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Calcium receptors respond to both intracellular and extracellular calcium. Activation of calcium receptor (CaSR) by extracellular calcium causes that activation of G protein G which stimulates phospholipase C (PLC) to hydrolyze PIP2 to inositol triphosphate (IP3), a second messenger. Activation of phospholipase C (PLC) increases the concentration of inositol triphosphate (IP3), which, in turn, opens the IP3 receptor and promotes calcium release from intracellular stores. Inositol triphosphate (IP3) is converted to diacylglycerol which activates protein kinase C (PKC). Furthermore, calcium influx into cells leads to activation of calcium ion channel transient receptor potential 6 (TRP6). Activation of the TRP6 channel contributes to the increased calcium influx and causes an increase in intracellular calcium which activates CaSR. The increase in intracellular calcium is regulated by the calcium pump which phosphorylates the calcium pump and mediates the sequestration of intracellular calcium to the endoplasmic reticulum, thus, reducing calcium levels in the cytosol (378,379). Finally, activation of TRP6 can be mimicked by the arachidonic acid serotonin cascade or the FDBK signal transduction cascade and abrogated by presenilin 2 (PS2) or calstabin2 (CalsB2). In addition, the FDBK cascade can be blocked by PKC inhibition ((374), and in turn FDBK activation by PS2 induces calcium influx through TRP6 channels (375). Thus, in addition to the effects of calcium on differentiation, calcium regulates calcium homeostasis. As a result, the calcium homeostasis of corneal cells is regulated by calcium receptors, intracellular calcium levels, calcium pump, calcium ion channels, and calcium pump recruitment to the plasma membrane. 7211a4ac4a