ArticleThe Journal of biological chemistry2016
Mechanisms of Calmodulin Regulation of Different Isoforms of Kv7.4 K+ Channels.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Redox regulation of KeLife · 2023Article
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Calmodulin acts as a state-dependent switch to control a cardiac potassium channel opening.Science advances · 2020Article
- Atomistic Insights of Calmodulin Gating of Complete Ion Channels.International journal of molecular sciences · 2020Review
- The S2-S3 Loop of Kv7.4 Channels Is Essential for Calmodulin Regulation of Channel Activation.Frontiers in physiology · 2020Article
- Calmodulin: A Multitasking Protein in Kv7.2 Potassium Channel Functions.Biomolecules · 2018Review
- A Calmodulin C-Lobe CaNeuron · 2018Article
- Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants.Channels (Austin, Tex.) · 2018Article
- Muscarinic Acetylcholine Receptors and M-Currents Underlie Efferent-Mediated Slow Excitation in Calyx-Bearing Vestibular Afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Modulation of Kv7 channels and excitability in the brain.Cellular and molecular life sciences : CMLS · 2017Review
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Authors and funding
10 authors.
Funding
Abstract
Calmodulin (CaM), a Ca(2+)-sensing protein, is constitutively bound to IQ domains of the C termini of human Kv7 (hKv7, KCNQ) channels to mediate Ca(2+)-dependent reduction of Kv7 currents. However, the mechanism remains unclear. We report that CaM binds to two isoforms of the hKv7.4 channel in a Ca(2+)-independent manner but that only the long isoform (hKv7.4a) is regulated by Ca(2+)/CaM. Ca(2+)/CaM mediate reduction of the hKv7.4a channel by decreasing the channel open probability and altering activation kinetics. We took advantage of a known missense mutation (G321S) that has been linked to progressive hearing loss to further examine the inhibitory effects of Ca(2+)/CaM on the Kv7.4 channel. Using multidisciplinary techniques, we demonstrate that the G321S mutation may destabilize CaM binding, leading to a decrease in the inhibitory effects of Ca(2+) on the channels. Our study utilizes an expression system to dissect the biophysical properties of the WT and mutant Kv7.4 channels. This report provides mechanistic insights into the critical roles of Ca(2+)/CaM regulation of the Kv7.4 channel under physiological and pathological conditions.
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