The voltage-gated K+ channel subunit Kv1.1 links kidney and brain

Research output: Contribution to journalComment/debate

10 Scopus citations

Abstract

Analysis of Mendelian Mg2+ wasting disorders helps us to unravel the mechanisms of Mg2+ homeostasis. In this issue of the JCI, Glaudemans and colleagues show that mutations in voltage-gated K+ channel subtype 1.1 (Kv1.1) cause autosomal dominant hypomagnesemia in humans (see the related article beginning on page 936). Interestingly, other mutations in the same protein cause the neurological disease episodic ataxia type 1. The authors show, using cells with heterologous expression of the wild-type and mutant channels, that the mutant channel is dysfunctional and speculate that Mg2+ wasting results from changes in apical membrane voltage along the nephron. Mechanisms by which the apical voltage is generated and how Kv1.1 fits within this context are discussed herein.

Original languageEnglish (US)
Pages (from-to)763-766
Number of pages4
JournalJournal of Clinical Investigation
Volume119
Issue number4
DOIs
StatePublished - Apr 1 2009

ASJC Scopus subject areas

  • Medicine(all)

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