Affinage

KCNC4

Voltage-gated potassium channel KCNC4 · UniProt Q03721

Length
635 aa
Mass
69.8 kDa
Annotated
2026-06-10
37 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCNC4 encodes Kv3.4, a voltage-gated A-type potassium channel that produces a fast-inactivating, high voltage-activated K+ current shaping action potential repolarization in excitable cells, most prominently nociceptive sensory neurons (PMID:22063632, PMID:36198500). Fast inactivation operates by an N-type ball-and-chain mechanism: the cytoplasmic N-terminal inactivation domain occludes the pore through a voltage-dependent association in which a hydrophobic segment blocks the pore and an adjacent positively charged region engages channel negative charges (PMID:7602512, PMID:8910203). This inactivation is dynamically tuned by PKC-dependent phosphorylation of four nonequivalent serines (S8, S9, S15, S21) in the inactivation domain; phosphorylation slows inactivation and thereby accelerates and sharpens action potential repolarization, a tuning lost when channel surface expression falls after spinal cord injury (PMID:22063632, PMID:36198500, PMID:25609640). Kv3.4 function is set by partner subunits and regulators: it assembles with the accessory subunit MiRP2/KCNE3 to form a subthreshold channel that sets resting membrane potential in skeletal muscle, where a MiRP2 R83H mutation causing periodic paralysis confers aberrant intracellular pH sensitivity (PMID:11207363, PMID:16449802), and it coassembles with Kv3.1 in fast-spiking neurons to enhance repolarizing efficiency and sustain high firing rates (PMID:12592408). Channel surface delivery and presynaptic targeting are promoted by a non-proteolytic physical interaction with BACE1, while expression and membrane localization are stabilized by a kinase-activity-dependent association with PKCε (PMID:29507146, PMID:33368632). Kv3.4 expression is transcriptionally and post-transcriptionally regulated by hypoxia—directly activated by HIF-1α at its promoter in carcinoma cells yet downregulated by chronic hypoxia and by 15-HETE via the 15-lipoxygenase pathway in pulmonary and carotid body tissues—linking channel abundance to oxygen sensing (PMID:31471334, PMID:15890707, PMID:18430420). Beyond electrical signaling, Kv3.4 activity influences cell-cycle progression, mitochondrial cytochrome c release and apoptotic signaling, and amyloid-β-associated synaptotoxicity (PMID:20093253, PMID:28522852, PMID:35359460).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1992 Medium

    Establishing the human gene's chromosomal location provided the molecular foothold for studying KCNC4 as a distinct potassium channel gene.

    Evidence Genomic cloning and chromosomal mapping localizing KCNC4 to human chromosome 1

    PMID:1740329

    Open questions at the time
    • No functional or channel property characterized at this stage
    • Gene structure and expression pattern not defined
  2. 1996 High

    Defining how the N-terminal inactivation peptide blocks the pore answered the long-standing mechanistic question of how Kv3.4 achieves fast N-type inactivation.

    Evidence Synthetic inactivation peptide application and systematic mutagenesis in mKv1.1-expressing CHO cells, plus chemical modification (NBA, chloramine-T)

    PMID:7602512 PMID:8910203

    Open questions at the time
    • Mechanism shown on a surrogate channel (mKv1.1), not full-length Kv3.4 tetramer
    • Physiological regulation of the inactivation domain not addressed
    • No structural model of the bound peptide
  3. 2001 High

    Identifying MiRP2/KCNE3 as a physical Kv3.4 partner explained how the channel sets resting membrane potential in muscle and linked it to a Mendelian disease.

    Evidence Co-immunoprecipitation, patch clamp, and patient family genetics in heterologous expression and skeletal muscle (MiRP2 R83H periodic paralysis)

    PMID:11207363

    Open questions at the time
    • Stoichiometry of the Kv3.4–MiRP2 complex not defined
    • How R83H disrupts membrane potential setting clarified only later
  4. 2003 High

    Showing Kv3.4 coassembles with Kv3.1 in fast-spiking neurons answered how heteromeric Kv3 channels tune high-frequency firing beyond homomeric channels.

