Ubiquitylation and the pathogenesis of hypertension

Research output: Contribution to journalArticle

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Abstract

Liddle syndrome is monogenic hypertension caused by mutations in the epithelial Na+ channel (ENaC) that interfere with its ubiquitylation by Nedd4-2. In this issue, Ronzaud and colleagues found that deleting Nedd4-2 from kidney tubules in adult mice led to ENaC accumulation, but not at the plasma membrane, as predicted from current models. Instead, abundance of the sodium chloride transporter NCC increased at the plasma membrane, and the mice have some features of increased NCC activity. Together, the results suggest that defective ubiquitylation of ENaC by Nedd4-2 may not fully explain Liddle syndrome and that Nedd4-2 modulates NCC more strongly.

Original languageEnglish (US)
Pages (from-to)546-548
Number of pages3
JournalJournal of Clinical Investigation
Volume123
Issue number2
DOIs
StatePublished - Feb 1 2013

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Epithelial Sodium Channels
Ubiquitination
Liddle Syndrome
Hypertension
Sodium Chloride Symporters
Cell Membrane
Kidney Tubules
Mutation

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Ubiquitylation and the pathogenesis of hypertension. / Ellison, David.

In: Journal of Clinical Investigation, Vol. 123, No. 2, 01.02.2013, p. 546-548.

Research output: Contribution to journalArticle

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