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Article

The ENaC channel as the primary determinant of two human diseases: Liddle syndrome and pseudohypoaldosteronism.

Nephrologie - 1 Jan 1996

Schild L

Abstract excerpt

The amiloride-sensitive epithelial sodium channel (ENaC) controls sodium reabsorption in the distal nephron. Its activity is under the control of aldosterone. The genes encoding ENaC have been identified and revealed an heteromultimeric structure of the protein composed of three homologous alpha...

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PMID: 8987044

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-8987044-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

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The ENaC channel as the primary determinant of two human diseases: Liddle syndrome and pseudohypoaldosteronism.PMID 8987044Read ↗

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Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases.Semantic proximity Read ↗

Liddle disease caused by a missense mutation of beta subunit of the epithelial sodium channel gene.Semantic proximity Read ↗

A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity.Semantic proximity Read ↗

Whole-exome sequencing reveals an inherited R566X mutation of the epithelial sodium channel β-subunit in a case of early-onset phenotype of Liddle syndrome.Semantic proximity Read ↗

A Missense Mutation in the Extracellular Domain of αENaC Causes Liddle SyndromeSemantic proximity Read ↗

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