Claudin-14 (CLDN14)

Claudin-14 (CLDN14) is an integral membrane protein and a key component of tight junctions in epithelial and endothelial cells[1][2][4]. Tight junctions form a seal between adjacent cells and restrict the free passage of solutes and water through the paracellular space. Claudin-14 is especially important in the kidney, where it regulates calcium reabsorption by controlling the permeability of the thick ascending limb of the loop of Henle[2][3]. It physically interacts with other claudins (notably CLDN16 and CLDN19), modulating cation selectivity and transport[3]. In the inner ear, CLDN14 maintains proper ion gradients critical for hearing; loss-of-function mutations cause a form of autosomal recessive nonsyndromic sensorineural deafness (DFNB29)[1][2][4]. Genetic variants in the CLDN14 gene are strongly associated with kidney stone formation and altered bone mineral density[2][3][4]. There is emerging evidence that dysregulation of CLDN14 may contribute to tumor angiogenesis and other pathologies, but its role as a direct drug target remains under investigation[1][2]. No drugs are currently known to directly target CLDN14.

Other names

Claudin-14CLDN14UNQ777/PRO1571DFNB29