Key result
Coexpression with the β1 subunit accelerated the inactivation of sodium currents and shifted the voltage dependence of channel activation by 6.6 mV in the direction of depolarization.
Population
HEK293 cells stably transformed to express the rat Nav1.6 sodium channel α subunit either alone or in…
Comparison
Coexpression of the rat Nav1.6 sodium channel α… vs Expression of the rat Nav1.6 sodium channel α…
Design
Preclinical
Authors
Loading...
These in vitro effects do not guide clinical practice; leaves open β1-Nav1.6 roles in cardiac disease models.
Mean Difference: 6.6
Absolute Event Rate: -28.6% vs -35.2%
p-value: p=<0.0005
The rat β1 subunit modulates rat Nav1.6 sodium channels in HEK293 cells by accelerating inactivation and shifting voltage dependence of activation and steady-state inactivation towards depolarization.
He et al. (2014) studied this question. Coexpression with the rat β1 subunit vs. Expression of rat Nav1.6 sodium channel α subunit alone was evaluated on Voltage dependence of channel activation (V0.5) (6.6 mV depolarizing shift, p=<0.0005). Coexpression with the β1 subunit accelerated the inactivation of sodium currents and shifted the voltage dependence of channel activation by 6.6 mV in the direction of depolarization.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: