ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
The axon-dendrite targeting of Kv3 (Shaw) channels is determined by a targeting motif that associates with the T1 domain and ankyrin G.
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 43 papers.
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Who cites it
43 citing papers in PubMed.
- Impacts of Kv3.1 Channels on Action Potentials in Fusiform Neurons From the Dorsal Cochlear Nucleus of Mice Before and After Hearing Onset.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- An epilepsy-associated KV3.1 potassium channel variant acts via dominant-positive effect.The Journal of general physiology · 2026Article
- Proper localization of the SCA13-linked KNeurobiology of disease · 2026Article
- AProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Structural insights into the function, dysfunction and modulation of Kv3 channels.Neuropharmacology · 2025Review
- Axons compensate for biophysical constraints of variable size to uniformize their action potentials.PLoS biology · 2024Article
- A cytoskeleton-membrane interaction conserved in fast-spiking neurons controls movement, emotion, and memory.Molecular psychiatry · 2023Article
- Developmental and epileptic encephalopathies: from genetic heterogeneity to phenotypic continuum.Physiological reviews · 2023Review
- Pleiotropic Ankyrins: Scaffolds for Ion Channels and Transporters.Channels (Austin, Tex.) · 2022Review
- The Mechanical Microenvironment Regulates Axon Diameters Visualized by Cryo-Electron Tomography.Cells · 2022Article
- Cryo-EM structure of the human Kv3.1 channel reveals gating control by the cytoplasmic T1 domain.Nature communications · 2022Article
- Article
- Review
- Immediate induction of varicosities by transverse compression but not uniaxial stretch in axon mechanosensation.Acta neuropathologica communications · 2022Article
- The Ankyrin Repeat Domain Controls Presynaptic Localization of Drosophila Ankyrin2 and Is Essential for Synaptic Stability.Frontiers in cell and developmental biology · 2019Article
- Balanced Activity between Kv3 and Nav Channels Determines Fast-Spiking in Mammalian Central Neurons.iScience · 2018Article
- Kv3 Channels: Enablers of Rapid Firing, Neurotransmitter Release, and Neuronal Endurance.Physiological reviews · 2017Review
- Polarity of varicosity initiation in central neuron mechanosensation.The Journal of cell biology · 2017Article
- Suppression of Inflammatory Demyelinaton and Axon Degeneration through Inhibiting Kv3 Channels.Frontiers in molecular neuroscience · 2017Article
- Membrane Distribution and Activity of a Neuronal Voltage-Gated K+ Channel is Modified by Replacement of Complex Type N-Glycans with Hybrid Type.Journal of glycobiology · 2017Article
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5 authors.
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Abstract
Kv3 (Shaw) channels regulate rapid spiking, transmitter release and dendritic integration of many central neurons. Crucial to functional diversity are the complex targeting patterns of channel proteins. However, the targeting mechanisms are not known. Here we report that the axon-dendrite targeting of Kv3.1 is controlled by a conditional interaction of a C-terminal axonal targeting motif (ATM) with the N-terminal T1 domain and adaptor protein ankyrin G. In cultured hippocampal neurons, although the two splice variants of Kv3.1, Kv3.1a and Kv3.1b, are differentially targeted to the somatodendritic and axonal membrane, respectively, the lysine-rich ATM is surprisingly common for both splice variants. The ATM not only directly binds to the T1 domain in a Zn2+-dependent manner, but also associates with the ankyrin-repeat domain of ankyrin G. However, the full-length channel proteins of Kv3.1b display stronger association to ankyrin G than those of Kv3.1a, suggesting that the unique splice domain at Kv3.1b C terminus influences ATM binding to T1 and ankyrin G. Because ankyrin G mainly resides at the axon initial segment, we propose that it may function as a barrier for axon-dendrite targeting of Kv3.1 channels. In support of this idea, disrupting ankyrin G function either by over-expressing a dominant-negative mutant or by siRNA knockdown decreases polarized axon-dendrite targeting of both Kv3.1a and Kv3.1b. We conclude that the conditional ATM masked by the T1 domain in Kv3.1a is exposed by the splice domain in Kv3.1b, and is subsequently recognized by ankyrin G to target Kv3.1b into the axon.
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