ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
K+ channel facilitation of exocytosis by dynamic interaction with syntaxin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- Circulating extracellular vesicles promote recovery in a preclinical model of intracerebral hemorrhage.Molecular therapy. Nucleic acids · 2023Article
- EVAP: A two-photon imaging tool to study conformational changes in endogenous Kv2 channels in live tissues.The Journal of general physiology · 2021Article
- Location, location, location: the organization and roles of potassium channels in mammalian motoneurons.The Journal of physiology · 2021Article
- The versatile Kv channels in the nervous system: actions beyond action potentials.Cellular and molecular life sciences : CMLS · 2020Review
- Kv2 channels create endoplasmic reticulum / plasma membrane junctions: a brief history of Kv2 channel subcellular localization.Channels (Austin, Tex.) · 2019Review
- Defining the Kv2.1-syntaxin molecular interaction identifies a first-in-class small molecule neuroprotectant.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A glucose-dependent spatial patterning of exocytosis in human β-cells is disrupted in type 2 diabetes.JCI insight · 2019Article
- Kv2 potassium channels form endoplasmic reticulum/plasma membrane junctions via interaction with VAPA and VAPB.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- KThe Journal of biological chemistry · 2018Article
- Kv2.1 Clustering Contributes to Insulin Exocytosis and Rescues Human β-Cell Dysfunction.Diabetes · 2017Article
- Disruption of KNeuroscience · 2017Article
- Targeting a Potassium Channel/Syntaxin Interaction Ameliorates Cell Death in Ischemic Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Association of KCNB1 polymorphisms with lipid metabolisms and insulin resistance: a case-control design of population-based cross-sectional study in Chinese Han population.Lipids in health and disease · 2015Article
- Mechanisms of activation of voltage-gated potassium channels.Acta naturae · 2014Article
- Syntaxin-binding domain of Kv2.1 is essential for the expression of apoptotic K+ currents.The Journal of physiology · 2014Article
- Kv2 channels regulate firing rate in pyramidal neurons from rat sensorimotor cortex.The Journal of physiology · 2013Article
- Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Regulation of Kv2.1 K(+) conductance by cell surface channel density.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Kv2.1 cell surface clusters are insertion platforms for ion channel delivery to the plasma membrane.Molecular biology of the cell · 2012Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Kv channels inhibit release indirectly by hyperpolarizing membrane potential, but the significance of Kv channel interaction with the secretory apparatus is not known. The Kv2.1 channel is commonly expressed in the soma and dendrites of neurons, where it could influence the release of neuropeptides and neurotrophins, and in neuroendocrine cells, where it could influence hormone release. Here we show that Kv2.1 channels increase dense-core vesicle (DCV)-mediated release after elevation of cytoplasmic Ca2+. This facilitation occurs even after disruption of pore function and cannot be explained by changes in membrane potential and cytoplasmic Ca2+. However, triggering release increases channel binding to syntaxin, a secretory apparatus protein. Disrupting this interaction with competing peptides or by deleting the syntaxin association domain of the channel at the C terminus blocks facilitation of release. Thus, direct association of Kv2.1 with syntaxin promotes exocytosis. The dual functioning of the Kv channel to influence release, through its pore to hyperpolarize the membrane potential and through its C-terminal association with syntaxin to directly facilitate release, reinforces the requirements for repetitive firing for exocytosis of DCVs in neuroendocrine cells and in dendrites.
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Registered trials
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.