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Article

Mechanism by which Liddle's syndrome mutations increase activity of a human epithelial Na+ channel

1 Dec 1995

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 8521520
DOI: 10.1016/0092-8674(95)90212-0

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Related research

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Mechanism by which Liddle's syndrome mutations increase activity of a human epithelial Na+ channelPMID 8521520Read ↗

Liddle's syndrome: genetics and mechanisms of Na+ channel defects.Semantic proximity Read ↗

Identification of a PY motif in the epithelial Na channel subunits as a target sequence for mutations causing channel activation found in Liddle syndrome.Semantic proximity Read ↗

Mutations causing Liddle syndrome reduce sodium-dependent downregulation of the epithelial sodium channel in the Xenopus oocyte expression system.Semantic proximity Read ↗

Roles of KCNA2 in Neurological Diseases: from Physiology to PathologySemantic proximity Read ↗

A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.Semantic proximity Read ↗

Genetic control of sodium channel function.Semantic proximity Read ↗

Liddle syndrome caused by P616R mutation of the epithelial sodium channel beta subunit.Semantic proximity Read ↗

Ion channel mutations in neuronal diseases: a genetics perspective.Semantic proximity Read ↗

Liddle syndrome: genetics and mechanisms of Na+ channel defects.Semantic proximity Read ↗

A Splice Mutation in the Human Canalicular Multispecific Organic Anion Transporter Gene Causes Dubin-Johnson SyndromeSemantic proximity Read ↗

Hereditary dysfunction of voltage-gated sodium channels: from clinical phenotype to molecular mechanisms.Semantic proximity Read ↗

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

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