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Prasanna Devaraneni

As seen in: The Journal of Biological Chemistry
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Articles by Prasanna Devaraneni

Pharmacological Correction of Trafficking Defects in ATP-sensitive Potassium Channels Caused by Sulfonylurea Receptor 1 Mutations

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By Gregory Martin, Emily A. Rex, Prasanna Devaraneni, Jerod S. Denton
| The Journal of Biological Chemistry Verified
ATP-sensitive potassium (K ) channels play a key role in mediating glucose-stimulated insulin secretion by coupling metabolic signals to ?-cell membrane potential. Loss of K channel function due to mutations in ABCC8 or KCNJ11, genes encoding the sulfonylurea receptor 1 (SUR1) or the inwardly rectifying potassium channel Kir6.2, respectively, results in congenital hyperinsulinism. Many SUR1 mutations prevent trafficking of channel proteins from the endoplasmic reticulum to the cell surface.
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Pharmacological Correction of Trafficking Defects in ATP-Sensitive Potassium Channels Caused by Sulfonylurea Receptor 1 Mutations

|
By Gregory Martin, Emily A. Rex, Prasanna Devaraneni, Jerod S. Denton
| The Journal of Biological Chemistry Verified
ATP-sensitive potassium (K ) channels play a key role in mediating glucose-stimulated insulin secretion by coupling metabolic signals to β-cell membrane potential. Loss of K channel function due to mutations in ABCC8 or KCNJ11, genes encoding the sulfonylurea receptor 1 (SUR1) or the inwardly rectifying potassium channel Kir6.2, respectively, results in congenital hyperinsulinism. Many SUR1 mutations prevent trafficking of channel proteins from the endoplasmic reticulum to the cell surface.
Open in Who Shared Issue with article?
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