    Evidence Molecular cloning, electrophysiology, pharmacology and immunohistochemistry in rat brain neurons

    PMID:12592408

    Open questions at the time
    • Subunit stoichiometry of native heteromers not quantified
    • In vivo behavioral relevance not tested
  5. 2006 High

    Dissecting MiRP2 phosphorylation and the R83H variant explained why the periodic paralysis mutation impairs channel function—via aberrant pH sensitivity rather than loss of PKC phosphorylation.

    Evidence Site-directed mutagenesis, PKC phosphorylation assays, and pH-dependent single-channel recording in heterologous cells

    PMID:16449802

    Open questions at the time
    • Physiological pH fluctuations driving the defect in muscle not demonstrated in vivo
    • Effect on Kv3.4 pore residues not separated from MiRP2 contribution
  6. 2004 Medium

    Mapping Kv3.4 to both presynaptic terminals and postsynaptic structures established candidate roles in transmitter release and postsynaptic excitability.

    Evidence Immunohistochemistry, confocal co-localization with synaptic markers, and electron microscopy in brainstem and spinal cord

    PMID:15207333

    Open questions at the time
    • Functional consequence of each localization not directly tested
    • Targeting mechanism to presynaptic terminals not yet known
  7. 2011 High

    Demonstrating that PKC slows N-type inactivation to accelerate AP repolarization in nociceptors established Kv3.4 as a dynamically tunable controller of sensory neuron firing.

    Evidence Cell-attached patch clamp, single-cell qPCR, siRNA knockdown, and GPCR/PKC pharmacology in DRG neurons and heterologous cells

    PMID:22063632

    Open questions at the time
    • Specific phosphorylated residues not yet mapped
    • Identity of the membrane-delimited GPCR signaling complex incomplete
  8. 2015 High

    Showing that spinal cord injury reduces Kv3.4 surface expression and abolishes PKC-driven AP shortening linked channel trafficking to pathological hyperexcitability.

    Evidence Patch clamp, immunohistochemistry, dynamic clamp, qPCR and Western blot in DRG nociceptors post-SCI

    PMID:25609640

    Open questions at the time
    • Molecular trigger for reduced surface trafficking unidentified
    • Whether restoring surface Kv3.4 reverses pain behavior not shown
  9. 2018 High

    Identifying a non-proteolytic BACE1–Kv3.4 interaction answered how the channel is trafficked to presynaptic terminals and gave BACE1 a channel-trafficking function.

    Evidence Reciprocal co-IP, surface biotinylation, synaptic fractionation, and slice electrophysiology in BACE1-/- mice plus heterologous co-expression

    PMID:29507146

    Open questions at the time
    • Trafficking step at which BACE1 acts not resolved
    • Whether the interaction is direct or bridged by another protein unknown
  10. 2021 Medium

    Showing PKCε physically associates with Kv3.4 and supports its expression and membrane localization separated a kinase-scaffolding role from gating modulation.

    Evidence Reciprocal co-IP and dominant-negative mutagenesis in heterologous cells and rat DRG neurons

    PMID:33368632

    Open questions at the time
    • Whether PKCε is the kinase phosphorylating the inactivation domain not established
    • Single lab; structural basis of the interaction unknown
  11. 2022 High

    Mapping four phosphorylatable serines (S8, S9, S15, S21) in the inactivation domain pinpointed the molecular substrate that converts PKC signaling into tunable AP repolarization.

    Evidence AAV-mediated phosphonull/phosphomimic and pore-mutant expression in rat DRG neurons with patch clamp

    PMID:36198500

    Open questions at the time
    • Site-specific stoichiometry and order of phosphorylation not resolved
    • Kinase responsible for each site not assigned
  12. 2022 Medium

    In vivo knockdown of Kv3.4 ameliorating dendritic spine loss in APP/PS1 mice extended the channel's role to amyloid-β-driven synaptotoxicity, building on earlier Aβ/NF-κB upregulation findings.

