Cardiac Na⁺ channel dysfunction in Brugada syndrome is aggravated by β₁-subunit

Keyphrases

• Na+ Channel 100%
• Brugada Syndrome 100%
• Idiopathic Ventricular Fibrillation 100%
• Xenopus Oocytes 66%
• Steady-state Inactivation 66%
• Co-expression 66%
• LQT3 66%
• Recovery from Inactivation 66%
• Skeletal muscle 33%
• Functional Impact 33%
• Voltage Dependence 33%
• Na + 33%
• Congenital Long QT Syndrome 33%
• Pathophysiological Mechanisms 33%
• Persistent Current 33%
• Functional Defects 33%
• Channel Activation 33%
• Current Decay 33%
• Background mutations 33%
• Chromosome 3 33%
• Window Current 33%
• Gating Kinetics 33%
• Negative Potential 33%
• Channel Inactivation 33%
• Positive Potential 33%
• Subunit Association 33%
• Activation Kinetics 33%
• Excitable Tissues 33%
• Current Recovery 33%

Biochemistry, Genetics and Molecular Biology

• Sodium Channel 100%
• Ventricular Fibrillation 100%
• Brugada Syndrome 100%
• Wild Type 66%
• Xenopus 66%
• Steady State 66%
• Isoform 33%
• Skeletal Muscle 33%
• Electric Potential 33%
• Chromosome 3 33%
• Long QT Syndrome 33%

Neuroscience

• Sodium Channel 100%
• Brugada Syndrome 100%
• In Vivo 33%
• Skeletal Muscle 33%
• Chromosome 3 33%
• Long QT Syndrome 33%