Claudin-10 (CLDN10)

Claudin-10 is an integral membrane protein of the claudin family, primarily involved in forming tight junctions that regulate the paracellular passage of ions and solutes between epithelial and endothelial cells[3]. The protein has several alternatively spliced isoforms, the two most functionally significant being claudin-10a (primarily in the kidney cortex; forms selective anion channels) and claudin-10b (widely expressed; forms selective cation channels)[1][2]. Claudin-10 is essential for epithelial barrier integrity and plays specialized roles in renal electrolyte handling and organ-specific epithelial development, such as in tooth amelogenesis. Mutations in CLDN10 are causative for HELIX syndrome, characterized by hypohidrosis, electrolyte imbalance, and ectodermal defects including enamel hypoplasia, highlighting its importance in ion homeostasis and tissue differentiation[1]. Expression deregulation in tumors may have prognostic value, but direct drug targeting and corresponding therapy are not established to date[3].

Other names

Claudin-10CLDN10OSP-likeOSP-LCPETRL3Oligodendrocyte-specific protein-likeHELIXOSPLclaudin-10OSP-like proteinoligodendrocyte-specific protein-like

Not applicable (no approved targeting drugs); Claudin-10 modulates paracellular ion selectivity, and alterations primarily result from genetic mutations[1][2]