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JCI early table of contents for Nov. 26, 2012
Date:11/26/2012

cle weakness and low serum potassium levels. It is caused be a genetic mutation in protein channels that pump calcium or sodium ions across the cell membrane, but it is unclear exactly how the calcium channel mutations cause muscle weakness. In this issue of the Journal of Clinical Investigation, researchers led by Stephen Cannon at the University of Texas Southwestern Medical Center created a mouse with the HypoPP-associated calcium channel mutation that had symptoms that were similar to human HypoPP. They found that the mutant calcium channel caused changes in the cellular membrane potential that altered the ability of the muscle fibers to contract. This study explains how an inherited mutation causes HypoPP in humans. In a companion commentary, Alfred George of Vanderbilt University discusses how inherited mutations in channels contribute to human disease.

TITLE:
A calcium channel mutant mouse model of hypokalemic periodic paralysis

AUTHOR CONTACT:
Stephen C. Cannon
Southwestern Medical School, Dallas, TX, USA
Phone: 214-648-2564; Fax: 214-648-6306; E-mail: steve.cannon@utsouthwestern.edu

View this article at: http://www.jci.org/articles/view/66091?key=0f8ffec321a1fe4d328b

ACCOMPANYING COMMENTARY

TITLE:
Leaky channels make weak muscles

AUTHOR CONTACT:
Alfred L George, Jr.
Vanderbilt University, Nashville, TN, USA
Phone: 615-936-2660; Fax: 615-936-2661; E-mail: al.george@vanderbilt.edu

View this article at: http://www.jci.org/articles/view/66535?key=6b5240ca1c7bbbfe9a54


A tale of two heme transporters

Erythropoiesis, or the production of red blood cells,
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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