Key result
Coexpression of the β1-subunit induced a 2.3-fold increase in Nav1.8 current density and hyperpolarizing shifts in activation and steady-state inactivation, whereas β-subunits weakly regulated Nav1.6.
Population
Small-diameter dorsal root ganglion (DRG) neurons and heterologous expression systems
Design
Preclinical
Authors
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Highlights β1 as regulator of Nav1.8; hypothesis-generating for pain pathways with no clinical implications yet.
Effect estimate: 2.3-fold increase
Absolute Event Rate: -165.7% vs 73.9%
p-value: p=<0.01
The intracellular COOH-terminal domain of the β1-subunit plays an essential role in regulating Nav1.8 expression and gating in peripheral nerve channels.
Zhao et al. (2011) studied Peripheral nerve Na+ channel regulation. Auxiliary beta-subunits (β1-β4) vs. Empty vector was evaluated on Nav1.8 current density (2.3-fold increase, p=<0.01). Coexpression of the β1-subunit induced a 2.3-fold increase in Nav1.8 current density and hyperpolarizing shifts in activation and steady-state inactivation, whereas β-subunits weakly regulated Nav1.6.
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