Our data suggest a potential role for δ-ENaC in controlling sodium reabsorption in the airways, and advance the plausibility of ENaC as a therapeutic target in CF.
Separately, an independently enriched rare variant in SCNN1D was identified in the Exome Variant Server database associated with a milder pulmonary disease phenotype.
The aim of this study was to investigate the expression pattern of δ ENaC in patients with temporal lobe epilepsy (TLE) and in a pilocarpine-induced rat model of epilepsy.
In contrast, knocking down δENaC, which is not a component of the glioma cation channel complex, had no effect on cyclin-dependent kinase inhibitor expression.