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Non steroid hormones cannot diffuse freely through the cell membrane, therefore they interact with membrane receptors. There are many different types of receptors, many of which result in an increase in cellular [Ca2+], and increased cellular [Ca2+] can have a myriad of effects including cytoskeleton restructuring, muscle fibre contraction, regulation of calcium-dependent enzymes, action potential generation, secretion of vesicles, and even apoptosis. The increase in cellular [Ca2+] can be caused by as simple as the opening of a ligand(hormone)-gated calcium channel. Another far more complex, but somewhat more common pathway involves the hormone binding to a G-protein coupled receptor or a receptor tyrosine kinase, causing the receptor to activate an enzyme called PLC (phospholipase C) that will cleave a membrane phospholipid (phosphatidylinositol bisphosphate, PIP2) into two components (Inositol triphosphate, IP3, and Diacylglycerol, DAG). IP3 localizes to the endoplasmic reticulum and releases sequestered Ca2+, and DAG provides an anchor for another enzyme, PKC (protein kinase C). Anchored PKC is activated by the released Ca2+ and it begins to perform its duty, which is to add a phosphate group onto specific substrates, activating or deactivating them, causing a general shift in cellular dynamics.

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Q: Explain how nonsteroid hormones may function through an increase intracellular calcium ion concentration?
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