Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: a quantitative approach (Q24653749)

2

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I Gautschi

3

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A M Mérillat

4

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E Schneeberger

5

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B C Rossier

Proceedings of the National Academy of Sciences of the United States of America

6

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publication date

24 December 1996

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language of work or name

English

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published in

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volume

93

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issue

26

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page(s)

15370-5

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cites work

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WW domains of Nedd4 bind to the proline-rich PY motifs in the epithelial Na+ channel deleted in Liddle's syndrome

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

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Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1

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Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits

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Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel

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Membrane topology of the epithelial sodium channel in intact cells

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Cloning and expression of the beta- and gamma-subunits of the human epithelial sodium channel

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A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system

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The highly selective low-conductance epithelial Na channel of Xenopus laevis A6 kidney cells

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