Claudins function as major constituents of the tight junction complexes that regulate the permeability of epithelia. While some claudin family members function as impermeable barriers, others mediate the permeability to ions and small molecules. Often, several claudin family members are coexpressed and interact with each other, and this determines the overall permeability. CLDN15 forms tight junctions that mediate the paracellular transport of small monovalent cations along a concentration gradient, due to selective permeability for Na(+), Li(+) and K(+) ions, but selects against Cl(-) ions. Plays an important role in paracellular Na(+) transport in the intestine and in Na(+) homeostasis. Required for normal Na(+)-dependent intestinal nutrient uptake. Can form linear homooligomers in the membrane, giving rise to tight junction strand-like structures. Tight junctions form continuous circumferential cell-cell contacts at the borders of apical and lateral cell membranes that seal the intercellular space and show up as strand-like structures in electron microscopy. Detected in duodenum, jejunum and ileum. Detected on intestinal villi and crypts (at protein level). Ubiquitous. Detected in small intestine, colon, jejunum, heart, kidney and lung. Palmitoylated when heterogeneously expressed in S.frugiperda cells. No visible phenotype at birth and during the first four weeks after birth. After about eight weeks, the upper part of the small intestine is abnormally increased both in length and in thickness with enlarged villi and crypts. The villi are about two times larger than normal, and each is associated with about forty abnormally large crypts instead of the normally observed ratio of ten crypts per villus. In contrast, there is no difference in the size of the lower part of the small intestine. The body weight of mutant mice does not differ from that of wild-type littermates (PubMed:18242218). According to PubMed:20727355, the intestinal mucosa from newborn and adult mutant mice displays strongly decreased transepithelial conductance with strongly reduced paracellular Na(+) permeability, but no major changes in paracellular permeability to Cl(-). Adults show strongly decreased Na(+) levels in the lumen of the small intestine. Mutant mice also display decreased intestinal glucose uptake, probably due to decreased Na(+) levels. According to PubMed:23089202, mutant mice lacking both Cldn2 and Cldn15 display no visible phenotype at birth, but show decreased growth after about 10 days, severe developmental retardation about 14 days after birth, and then die from malnutrition. None survive more than 25 days after birth. Mice lacking both Cldn2 and Cldn15 show abnormally low Na(+) levels in the intestine, leading to decreased intestinal glucose uptake; glucose uptake can be restored to normal levels by addition of Na(+). Likewise, mice lacking both Cldn2 and Cldn15 show decreased intestinal uptake of milk fat, fatty acids, bile acids and amino acids; again, normal bile acid and amino acid uptake can be restored by the addition of Na(+). Belongs to the claudin family.