    Evidence AAV-CRISPR Kv3.4 knockdown with dendritic spine analysis in APP/PS1 cortex; earlier RT-PCR/patch clamp showing Aβ-induced, NF-κB-dependent upregulation

    PMID:17495071 PMID:35359460

    Open questions at the time
    • Mechanistic link between channel activity and spine maintenance not defined
    • Therapeutic window and behavioral rescue not established
  13. 2019 Medium

    Identifying HIF-1α direct promoter binding and divergent hypoxic regulation explained how Kv3.4 abundance is coupled to oxygen status across tissues.

    Evidence ChIP and luciferase reporter with CRISPR HIF-1α knockout in oral carcinoma; chronic hypoxia and 15-HETE/15-LOX downregulation in carotid body and pulmonary smooth muscle

    PMID:15890707 PMID:18430420 PMID:31471334

    Open questions at the time
    • Why HIF-1α activates Kv3.4 in carcinoma but hypoxia suppresses it in vascular/chemoreceptor cells unresolved
    • Promoter context determining direction of regulation unknown
  14. 2018 Medium

    Linking Kv3.4 to mitochondrial cytochrome c release and cell-cycle control broadened its role beyond plasma-membrane electrical signaling into apoptosis and proliferation.

    Evidence Pharmacological block (BDS), siRNA, Ca2+ imaging, mitochondrial potential and cytochrome c assays, and flow cytometry across SH-SY5Y, smooth muscle, and leukemia cells

    PMID:20093253 PMID:23443853 PMID:28522852

    Open questions at the time
    • Whether a genuine mitochondrial Kv3.4 pool exists is inferred pharmacologically
    • Direct molecular coupling to cell-cycle machinery not defined
  15. 2025 Medium

    Demonstrating that N-glycosylation, modulated by glucose availability, alters inactivation delay revealed a metabolic input to Kv3.4 gating.

    Evidence Voltage clamp characterization with glycosylation/glucose manipulation in heterologous cells

    PMID:40995118

    Open questions at the time
    • Glycosylation sites responsible not mapped
    • Physiological relevance in native neurons not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How Kv3.4 mechanistically drives cancer cell migration, EMT, and proliferation—and whether these reflect canonical channel conductance or non-conducting roles—remains unresolved.
  • Molecular link between Kv3.4 and EMT/FAK-integrin machinery not established
  • Cancer findings rest on single-lab knockdown/overexpression without channel-independent controls
  • No structural model of the full-length human channel or its inactivation domain

