
Klotho, a hormone and enzyme, is a powerful regulator of ageing and life span. Klotho deficiency leads to cardiac arrythmia and sudden cardiac death. We thus explored whether klotho modifies cardiac K+‐channel hERG. Current was determined utilizing dual electrode voltage clamp and hERG protein abundance utilizing immunohistochemistry and chemiluminescence in Xenopus oocytes expressing hERG with or without klotho. Coexpression of klotho increased cell membrane hERG‐protein abundance and hERG current at any given voltage without significantly modifying the voltage required to activate the channel. The effect of klotho coexpression was mimicked by recombinant klotho protein and reversed by β‐glucuronidase‐inhibitor d‐saccharic acid‐1,4‐lactone.
570, ERG1 Potassium Channel, Patch-Clamp Techniques, K+ channel, Xenopus, 610, Heart, 530, Ether-A-Go-Go Potassium Channels, Membrane Potentials, RNA, Complementary, Electrophysiology, Glucaric Acid, Lactones, Cardiac action potential, Oocytes, Animals, Ion Channel Gating, Klotho Proteins, Cells, Cultured, Glucuronidase
570, ERG1 Potassium Channel, Patch-Clamp Techniques, K+ channel, Xenopus, 610, Heart, 530, Ether-A-Go-Go Potassium Channels, Membrane Potentials, RNA, Complementary, Electrophysiology, Glucaric Acid, Lactones, Cardiac action potential, Oocytes, Animals, Ion Channel Gating, Klotho Proteins, Cells, Cultured, Glucuronidase
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