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Article

Deletion of claudin-10 rescues claudin-16-deficient mice from hypomagnesemia and hypercalciuria.

Kidney international - 1 Mar 2018

Breiderhoff Tilman, Himmerkus Nina, Drewell Hoora, Plain Allein, Günzel Dorothee, Mutig Kerim, Willnow Thomas E, Müller Dominik, Bleich Markus

Abstract excerpt

The tight junction proteins claudin-10 and -16 are crucial for the paracellular reabsorption of cations along the thick ascending limb of Henle's loop in the kidney. In patients, mutations in CLDN16 cause familial hypomagnesemia with hypercalciuria and nephrocalcinosis, while mutations in CLDN10 impair kidney function. Mice lacking claudin-16 display magnesium and calcium wasting, whereas absence of claudin-10...

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Source

Identifiers

PMID: 29129401
DOI: 10.1016/j.kint.2017.08.029

Genes

CLDN10
CLDN16

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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