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4
Localization
GO:0005886 plasma membrane 3 GO:0005739 mitochondrion 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-8953897 Cellular responses to stimuli 3
Partners
BACE1KCNC1KCNE3PRKCE
Complex memberships
Kv3.4–Kv3.1 heteromeric channelKv3.4–MiRP2 (KCNE3) channel complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 MiRP2 (KCNE3) physically assembles with Kv3.4 (KCNC4) in skeletal muscle to form a subthreshold voltage-gated potassium channel complex. MiRP2 modifies Kv3.4 channel properties including unitary conductance, voltage-dependent activation, recovery from inactivation, steady-state open probability, and block by peptide toxin. The complex sets resting membrane potential without producing afterhyperpolarization or cumulative inactivation. A missense mutation in MiRP2 (R83H) reduces current density and diminishes capacity to set resting membrane potential, causing periodic paralysis. Electrophysiology (patch clamp), Co-immunoprecipitation, heterologous expression, genetic analysis of patient families Cell High 11207363
2003 A splice variant of Kv3.4 coassembles with Kv3.1 subunits in rat brain fast-spiking neurons to form heteromeric channels. This coassembly enhances spike repolarizing efficiency, reduces spike duration, and enables higher repetitive spike rates compared to Kv3.1 homomeric channels. Molecular cloning, electrophysiology, pharmacology, immunohistochemistry in rat brain neurons Nature neuroscience High 12592408
2006 MiRP2-Kv3.4 channel function requires PKC phosphorylation of MiRP2 at serine 82. The periodic paralysis-associated R83H variant does not prevent S82 phosphorylation but instead confers sensitivity to intracellular pH changes (pKa ~7.3, consistent with histidine protonation), reducing single-channel current as internal pH is lowered, whereas wild-type channels are largely insensitive to pH. Electrophysiology (patch clamp), site-directed mutagenesis, PKC phosphorylation assays, heterologous expression FASEB journal High 16449802
2011 Kv3.4 channels underlie a robust high voltage-activated A-type K+ current (I_AHV) in nociceptive dorsal root ganglion neurons. PKC activation causes 4-fold slowing of Kv3.4 N-type inactivation via phosphorylation of the N-terminal inactivation gate, accelerating action potential repolarization by 22% and shortening AP duration by 14%. GPCR agonists eliminate I_AHV fast inactivation in a membrane-delimited manner via a Kv3.4 signaling complex. Kv3.4 siRNA knockdown prolongs AP by 25% and abolishes GPCR agonist-induced AP repolarization acceleration. Cell-attached patch clamp, single-cell qPCR, siRNA knockdown, pharmacology (PKC inhibitor, GPCR agonists), heterologous expression The Journal of physiology High 22063632
2015 Following spinal cord injury (SCI), Kv3.4 channel inactivation is impaired in DRG nociceptors at 1 week post-laminectomy. At 2–6 weeks post-SCI, Kv3.4 currents are downregulated and remain slow-inactivating, primarily due to decreased surface expression of the channel (while total protein and mRNA levels are unchanged). PKC activation fails to shorten AP duration in small-diameter DRG neurons post-SCI. Re-expression of synthetic Kv3.4 currents via dynamic clamp dampens repetitive spiking in SCI neurons. Patch clamp electrophysiology, immunohistochemistry, dynamic clamp, qPCR, Western blot The Journal of neuroscience High 25609640
1995 The N-terminal inactivation domain (ball peptide) of human Kv3.4 causes N-type (ball-and-chain) inactivation of mKv1.1 channels when applied intracellularly. Chemical modification reagents NBA and chloramine-T remove hKv3.4 peptide-induced inactivation in a manner critically dependent on cysteine at position 6 of the inactivation peptide. Whole-cell patch clamp in CHO cells expressing mKv1.1, chemical modification with N-bromoacetamide and chloramine-T, synthetic peptide application The Journal of physiology High 7602512
