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CLDN 12 expression could be clinically useful for predicting the survival of the estrogen receptor (ER)-negative subgroup of patients with breast cancer.
Knockdown of claudin-3, claudin-4, and claudin-12, but not claudin-1, increased breast cancer MCF-7 cell migration with maximal effects observed in claudin-12 siRNA-transfected cells.
Differential expression of genes encoding claudins in colorectal cancer suggests that these tight junction proteins may be associated to and involved in tumorigenesis.
These findings strongly suggest that claudin-2- and/or claudin-12-based tight junctions form paracellular Ca(2+) channels in intestinal epithelia, and they highlight a novel mechanism behind vitamin D-dependent calcium homeostasis.
Claudin-12 is expressed at the variety of epithelial tissues in inner ear including Organ of Corti, stria vascularis, Reissner's membrane, spiral limbus, vestibular sensory epithelia, and dark cell area.
1,25(OH)2D3 downregulates cadherin-17 and upregulates claudin-2 and claudin-12 in the intestine, suggesting that 1,25(OH)2D3, by regulating these epithelial cell junction proteins, can route calcium through the paracellular path
This gene encodes a member of the claudin family. Claudins are integral membrane proteins and components of tight junction strands. Tight junction strands serve as a physical barrier to prevent solutes and water from passing freely through the paracellular space between epithelial or endothelial cell sheets, and also play critical roles in maintaining cell polarity and signal transductions. This gene is expressed in the inner ear and bladder epithelium, and it is over-expressed in colorectal carcinomas. This protein and claudin 2 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. Multiple alternatively spliced transcript variants encoding the same protein have been found.