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Bernard C. Rossier
Researcher at University of Lausanne
Publications - 220
Citations - 25084
Bernard C. Rossier is an academic researcher from University of Lausanne. The author has contributed to research in topics: Epithelial sodium channel & Aldosterone. The author has an hindex of 75, co-authored 218 publications receiving 24110 citations. Previous affiliations of Bernard C. Rossier include University of North Carolina at Chapel Hill.
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Journal ArticleDOI
Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits.
Cecilia M. Canessa,Laurent Schild,Gary Buell,Bernard Thorens,Ivan Gautschi,Jean-Daniel Horisberger,Bernard C. Rossier +6 more
TL;DR: The ion-selective permeability, the gating properties and the pharmacological profile of the channel formed by coexpressing the three subunits in oocytes are similar to that of the native channel.
Journal ArticleDOI
Liddle's syndrome: Heritable human hypertension caused by mutations in the β subunit of the epithelial sodium channel
Richard A. Shimkets,David G. Warnock,Christopher M. Bositis,Carol Nelson-Williams,Joni H. Hansson,Morris Schambelan,John R. Gill,Stanley Ulick,Robert V. Milora,James W. Findling,Cecilia M. Canessa,Bernard C. Rossier,Richard P. Lifton +12 more
TL;DR: It is demonstrated that Liddle's syndrome is caused by mutations in the beta subunit of the epithelial sodium channel and have implications for the regulation of this epithelial ion channel as well as blood pressure homeostasis.
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CFTR as a cAMP-dependent regulator of sodium channels.
M. J. Stutts,Cecilia M. Canessa,John C. Olsen,M Hamrick,Jonathan A. Cohn,Bernard C. Rossier,Richard C. Boucher +6 more
TL;DR: In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport.
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Epithelial sodium channel related to proteins involved in neurodegeneration
TL;DR: The gene encoding this rat sodium channel subunit shares significant sequence similarity with mec-4 and deg-1, members of a family of Caenorhabditis elegans genes involved in sensory touch transduction and, when mutated, neuronal degeneration, and it is proposed that the gene products of these three genes are member of a gene family coding for cation channels.
Journal ArticleDOI
Early death due to defective neonatal lung liquid clearance in alpha-ENaC-deficient mice
Edith Hummler,Pierre M. Barker,John T. Gatzy,Friedrich Beermann,Chantal Verdumo,Andrea Schmidt,Richard C. Boucher,Bernard C. Rossier +7 more
TL;DR: It is shown that ENaC plays a critical role in the adaptation of the newborn lung to air breathing and was abolished in airway epithelia from αENaC(−/−) mice that developed respiratory distress and died within 40 h of birth from failure to clear their lungs of liquid.