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Molecular and cellular neuroscience

Publication date: 2003-10-01
Volume: 24 Pages: 357 - 366
Publisher: Academic press inc elsevier science

Author:

Van Hoorick, D
Raes, Adam ; Keysers, W ; Mayeur, E ; Snyders, DJ

Keywords:

secondary structure prediction, transient outward current, channel-interacting protein-2, closed-state inactivation, k+ channel, potassium channels, alpha-subunits, a-current, i-to, expression, Science & Technology, Life Sciences & Biomedicine, Neurosciences, Neurosciences & Neurology, SECONDARY STRUCTURE PREDICTION, TRANSIENT OUTWARD CURRENT, CHANNEL-INTERACTING PROTEIN-2, CLOSED-STATE INACTIVATION, K+ CHANNEL, POTASSIUM CHANNELS, ALPHA-SUBUNITS, A-CURRENT, I-TO, EXPRESSION, Alternative Splicing, Amino Acid Sequence, Animals, Base Sequence, Calcium-Binding Proteins, Genetic Variation, Humans, Kv Channel-Interacting Proteins, Mice, Molecular Sequence Data, Potassium Channels, Potassium Channels, Voltage-Gated, Shal Potassium Channels, 1109 Neurosciences, 1701 Psychology, 1702 Cognitive Sciences, Neurology & Neurosurgery, 3101 Biochemistry and cell biology, 3209 Neurosciences

Abstract:

The beta-subunits of the KChIP family modulate properties and expression level of Kv4 channels. We report the cloning of the first splice variant of KChIP1 (KChIP1b) which contains an extra exon, rich in aromatic residues, in the amino terminus. Both splice variants interacted equally well with Kv4.2 subunits based on confocal imaging and upregulation of current density (more than five-fold). No effects on the voltage dependence of activation or inactivation were noted. However, the effects on the kinetics of recovery from inactivation were opposite: KChIP1b induced a slow component in the recovery (tau similar to 1.2 s), in contrast to the increased recovery rate (tau = 125 ms) with KChIP1a. Accordingly, frequency-dependent accumulation of inactivation was enhanced by KChIP1b but reduced by KChIP1a. Since Kv4.2 channels are involved in protection against back propagating action potentials in dendritic spines, a differential expression of either splice variant could shape the dendritic function. (C) 2003 Elsevier Science (USA). All rights reserved.