Derst, C <br/><br/>
A hyperprostaglandin E syndrome mutation in Kir1.1 (renal outer medullary potassium) channels reveals a crucial residue for channel function in Kir1.3 channels.  [electronic resource] 

 -  The Journal of biological chemistry  Sep 1998 
 - 23884-91 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>0021-9258 
<br/><br/><label>Standard No.: </label>10.1074/jbc.273.37.23884  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Amino Acid Sequence<br/>Animals<br/>Bartter Syndrome--embryology<br/>COS Cells<br/>Cloning, Molecular<br/>Female<br/>Humans<br/>Kidney Medulla--metabolism<br/>Molecular Sequence Data<br/>Mutagenesis, Site-Directed<br/>Oocytes--physiology<br/>Point Mutation<br/>Polymerase Chain Reaction<br/>Polymorphism, Single-Stranded Conformational<br/>Potassium Channels--chemistry<br/>Potassium Channels, Inwardly Rectifying<br/>Prostaglandins E--metabolism<br/>Recombinant Proteins--chemistry<br/>Sequence Alignment<br/>Sequence Homology, Amino Acid<br/>Syndrome<br/>Transfection<br/>Xenopus laevis<br/>Kcnj10 Channel