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Fig. 5. Model for Ca²⁺ regulation of receptor-triggered PLC activity in insulin-secreting cells. Agonist (A) stimulation of G-protein-coupled receptors (GPCR) leads to partial activation of PLC via the Gq family of heterotrimeric G proteins. The resulting hydrolysis of membrane PIP₂ leads to formation of diacylglycerol (DAG) and sufficient amounts of IP₃ to mobilize Ca²⁺ via IP₃ receptors (IP₃R) in the endoplasmic reticulum (ER). The elevation of [Ca²⁺]_i further activates PLC to stimulate formation of more IP₃, which leads to further elevation of [Ca²⁺]_i, etc. The drop of Ca²⁺ concentration inside the ER triggers activation of store-operated channels (SOC) in the plasma membrane. This store-operated Ca²⁺ entry acts to increase [Ca²⁺]_i and to stimulate PLC activity during prolonged receptor stimulation.

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