ArticlePhysiological reports2015
Direct interactions between ENaC gamma subunit and ClCN2 in cystic fibrosis epithelial cells.
Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Association of cystic fibrosis transmembrane conductance regulator with epithelial sodium channel subunits carrying Liddle's syndrome mutations.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Downregulation of epithelial sodium channel (ENaC) activity in human airway epithelia after low temperature incubation.BMJ open respiratory research · 2021Article
- Role of CBS and Bateman Domains in Phosphorylation-Dependent Regulation of a CLC Anion Channel.Biophysical journal · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cystic fibrosis (CF) is a lethal disease caused by mutations in the chloride channel CFTR gene. The disease is characterized by decreased chloride secretion and unregulated sodium absorption through the epithelial sodium channel (ENaC) in the airway epithelium and other affected organs. We hypothesize that a non-CFTR alternative chloride channel ClCN2 can be activated to negatively regulate ENaC in CF epithelial cell cultures. We identified a novel interaction between ClCN2 and the ENaCγ subunit in CF airway epithelial cells and show that the upregulation of ClCN2 leads to decreased expression of ENaCγ via a K63 ubiquitination mechanism. These regulatory effects of ClCN2 on ENaCγ appear to be dependent on the CBS-1 domain located within the c-terminus of ClCN2, which is necessary for the targeting of ClCN2 to the apical surface. In sum, these results suggest the ability of ClCN2 to negatively regulate sodium absorption through ENaC, supporting its role as a therapeutic target for the treatment of CF.
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