WT hH1a clone was used.
N.S. : non different from WT ; N.A.: not available

COMMENTS ON IN VITRO DATA
DelF1617 was originally reported by Splawski et al. and it has been characterized in vitro by Chen et al. in order to assess if the biophysical properties of the mutant channel were consistent with the LQT3 phenotype. The authors concluded that this mutation causes a very complex in vitro phenotype that alters the voltage dependence of fast inactivation by a reduction in the gating charge contributed by S4-DIV, and can cause either a gain or loss of sodium current depending upon the membrane potential. Specifically a late component of INa was evident only at positive potentials, close to action potential plateau, Therefore the link with the reported phenotype at the clinical level (LQT3) remains difficult to explain. Overall the results of in vitro expression displayed a potential for this mutation to induce an overlapping BrS-LQT3 phenotype. No clinical data are currently available to support this hypothesis.