ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Regulation of neuronal M-channel gating in an isoform-specific manner: functional interplay between calmodulin and syntaxin 1A.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Calmodulin assists during co-translational folding of the KProtein science : a publication of the Protein Society · 2026Article
- Electrophysiological Abnormalities and Pharmacological Corrections of Pathogenic Missense Variants in KCNQ3.Neuroscience bulletin · 2025Article
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- Phosphoproteome Analysis Identifies a Synaptotagmin-1-Associated Complex Involved in Ischemic Neuron Injury.Molecular & cellular proteomics : MCP · 2022Article
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Epileptic channelopathies caused by neuronal Kv7 (KCNQ) channel dysfunction.Pflugers Archiv : European journal of physiology · 2020Review
- A mutually induced conformational fit underlies CaThe Journal of biological chemistry · 2019Article
- Reduced axonal surface expression and phosphoinositide sensitivity in KNeurobiology of disease · 2018Article
- Calmodulin: A Multitasking Protein in Kv7.2 Potassium Channel Functions.Biomolecules · 2018Review
- Modulation of Kv7 channels and excitability in the brain.Cellular and molecular life sciences : CMLS · 2017Review
- Distinct Functions of Syntaxin-1 in Neuronal Maintenance, Synaptic Vesicle Docking, and Fusion in Mouse Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Raised Intracellular Calcium Contributes to Ischemia-Induced Depression of Evoked Synaptic Transmission.PloS one · 2016Article
- Interactions between N and C termini of α1C subunit regulate inactivation of CaV1.2 L-type Ca(2+) channel.Channels (Austin, Tex.) · 2016Article
- Cooperative endocytosis of the endosomal SNARE protein syntaxin-8 and the potassium channel TASK-1.Molecular biology of the cell · 2014Article
- Polarized axonal surface expression of neuronal KCNQ potassium channels is regulated by calmodulin interaction with KCNQ2 subunit.PloS one · 2014Article
- Quantitative properties and receptor reserve of the DAG and PKC branch of G(q)-coupled receptor signaling.The Journal of general physiology · 2013Article
- Structural insights into neuronal K+ channel-calmodulin complexes.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- M channel enhancers and physiological M channel block.The Journal of physiology · 2012Article
- Regions of KCNQ K(+) channels controlling functional expression.Frontiers in physiology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whereas neuronal M-type K(+) channels composed of KCNQ2 and KCNQ3 subunits regulate firing properties of neurons, presynaptic KCNQ2 subunits were demonstrated to regulate neurotransmitter release by directly influencing presynaptic function. Two interaction partners of M-channels, syntaxin 1A and calmodulin, are known to act presynaptically, syntaxin serving as a major protein component of the membrane fusion machinery and calmodulin serving as regulator of several processes related to neurotransmitter release. Notably, both partners specifically modulate KCNQ2 but not KCNQ3 subunits, suggesting selective presynaptic targeting to directly regulate exocytosis without interference in neuronal firing properties. Here, having first demonstrated in Xenopus oocytes, using analysis of single-channel biophysics, that both modulators downregulate the open probability of KCNQ2 but not KCNQ3 homomers, we sought to resolve the channel structural determinants that confer the isoform-specific gating downregulation and to get insights into the molecular events underlying this mechanism. We show, using optical, biochemical, electrophysiological, and molecular biology analyses, the existence of constitutive interactions between the N and C termini in homomeric KCNQ2 and KCNQ3 channels in living cells. Furthermore, rearrangement in the relative orientation of the KCNQ2 termini that accompanies reduction in single-channel open probability is induced by both regulators, strongly suggesting that closer N-C termini proximity underlies gating downregulation. Different structural determinants, identified at the N and C termini of KCNQ3, prevent the effects by syntaxin 1A and calmodulin, respectively. Moreover, we show that the syntaxin 1A and calmodulin effects can be additive or blocked at different concentration ranges of calmodulin, bearing physiological significance with regard to presynaptic exocytosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.