Cystic Fibrosis Transmembrane Conductance Regulator-dependent Up-regulation of Kir1.1 (ROMK) Renal K+ Channels by the Epithelial Sodium Channel
Open Access
- 1 July 2002
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 277 (28) , 25377-25384
- https://doi.org/10.1074/jbc.m201925200
Abstract
No abstract availableKeywords
This publication has 41 references indexed in Scilit:
- The cystic fibrosis transmembrane conductance regulator (CFTR) inhibits ENaC through an increase in the intracellular Cl− concentrationEMBO Reports, 2001
- Non‐specific activation of the epithelial sodium channel by the CFTR chloride channelEMBO Reports, 2001
- Epithelial Sodium Channels Regulate Cystic Fibrosis Transmembrane Conductance Regulator Chloride Channels in XenopusOocytesJournal of Biological Chemistry, 2000
- Activation of the epithelial Na+ channel (ENaC) requires CFTR Cl- channel functionNature, 1999
- Downregulation of Epithelial Sodium Channel (ENaC) by CFTR Co-expressed in Xenopus Oocytes is Independent of Cl − ConductanceThe Journal of Membrane Biology, 1999
- CFTR Is a Conductance Regulator as well as a Chloride ChannelPhysiological Reviews, 1999
- Epithelial sodium channels: function, structure, and regulationPhysiological Reviews, 1997
- Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1Nature Genetics, 1996
- CFTR as a cAMP-Dependent Regulator of Sodium ChannelsScience, 1995
- Liddle's syndrome: Heritable human hypertension caused by mutations in the β subunit of the epithelial sodium channelCell, 1994