Mutations in the carboxy terminus of the β and γ subunits of the epithelial sodium channel are not present in patients with hypertensive crisis

This publication has 15 references indexed in Scilit:

• Genotype–phenotype analysis of a newly discovered family with Liddleʼs syndrome
  Journal Of Hypertension, 1997
• Liddle disease caused by a missense mutation of beta subunit of the epithelial sodium channel gene.
  Journal of Clinical Investigation, 1996
• Hypertensive Urgencies and Emergencies
  Hypertension, 1996
• A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity.
  Proceedings of the National Academy of Sciences, 1995
• Mechanism by which Liddle's syndrome mutations increase activity of a human epithelial Na+ channel
  Cell, 1995
• Hypertension caused by a truncated epithelial sodium channel γ subunit: genetic heterogeneity of Liddle syndrome
  Nature Genetics, 1995
• A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.
  Proceedings of the National Academy of Sciences, 1995
• Liddle's syndrome: Heritable human hypertension caused by mutations in the β subunit of the epithelial sodium channel
  Cell, 1994
• Epithelial sodium channels
  Current Opinion in Nephrology and Hypertension, 1994
• The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V)
  Archives of internal medicine (1960), 1993