1996 The hKv3.4 N-terminal inactivation peptide blocks the mKv1.1 channel pore through a voltage-dependent association rate (kon increases with depolarization) while dissociation rate (koff) is voltage-independent. The hydrophobic N-terminal region of the inactivation peptide blocks the channel pore while the adjacent positively charged region interacts with negative charges on the channel. Disulfide bridge between C6 and C24 is not required for inactivation; substitutions at C24 (not C6) reduce kon. Whole-cell patch clamp in CHO cells, synthetic peptide variants, mutagenesis of inactivation peptide The Journal of physiology High 8910203
2004 Kv3.4 channels localize to both presynaptic terminals (co-localizing with synaptic vesicle protein SV2 and glutamate/glycine vesicle markers VGluT1, VGluT2, GlyT2) and postsynaptic dendritic/somatic structures (at synaptic junctions) in brainstem and spinal cord, as confirmed by electron microscopy. This dual localization suggests roles in both transmitter release control and regulation of neuronal excitability. Immunohistochemistry, confocal co-localization with synaptic markers, electron microscopy Neuroscience Medium 15207333
2007 Amyloid-beta (Aβ1-42) peptide upregulates Kv3.4 and MiRP2 transcripts and proteins in hippocampal neurons and PC-12 cells via NF-κB nuclear translocation. This increases I_A current amplitude carried by Kv3.4 channels. Inhibition of NF-κB translocation (with SN-50) or Kv3.4 blockade (with BDS-I) prevents the increase in Kv3.4 current and protects against Aβ-induced neuronal death. RT-PCR, Western blot, whole-cell patch clamp, pharmacological inhibition (SN-50, BDS-I) in hippocampal neurons and PC-12 cells Molecular pharmacology Medium 17495071
2018 BACE1 (β-secretase) physically interacts with Kv3.4 and promotes its surface expression at hippocampal mossy fiber presynaptic terminals through a non-proteolytic mechanism. In BACE1-/- mice, Kv3.4 surface expression is significantly reduced in hippocampus and synaptic fractions specifically. Loss of presynaptic Kv3.4 affects excitatory transmission strength at mossy fiber–CA3 synapses. BACE1 co-transfection in heterologous cells upregulates Kv3.4 surface level and current. Co-immunoprecipitation, surface biotinylation, synaptic fractionation, hippocampal slice electrophysiology in BACE1-/- mice, heterologous co-expression The Journal of neuroscience High 29507146
2021 PKCε physically associates with Kv3.4 in both heterologous cells and rat DRG neurons. PKCε kinase activity positively regulates Kv3.4 expression and membrane localization: a catalytically inactive dominant-negative PKCε inhibits Kv3.4 expression and membrane localization, whereas wild-type and constitutively active PKCε do not affect Kv3.4 gating properties. Co-immunoprecipitation, Western blot, dominant-negative mutagenesis, heterologous expression, rat DRG neurons FASEB journal Medium 33368632
2022 PKC-dependent phosphorylation of the Kv3.4 cytoplasmic N-terminal inactivation domain (NTID) at four nonequivalent serine sites (S8, S9, S15, S21) confers tunable action potential repolarization in DRG neurons. Phosphonull (S→A) mutant retains fast inactivation; phosphomimic (S→D) mutant shows impaired inactivation. The dominant-negative (W429F) pore mutant abolishes endogenous Kv3.4 current. AP width and maximum repolarization rate are negatively correlated with Kv3.4 inactivation speed. AAV-mediated expression of Kv3.4 mutants in rat DRG neurons, patch clamp electrophysiology, fluorescence microscopy The Journal of neuroscience High 36198500
2022 Reducing Kv3.4 expression in neurons of APP/PS1 mice via AAV-CRISPR ameliorates dendritic spine loss and changes spine morphology, indicating a role for Kv3.4 in Aβ-induced synaptotoxicity in vivo. AAV-CRISPR-mediated Kv3.4 knockdown in APP/PS1 mouse somatosensory cortex, dendritic spine analysis Brain and neuroscience advances Medium 35359460
2010 Kv3.4 channel expression cycles during the cell cycle in human uterine artery smooth muscle cells; current amplitude and channel contribution to cell excitability are increased in proliferating cells. Kv3.4 channel blockers and siRNA knockdown reduce the proportion of proliferating VSMCs, inducing cell cycle arrest after G2/M phase completion, suggesting a permissive role in cell cycle progression mediated at least partly through modulation of resting membrane potential. Real-time PCR, Western blot, patch clamp, flow cytometry, BrdU incorporation, siRNA knockdown, pharmacological blockade Cardiovascular research Medium 20093253
