Abnormal regulatory interactions of I148T-CFTR and the epithelial Na+ channel in Xenopus oocytes (Q50647280)

17 March 2018

title

Abnormal regulatory interactions of I148T-CFTR and the epithelial Na+ channel in Xenopus oocytes (English)

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author

Ronald C. Rubenstein

series ordinal

3

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author name string

Laurence Suaud

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1

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17 March 2018

Wusheng Yan

series ordinal

2

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publication date

5 July 2006

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American Journal of Physiology - Cell Physiology

published in

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volume

292

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issue

1

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page(s)

C603-11

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Cl- interference with the epithelial Na+ channel ENaC

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Cl- transport by cystic fibrosis transmembrane conductance regulator (CFTR) contributes to the inhibition of epithelial Na+ channels (ENaCs) in Xenopus oocytes co-expressing CFTR and ENaC.

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Are p.I148T, p.R74W and p.D1270N cystic fibrosis causing mutations?

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The cystic fibrosis transmembrane conductance regulator (CFTR) inhibits ENaC through an increase in the intracellular Cl- concentration

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Wild type but not deltaF508 CFTR inhibits Na+ conductance when coexpressed in Xenopus oocytes

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CFTR fails to inhibit the epithelial sodium channel ENaC expressed in Xenopus laevis oocytes

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Genistein improves regulatory interactions between G551D-cystic fibrosis transmembrane conductance regulator and the epithelial sodium channel in Xenopus oocytes

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21 January 2018

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21 January 2018

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Differential modulation of a polymorphism in the COOH terminus of the alpha-subunit of the human epithelial sodium channel by protein kinase Cdelta

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Disease-Associated Mutations in Cytoplasmic Loops 1 and 2 of Cystic Fibrosis Transmembrane Conductance Regulator Impede Processing or Opening of the Channel†

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21 January 2018

Identifiers

DOI

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17 March 2018

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17 March 2018