Human FXYD2 G41R mutation responsible for renal hypomagnesemia behaves as an inward-rectifying cation channel

Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri Submitted 5 November 2007 ; accepted in final form 25 April 2008 A mutation in the human FXYD2 polypeptide (Na-K-ATPase subunit) that changes a conserved transmembrane glycine to arginine is link...

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Veröffentlicht in:	American Journal of Physiology. Renal Physiology 2008-07, Vol.295 (1), p.F91-F99
Hauptverfasser:	Sha, Qun, Pearson, Wade, Burcea, Lauren C, Wigfall, Darian A, Schlesinger, Paul H, Nichols, Colin G, Mercer, Robert W
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenosine triphosphatase Amino Acid Substitution Animals Calcium Channels - physiology Dogs Humans Kidneys Magnesium - blood Membrane Potentials - physiology Mutation Oocytes - physiology Peptides Potassium Renal Tubular Transport, Inborn Errors - genetics Renal Tubular Transport, Inborn Errors - physiopathology Ribonucleic acid RNA Sodium Sodium-Potassium-Exchanging ATPase - genetics Xenopus laevis
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