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|
|Aliases||Paracellin-1, PCLN-1, PCLN1|
|Organism||Homo sapiens (Human)|
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
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.
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.
The article indicates that 1,25(OH)2 VitD transcriptionally inhibits the expression of claudin-16 by a mechanism sensitive to Mg2+ and CaSR.
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.
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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