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The Journal of Neuroscience, December 17, 2003, 23(37):11681-11691
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Cellular/Molecular
Slick (Slo2.1), a Rapidly-Gating Sodium-Activated Potassium Channel Inhibited by ATP
Arin Bhattacharjee,1 * William J. Joiner,4 * Meilin Wu,2 Youshan Yang,3 Fred J. Sigworth,3 andLeonard K. Kaczmarek1,3 Departments of 1Pharmacology, 2Cell Biology, and 3Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520, and 4Department of Neuroscience, University of Pennsylvania, Philadelphia, Pennsylvania 94080
Neuronal stressors such as hypoxia and firing of action potentials at very high frequencies cause intracellular Na+ to rise and ATP to be consumed faster than it can be regenerated. We report the cloning of a gene encoding a K+ channel, Slick, and demonstrate that functionally it is a hybrid between two classes of K+ channels, Na+-activated (KNa) and ATP-sensitive (KATP) K+ channels. The Slick channel is activated by intracellular Na+ and Cl- and is inhibited by intracellular ATP. Slick is widely expressed in the CNS and is detected in heart. We identify a consensus ATP binding site near the C terminus of the channel that is required for ATP and its nonhydrolyzable analogs to reduce open probability. The convergence of Na+, Cl-, and ATP sensitivity in one channel may endow Slick with the ability to integrate multiple indicators of the metabolic state of a cell and to adjust electrical activity appropriately.
Key words: channel; chloride; hippocampus; metabolism; potassium; sodium
Received Sep 2, 2003; revised October 7, 2003; accepted October 30, 2003.
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