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• W1603322339 startingPage "27787" @default.
• W1603322339 abstract "Glucose stimulation of pancreatic beta-cell insulin secretion is closely coupled to alterations in ion channel conductances and intracellular Ca2+ ([Ca2+]i). To further examine this relationship after augmentation of voltage-dependent K+ channel expression, transgenic mice were produced which specifically overexpress a human insulinoma-derived, tetraethylammonium (TEA)-insensitive delayed rectifier K+ channel in their pancreatic beta-cells as shown by immunoblot of isolated islets and immunohistochemical analysis of pancreas sections. Whole-cell current recordings confirmed the presence of high amplitude TEA-resistant K+ currents in transgenic islet cells, whose expression correlated with hyperglycemia and hypoinsulinemia. Stable overexpression of the channel in insulinoma cells attenuated glucose-activated increases in [Ca2+]i and prevented the induction of TEA-dependent [Ca2+]i oscillations. These results, employing the first ion channel transgenic mouse, demonstrate the importance of membrane potential regulation in excitation-secretion coupling in the pancreatic beta-cell." @default.
• W1603322339 created "2016-06-24" @default.
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• W1603322339 date "1994-11-01" @default.
• W1603322339 modified "2023-09-27" @default.
• W1603322339 title "Delayed rectifier K+ channel overexpression in transgenic islets and beta-cells associated with impaired glucose responsiveness." @default.
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• W1603322339 doi "https://doi.org/10.1016/s0021-9258(18)46851-2" @default.
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