Claudin-19 (CLDN19) is a member of the claudin family, transmembrane proteins critical for forming tight junctions that regulate paracellular permeability and maintain cell polarity. CLDN19 is particularly abundant in the kidney and retina. In the kidney, it co-expresses with CLDN16 in the thick ascending limb of Henle’s loop, forming a selective paracellular barrier for magnesium and calcium reabsorption. Mutations in *CLDN19* are linked to familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), a rare autosomal recessive disorder characterized by renal magnesium wasting, kidney stones, and progressive renal failure. In the retina, CLDN19 contributes to the blood-retinal barrier, and its dysfunction may underlie ocular abnormalities observed in some FHHNC patients.
CLDN19-specific antibodies are essential tools for studying its localization, expression, and functional roles in health and disease. They enable detection of CLDN19 in tissue samples via immunohistochemistry, Western blotting, or immunofluorescence, aiding in diagnosing CLDN19-related pathologies or validating experimental models. Research using these antibodies has clarified how CLDN19 interacts with other claudins (e.g., CLDN16) and how mutations disrupt tight junction integrity. Therapeutic applications, such as antibody-based targeting to modulate tight junction function, remain exploratory but hold potential for treating electrolyte disorders or barrier-related diseases. Overall, CLDN19 antibodies are pivotal in advancing understanding of epithelial barrier biology and translational research.