Salt and acid-base metabolism in claudin-16 knockdown mice: impact for the pathophysiology of FHHNC patients

Claudin-16 is defective in familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). Claudin-16 knockdown (CLDN16 KD) mice show reduced cation selectivity in the thick ascending limb. The defect leads to a collapse of the lumen-positive diffusion voltage, which drives Ca(2+) and Mg(2...

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Auteurs principaux: Himmerkus, Nina, Shan, Qixian, Goerke, Boeren, Hou, Jianghui, Goodenough, Daniel A., Bleich, Markus
Format: Artigo
Langue:Inglês
Publié: American Physiological Society 2008
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Articles
Accès en ligne:https://ncbi.nlm.nih.gov/pmc/articles/PMC2604832/
https://ncbi.nlm.nih.gov/pubmed/18784260
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1152/ajprenal.90388.2008
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