Associated Papers
Mouse Models of Human Claudin-Associated Disorders: Benefits and Limitations.
Seker M et al.
International Journal of Molecular Sciences, 2019
Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis: clinical and molecular characteristics.
Claverie-Martin F
Clinical Kidney Journal, 2015
First report of a novel missense CLDN19 mutations causing familial hypomagnesemia with hypercalciuria and nephrocalcinosis in a Chinese family.
Yuan T et al.
Calcified Tissue International, 2015
Claudin-19 mutations and clinical phenotype in Spanish patients with familial hypomagnesemia with hypercalciuria and nephrocalcinosis.
Claverie-Martín F et al.
Plos One, 2013
Impaired paracellular ion transport in the loop of Henle causes familial hypomagnesemia with hypercalciuria and nephrocalcinosis.
Haisch L et al.
Annals of the New York Academy of Sciences, 2012
The role of tight junctions in paracellular ion transport in the renal tubule: lessons learned from a rare inherited tubular disorder.
Haisch L et al.
American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation, 2011
Mutation in the tight-junction gene claudin 19 (CLDN19) and familial hypomagnesemia, hypercalciuria, nephrocalcinosis (FHHNC) and severe ocular disease.
Naeem M et al.
American Journal of Nephrology, 2011
Claudin-16 and claudin-19 interact and form a cation-selective tight junction complex.
Hou J et al.
The Journal of Clinical Investigation, 2008
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