Papers on
CLDN14
Claudins and the kidney.Yu, Kansas City, United States. In J Am Soc Nephrol, 2015
Genetic mutations in claudin-16 and -19 cause familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphisms in claudin-14 are associated with kidney stone risk.
Idiopathic calcium nephrolithiasis: a review of pathogenic mechanisms in the light of genetic studies.Vezzoli et al., Milano, Italy. In Am J Nephrol, 2013
Polymorphisms of eleven genes have been associated with stones in genome-wide association studies and replicated candidate-gene association studies: VDR, SLC34A1, SLC34A4, CLDN14, and CaSR genes coding for proteins regulating tubular phosphate and calcium reabsorption; CaSR, MGP, OPN, PLAU, and UMOD genes coding for proteins preventing calcium salt precipitation; AQP1 gene coding for a water channel in the proximal tubule.
The role of claudin in hypercalciuric nephrolithiasis.Hou, Saint Louis, United States. In Curr Urol Rep, 2013
The susceptible genes include NKCC2, ROMK and ClCkb/Barttin that underlie renal salt excretion; claudin-14, -16 and -19 that underlie renal Ca(++) excretion; and CaSR that provides a sensing mechanism for the kidney to regulate salt, water and Ca(++) homeostasis.
Claudins and the kidney.Yu et al., Saint Louis, United States. In Annu Rev Physiol, 2012
Recent evidence has identified claudin-2 as constituting the cation-reabsorptive pathway in the proximal tubule; claudin-14, -16, and -19 as forming a complex that regulates calcium transport in the thick ascending limb of the loop of Henle; and claudin-4, -7, and -8 as determinants of collecting duct chloride permeability.