Expression and function of the CaSR have been shown in some mammalian taste buds 
and basal cells of the esophagus. Signaling cascades responsible for 
CaSR-mediated stimulation of H(+)-K(+)-ATPase on human parietal cells have been 
defined. Transgenic mice and reductionistic cell culture models have shown that 
the CaSR promotes gastrin secretion from G cells, cholecystokinin (CCK) 
secretion from duodenal I cells and BMP-2 secretion from sub-epithelial 
myofibroblasts. In addition, the CaSR mediates a novel paracrine relationship 
between myofibroblasts and overlying epithelial cells in the colon. Thus, CaSR 
activators stimulate secretion of Wnt5a from myofibroblasts and expression of 
the Wnt5a receptor Ror2 in epithelial cells. CaSR-mediated Wnt5a/Ror2 engagement 
stimulates epithelial differentiation and reduces expression of the receptor for 
tumor necrosis factor (TNFR1). CaSR activators also modulate intestinal 
motility, inhibit Cl(-) secretion and stimulate Na(+) absorption in both the 
small intestine and colon. Colonic epithelia from conditional and global CaSR 
knockout mice exhibit increased proliferation with increased Wnt/β-catenin 
signaling, demonstrating that the CaSR negatively modulates colonic epithelial 
growth.