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

@article{Snyder1995MechanismBW,
  title={Mechanism by which Liddle's syndrome mutations increase activity of a human epithelial Na+ channel},
  author={Peter M. Snyder and Margaret P. Price and Fiona J. McDonald and Christopher M Adams and Kenneth A. Volk and Bernhardt G. Zeiher and John B. Stokes and Michael J. Welsh},
  journal={Cell},
  year={1995},
  volume={83},
  pages={969-978}
}
Liddle's syndrome is an inherited form of hypertension caused by mutations that truncate the C-terminus of human epithelial Na+ channel (hENaC) subunits. Expression of truncated beta and gamma hENaC subunits increased Na+ current. However, truncation did not alter single-channel conductance or open state probability, suggesting there were more channels in the plasma membrane. Moreover, truncation of the C-terminus of the beta subunit increased apical cell-surface expression of hENaC in a renal… CONTINUE READING

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