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KCNQ1-dependent transport in renal and gastrointestinal epithelia.

Authors: Vallon, V  Grahammer, F  Volkl, H  Sandu, CD  Richter, K  Rexhepaj, R  Gerlach, U  Rong, Q  Pfeifer, K  Lang, F 
Citation: Vallon V, etal., Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17864-9. Epub 2005 Nov 28.
Pubmed: (View Article at PubMed) PMID:16314573
DOI: Full-text: DOI:10.1073/pnas.0505860102

Mutations in the gene encoding for the K+ channel alpha-subunit KCNQ1 have been associated with long QT syndrome and deafness. Besides heart and inner ear epithelial cells, KCNQ1 is expressed in a variety of epithelial cells including renal proximal tubule and gastrointestinal tract epithelial cells. At these sites, cellular K+ ions exit through KCNQ1 channel complexes, which may serve to recycle K+ or to maintain cell membrane potential and thus the driving force for electrogenic transepithelial transport, e.g., Na+/glucose cotransport. Employing pharmacologic inhibition and gene knockout, the present study demonstrates the importance of KCNQ1 K+ channel complexes for the maintenance of the driving force for proximal tubular and intestinal Na+ absorption, gastric acid secretion, and cAMP-induced jejunal Cl- secretion. In the kidney, KCNQ1 appears dispensable under basal conditions because of limited substrate delivery for electrogenic Na+ reabsorption to KCNQ1-expressing mid to late proximal tubule. During conditions of increased substrate load, however, luminal KCNQ1 serves to repolarize the proximal tubule and stabilize the driving force for Na+ reabsorption. In mice lacking functional KCNQ1, impaired intestinal absorption is associated with reduced serum vitamin B12 concentrations, mild macrocytic anemia, and fecal loss of Na+ and K+, the latter affecting K+ homeostasis.


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RGD Object Information
RGD ID: 10412292
Created: 2015-11-14
Species: All species
Last Modified: 2015-11-14
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.