Mexiletine rescues a mixed biophysical phenotype of the cardiac sodium channel arising from the SCN5A mutation, N406K, found in LQT3 patients

פריטים דומים

• Expression defect of the rare variant/Brugada mutation R1512W depends upon the SCN5A splice variant background and can be rescued by mexiletine and the common polymorphism H558R
  מאת: Hu, Rou-Mu, et al.
  יצא לאור: (2021)
• Arrhythmogenic Biophysical Phenotype for SCN5A Mutation S1787N Depends upon Splice Variant Background and Intracellular Acidosis
  מאת: Hu, Rou-Mu, et al.
  יצא לאור: (2015)
• Digenic inheritance novel mutations in SCN5a and SNTA1 increase late I(Na) contributing to LQT syndrome
  מאת: Hu, Rou-Mu, et al.
  יצא לאור: (2013)
• Epidemiologic, molecular, and functional evidence suggest A572D-SCN5A should not be considered an independent LQT3-susceptibility mutation
  מאת: Tester, David J., et al.
  יצא לאור: (2010)
• The common African American polymorphism SCN5A-S1103Y interacts with mutation SCN5A-R680H to increase late Na current
  מאת: Cheng, Jianding, et al.
  יצא לאור: (2011)