檢索結果 - Gautschi, I

Mutations causing Liddle syndrome reduce sodium-dependent downregulation of the epithelial sodium channel in the Xenopus oocyte expression system. 由 Kellenberger, S, Gautschi, I, Rossier, B C, Schild, L

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The heterotetrameric architecture of the epithelial sodium channel (ENaC). 由 Firsov, D, Gautschi, I, Merillat, A M, Rossier, B C, Schild, L

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Regulation of stability and function of the epithelial Na+ channel (ENaC) by ubiquitination. 由 Staub, O, Gautschi, I, Ishikawa, T, Breitschopf, K, Ciechanover, A, Schild, L, Rotin, D

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Identification of a PY motif in the epithelial Na channel subunits as a target sequence for mutations causing channel activation found in Liddle syndrome. 由 Schild, L, Lu, Y, Gautschi, I, Schneeberger, E, Lifton, R P, Rossier, B C

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A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system. 由 Schild, L, Canessa, C M, Shimkets, R A, Gautschi, I, Lifton, R P, Rossier, B C

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A mutation causing pseudohypoaldosteronism type 1 identifies a conserved glycine that is involved in the gating of the epithelial sodium channel. 由 Gründer, S, Firsov, D, Chang, S S, Jaeger, N F, Gautschi, I, Schild, L, Lifton, R P, Rossier, B C

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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... 由 Hansson, J H, Schild, L, Lu, Y, Wilson, T A, Gautschi, I, Shimkets, R, Nelson-Williams, C, Rossier, B C, Lifton, R P

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