English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Non-specific activation of the epithelial sodium channel by the CFTR chloride channel

MPS-Authors
/persons/resource/persons137819

Nagel,  Georg
Department of Biophysical Chemistry, Max Planck Institute of Biophysics, Max Planck Society;

/persons/resource/persons137913

Szellas,  Tanjef
Department of Biophysical Chemistry, Max Planck Institute of Biophysics, Max Planck Society;

/persons/resource/persons137658

Friedrich,  Thomas
Department of Biophysical Chemistry, Max Planck Institute of Biophysics, Max Planck Society;

/persons/resource/persons137696

Hartung,  Klaus
Department of Biophysical Chemistry, Max Planck Institute of Biophysics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Nagel, G., Szellas, T., Riordan, J. R., Friedrich, T., & Hartung, K. (2001). Non-specific activation of the epithelial sodium channel by the CFTR chloride channel. EMBO Reports, 2(3), 249-254. doi:10.1093/embo-reports/kve045.


Cite as: https://hdl.handle.net/21.11116/0000-0007-1FEF-B
Abstract
The genetic disease cystic fibrosis is caused by mutation of the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR). Controversial studies reported regulation of the epithelial sodium channel (ENaC) by CFTR. We found that uptake of 22Na+ through ENaC is modulated by activation of CFTR in oocytes, coexpressing CFTR and ENaC, depending on extracellular chloride concentration. Furthermore we found that the effect of CFTR activation could be mimicked by other chloride channels. Voltage- and patch-clamp measurements, however, showed neither stimulation nor inhibition of ENaC-mediated conductance by activated CFTR. We conclude that the observed modulation of 22Na+ uptake by activated CFTR is due to the effect of CFTR-mediated chloride conductance on the membrane potential. These findings argue against the notion of a specific influence of CFTR on ENaC and emphasize the chloride channel function of CFTR.