Processing of ENaC in mouse kidney: effects of aldosterone and a Liddle syndrome mutation
Abstract
Using a mouse model of Liddle syndrome we show that the effects of the mutation on ENaC activity do not correlate with effects on channel processing. We conclude that the hyperactivity of the channels likely results from increased activity of processed channels residing in the apical membrane.
Fields of Study & Subjects
Ion Transport and Channel Regulation
Hormonal Regulation and Hypertension
Ion channel regulation and function
Publication details
- Journal / source
- American Journal of Physiology-Renal Physiology
- Volume
- 330
- Issue
- 3
- Pages
- F285–F293
- Publication date
- 8 January 2026
- Language
- EN