathophysiology of Takotsubo Syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia
- Inhibitors of Intracellular RyR2 Calcium Release Channels as Therapeutic Agents in Arrhythmogenic Heart Diseases
- Structure Activity Optimization of Ryanodine Receptor Modulators for the Treatment of Catecholaminergic Polymorphic Ventricular Tachycardia
- Structure-activity optimization of ryanodine receptor modulators for the treatment of catecholaminergic polymorphic ventricular tachycardia
- Generation of a human induced pluripotent stem cell line (KSCBi016-A) from a CPVT patient with an RYR2 mutation