Mutations in the beta-subunit of the epithelial Na+ channel in patients with a cystic fibrosis-like syndrome.

Article Details

Citation

Sheridan MB, Fong P, Groman JD, Conrad C, Flume P, Diaz R, Harris C, Knowles M, Cutting GR

Mutations in the beta-subunit of the epithelial Na+ channel in patients with a cystic fibrosis-like syndrome.

Hum Mol Genet. 2005 Nov 15;14(22):3493-8. Epub 2005 Oct 5.

PubMed ID
16207733 [ View in PubMed
]
Abstract

Cystic fibrosis (CF) is an autosomal recessive disorder of Cl(-) and Na(+) transport. The vast majority of CF patients have deleterious mutations in an epithelial Cl(-) channel called the CF transmembrane conductance regulator (CFTR). In contrast, defects in the epithelial Na(+) channel (SCNN1) have been associated with phenotypes dominated by renal disease (systemic pseudohypoaldosteronism type I and Liddle syndrome). We report two non-classic CF patients without CFTR mutations who have novel deleterious mutations in the beta-subunits of SCNN1 in the absence of overt renal disease.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Amiloride-sensitive sodium channel subunit betaP51168Details
Amiloride-sensitive sodium channel subunit alphaP37088Details