Associated Papers
Functional reassessment of Nav1.5 T559A reveals loss-of-function in a variant commonly used as wild type.
Melgari D et al.
American Journal of Physiology. Cell Physiology, 2025
Calmodulin binds to the N-terminal domain of the cardiac sodium channel Nav1.5.
Wang Z et al.
Channels (austin, Tex.), 2020
Predicting changes to INa from missense mutations in human SCN5A.
Clerx M et al.
Scientific Reports, 2018
Mutations in sodium channel β-subunit SCN3B are associated with early-onset lone atrial fibrillation.
Olesen MS et al.
Cardiovascular Research, 2011
Partial expression defect for the SCN5A missense mutation G1406R depends on splice variant background Q1077 and rescue by mexiletine.
Tan BH et al.
American Journal of Physiology. Heart and Circulatory Physiology, 2006
A ubiquitous splice variant and a common polymorphism affect heterologous expression of recombinant human SCN5A heart sodium channels.
Makielski JC et al.
Circulation Research, 2003
A common human SCN5A polymorphism modifies expression of an arrhythmia causing mutation.
Ye B et al.
Physiological Genomics, 2003
Temperature dependence of early and late currents in human cardiac wild-type and long Q-T DeltaKPQ Na+ channels.
Nagatomo T et al.
The American Journal of Physiology, 1998
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