A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.
Schild L, Canessa C, Shimkets R, Gautschi I, Lifton R, Rossier B. A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system. Proceedings Of The National Academy Of Sciences Of The United States Of America 1995, 92: 5699-5703. PMID: 7777572, PMCID: PMC41764, DOI: 10.1073/pnas.92.12.5699.Peer-Reviewed Original ResearchMeSH KeywordsAmilorideAnimalsEpitheliumHypertensionMutationOocytesSequence DeletionSodium ChannelsXenopus laevisConceptsLiddle's diseaseSalt-sensitive hypertensionSalt-sensitive formsChannel activityXenopus laevis oocyte expression systemDirect physiological evidenceChannel beta subunitsEpithelial sodium channelChannel hyperactivityOocyte expression systemPharmacological propertiesSodium channelsGamma subunitsMolecular targetsBeta subunitDiseaseXenopus laevis oocytesHypertensionPremature stop codonPhysiological evidenceHeritable formTruncation mutationsOverall channel activityFunctional consequencesLaevis oocytes