CLDN16 Membrane Protein Introduction

Introduction of CLDN16

Claudin-16 is a protein that belongs to the group of claudins. It is encoded by the CLDN16 gene in human. This gene and the CLDN1 gene are clustered on chromosome 3q28. Claudin-16 protein is an integral membrane protein and a component of tight junction strands. It is mainly found in the kidneys, especially in the Henle’s thick ascending limb. Claudin-16 acts as either an intercellular pore or ion concentration sensor to regulate the paracellular resorption of magnesium ions.

Basic Information of CLDN16
Protein Name	Claudin-16
Gene Name	CLDN16
Aliases	Paracellin-1, PCLN-1, PCLN1
Organism	Homo sapiens (Human)
UniProt ID	Q9Y5I7
Transmembrane Times	4
Length (aa)	305
Sequence	MTSRTPLLVTACLYYSYCNSRHLQQGVRKSKRPVFSHCQVPETQKTDTRHLSGARAGVCPCCHPDGLLATMRDLLQYIACFFAFFSAGFLIVATWTDCWMVNADDSLEVSTKCRGLWWECVTNAFDGIRTCDEYDSILAEHPLKLVVTRALMITADILAGFGFLTLLLGLDCVKFLPDEPYIKVRICFVAGATLLIAGTPGIIGSVWYAVDVYVERSTLVLHNIFLGIQYKFGWSCWLGMAGSLGCFLAGAVLTCCLYLFKDVGPERNYPYSLRKAYSAAGVSMAKSYSAPRTETAKMYAVDTRV

Function of CLDN16 Membrane Protein

Claudin-16 protein is critical in tight junction-specific obliteration of the intercellular space by calcium-independent cell-adhesion activity. It is involved in paracellular magnesium reabsorption and is required for selective paracellular conductance. Claudin-16 may form intercellular pores either alone or in combination with other components, which allow the cells of magnesium and calcium ions to pass through their electrochemical gradients. Alternatively, it can be a magnesium concentration sensor that can alter the paracellular permeability mediated by other factors. Defects in CLDN16 gene are responsible for the primary hypomagnesemia, characterized by a large amount of renal magnesium wasting with hypomagnesemia and hypercalciuria, leading to nephrocalcinosis and renal failure. Several diseases are associated with CLDN16, such as hypomagnesemia 3, renal and primary hypomagnesemia. Related pathways include sertoli-sertoli cell junction dynamics and blood-brain barrier and immune cell transmigration: VCAM-1/CD106 signaling pathways.

Fig.1 (A) Genomic organization of CLDN16. Mutations are depicted above the schematic presentation of CLDN16 (novel mutations in bold). (B) Claudin-16 protein model deduced from hydrophilicity plots. (Radulescu, 2013)

Application of CLDN16 Membrane Protein in Literature

Lv F., et al. A novel mutation in CLDN16 results in rare familial hypomagnesaemia with hypercalciuria and nephrocalcinosis in a Chinese family. Clin Chim Acta. 2016, 457: 69-74. PubMed ID: 27067446

Authors in this group detected a novel mutation in CLDN16 for the first time. The mutation results in rare familial hypomagnesaemia with hypercalciuria and nephrocalcinosis in a Chinese family.
Bardet C., et al. Claudin-16 deficiency impairs tight junction function in ameloblasts, leading to abnormal enamel formation. J Bone Miner Res. 2016, 31(3): 498-513. PubMed ID: 26426912

The article reveals that claudin-16 deficiency impairs tight junction function in ameloblasts, which leads to abnormal enamel formation. The study indicates the importance of a TJ protein in tooth formation for the first time.
Kladnitsky O., et al. The claudin-16 channel gene is transcriptionally inhibited by 1,25-dihydroxyvitamin D. Exp Physiol. 2015, 100(1): 79-94. PubMed ID: 25557732

The article indicates that 1,25(OH)2 VitD transcriptionally inhibits the expression of claudin-16 by a mechanism sensitive to Mg²⁺ and CaSR.
Sikora P., et al. Retrospective cohort study of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis due to CLDN16 mutations. Nephrol Dial Transplant. 2015, 30(4):636-44. PubMed ID: 25477417

This article focuses on one of the largest cohorts of FHHNC cases caused by CLDN16 mutations. It shows that familial hypomagnesaemia with hypercalciuria and nephrocalcinosis is due to CLDN16 mutations.
Ikari A., et al. Tight junctional localization of claudin-16 is regulated by syntaxin 8 in renal tubular epithelial cells. J Biol Chem. 2014, 289(19):13112-23. PubMed ID: 24659781

This article reports that STX8 mediates the recycling of CLDN16, which constitutes a key component of the CLDN16 trafficking machinery in the kidney.

CLDN16 Preparation Options

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Reference

Konrad M, et al. (2008). CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis. J Am Soc Nephrol. 19(1), 171-81.

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