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Background:  The pore-forming subunit of the cardiac sodium channel, Na  v 1.5, has been previously found to be mutated in genetically determined arrhythmias. Na  v 1.5 associates with many proteins that regulate its function and cellular localisation. In order to identify more  in situ  Na  v 1.5 interacting proteins, genetically-modified mice with a high-affinity epitope in the sequence of Na  v 1.5 can be generated.    Methods:  In this short study, we (1) compared the biophysical properties of the sodium current (I  Na ) generated by the mouse Na  v 1.5 (mNa  v 1.5) and human Na  v 1.5 (hNa  v 1.5) constructs that were expressed in HEK293 cells, and (2) investigated the possible alterations of the biophysical properties of the human Na  v 1.5 construct that was modified with specific epitopes.    Results:  The biophysical properties of mNa  v 1.5 were similar to the human homolog. Addition of epitopes either up-stream of the N-terminus of hNa  v 1.5 or in the extracellular loop between the S5 and S6 transmembrane segments of domain 1, significantly decreased the amount of I  Na  and slightly altered its biophysical properties. Adding green fluorescent protein (GFP) to the N-terminus did not modify any of the measured biophysical properties of hNa  v 1.5.    Conclusions:  These findings have to be taken into account when planning to generate genetically-modified mouse models that harbour specific epitopes in the gene encoding mNa  v 1.5.

Electrophysiological properties of mouse and epitope-tagged human cardiac sodium channel Nav1.5 expressed in HEK293 cells