[7] In the kidney it has an inhibitory effect on the reabsorption of calcium, potassium, sodium, and water depending on which segment of the tubule is being activated.

1993, Brown et al.[10] isolated a clone named BoPCaR (bovine parathyroid calcium receptor) which replicated the effect when introduced to polyvalent cations.

The CryoEM structures of CasR homodimer was recently solved The VFT extends outside the cell and is composed of two lobe subdomains.

The inactive state of the receptor has two extracellular domains, oriented in an open conformation with an empty intradomain part.

That behavior makes the binding of calcium at site 4 to hold a major role in stabilization.

[23] Other mutations that activate CaSR are the cause of autosomal dominant hypocalcemia[24] or Type 5 Bartter syndrome.

An alternatively spliced transcript variant encoding 1088 aa has been found for this gene, but its full-length nature has not been defined.

[25] In CKD, the dysregulation of CaSR leads to a secondary hyperparathyroidism linked with osteoporosis, which considered as one of the main complications.

Patients suffers from secondary hyperparathyroidism require to make changes in their diet in order to balance the disease.

Calcilytic drugs, which block CaSR, produce increased bone density in animal studies and have been researched for the treatment of osteoporosis.

Unfortunately clinical trial results in humans have proved disappointing, with sustained changes in bone density not observed despite the drug being well tolerated.

It is defined as a sensation that enhances existing flavors and creates feelings of roundness, complexity, and richness in the mouth.

In the mouth, unlike in other tissues, the influx of the extracellular Calcium does not affect the receptor activity.

The simultaneous binding of gamma glutamine peptides to the CaSR increases the level of the intracellular calcium, and that intensify the taste perception.