Skip to main content
Article thumbnail
Location of Repository

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

By David H. Ellison


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

Topics: Commentary
Publisher: American Society for Clinical Investigation
OAI identifier:
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.