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Specifically, the G subunit can directly interact with the G protein-gated inwardly rectifying potassium channel (GIRK), Kir3, resulting in cellular hyperpolarization and the inhibition of tonic neural activity [31, 32] while the directly binding of the dissociated G subunit to calcium channels inhibits calcium conductance by reducing voltage activation of channel pore opening [33]

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This is accompanied by deposition of calcium oxalate crystals in the kidney, which may contribute to a persistent inflammatory reaction and interstitial fibrosis

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