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Updated: Jul 15, 2026

A Fluorescence-Based Assay of Membrane Potential for High-Throughput Functional Study of Two Endogenous Ion Channels in Two Epithelial Cell Lines
Published on: June 22, 2022
CFTR stabilizes ENaC at the plasma membrane
1Program in Cell Biology, The Hospital for Sick Children, and Biochemistry Department, University of Toronto, 555 University Ave, Toronto, Ontario, Canada M5G 1X8.
Cystic fibrosis transmembrane conductance regulator (CFTR) surprisingly stabilizes epithelial sodium channel (ENaC) at the cell surface. This suggests CFTR impacts ENaC stability rather than just its opening.
Area of Science:
- Cell Biology
- Ion Channel Physiology
- Molecular Medicine
Background:
- Epithelial sodium channel (ENaC) activity is crucial for ion and fluid transport.
- The cystic fibrosis transmembrane conductance regulator (CFTR) is known to modulate ENaC channel opening.
- Previous understanding suggested CFTR primarily affects ENaC gating.
Purpose of the Study:
- To investigate the effect of CFTR on ENaC stability at the plasma membrane.
- To determine if CFTR influences ENaC cell-surface half-life.
Main Methods:
- Generation of MDCK-I cell lines stably expressing ENaC alone or with CFTR.
- Development of an assay to quantify ENaC cell-surface half-life.
Main Results:
- Co-expression of CFTR with ENaC led to stabilization of ENaC at the plasma membrane.
- CFTR significantly increased the cell-surface half-life of ENaC.
Conclusions:
- CFTR plays a role in regulating ENaC stability at the cell surface.
- The findings suggest CFTR's influence on ENaC extends beyond channel opening to membrane trafficking and stability.
More Related Videos
08:56Demonstration of Proteolytic Activation of the Epithelial Sodium Channel (ENaC) by Combining Current Measurements with Detection of Cleavage Fragments
Published on: July 5, 2014
09:59Functional Reconstitution and Channel Activity Measurements of Purified Wildtype and Mutant CFTR Protein
Published on: March 9, 2015
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