2013 Ionizing radiation activates Kv3.4-like voltage-gated potassium channels in chronic myeloid leukemia cells, which in turn enhances Ca2+ entry, activates Ca2+/calmodulin-dependent kinase II, and inactivates phosphatase cdc25B and cyclin-dependent kinase cdc2, leading to G2/M arrest. Channel inhibition (TEA, BDS-1/2) or siRNA knockdown releases cells from G2/M arrest, increases apoptosis, and decreases clonogenic survival. Patch clamp, Ca2+ imaging (fura-2), immunoblotting, flow cytometry, RNA interference, clonogenic survival assay Pflugers Archiv Medium 23443853
2005 Chronic hypoxia (24–48 h) downregulates Kv3.4 channel expression in rabbit carotid body chemoreceptor cells, reducing the amplitude of a fast-inactivating, BDS- and TEA-sensitive K+ current component. This Kv3.4 downregulation increases the relative contribution of the oxygen-sensitive K+ current (IKO2), thereby sensitizing chemoreceptors to acute hypoxia. Patch clamp electrophysiology, immunocytochemistry, qPCR, pharmacological characterization (BDS, TEA) in primary carotid body cultures The Journal of physiology Medium 15890707
2008 Subacute hypoxia suppresses Kv3.4 channel mRNA and protein expression in pulmonary arterial smooth muscle cells via the 15-lipoxygenase/15-HETE pathway. Blockade of 15-LOX (with CDC or NDGA) upregulates Kv3.4 expression and partially restores whole-cell K+ currents. 15-HETE selectively downregulates Kv3.4, whereas 5-HETE has no effect. Whole-cell patch clamp, semi-quantitative PCR, ELISA, Western blot, pharmacological inhibition in pulmonary artery smooth muscle cells European journal of pharmacology Medium 18430420
2019 HIF-1α directly regulates Kv3.4 transcription in oral squamous cell carcinoma cells under hypoxia, as shown by chromatin immunoprecipitation and luciferase reporter assay identifying HIF-1α binding sites in the Kv3.4 promoter. Knockout of HIF-1α reduces Kv3.4 expression; overexpression of Kv3.4 after HIF-1α knockdown partially restores cell proliferation and invasion. Chromatin immunoprecipitation (ChIP), luciferase reporter assay, CRISPR knockout, Western blot, qRT-PCR, Transwell and CCK-8 assays Annals of clinical and laboratory science Medium 31471334
2017 HIF-1α downregulates Kv3.4 channel function and expression in SH-SY5Y neuronal cells under CoCl2-induced oxidative stress. Mitochondrial Kv3.4 is more sensitive to CoCl2. Blocking Kv3.4 with BDS-II inhibits MPP+-induced cytochrome c release from the mitochondrial intermembrane space to the cytosol and prevents mitochondrial membrane potential depolarization, protecting against apoptotic neuronal death. Patch clamp, Western blot, pharmacological inhibition (BDS-II), mitochondrial membrane potential assay, cytochrome c release assay in SH-SY5Y cells Scientific reports Medium 28522852
1992 Human Kv3.4 (KCNC4) was mapped to human chromosome 1 using genomic cloning and chromosomal localization. Genomic cloning, chromosomal mapping (somatic cell hybrids/FISH) Genomics Medium 1740329
2025 N-glycosylation causes heterogeneity in the inactivation delay kinetics of Kv3.4 channels. Changes in glucose availability directly affect N-glycosylation and consequently alter Kv3.4 inactivation kinetics. Electrophysiology (voltage clamp characterization of Kv3.4 kinetics), glycosylation manipulation (glucose availability), heterologous expression system iScience Medium 40995118
2024 Kv3.4 regulates cancer cell migration and invasion through TGF-β-induced epithelial-mesenchymal transition (EMT) in A549 lung carcinoma cells. Kv3.4 knockdown blocks EMT progression and reduces migration/invasion; Kv3.4 overexpression promotes mesenchymal characteristics and synergizes with TGF-β to promote migration. siRNA knockdown, overexpression, Transwell assay, wound healing assay, Western blot, TGF-β treatment in A549 cells Scientific reports Low 38280903
2025 BPA treatment increases Kv3.4 expression and promotes cell migration in MCF7 breast cancer cells via integrin β and integrin-regulated FAK signaling; Kv3.4 silencing abolishes BPA-induced migration and FAK signaling. siRNA knockdown, Western blot, qRT-PCR, wound healing assay, immunoblotting for FAK signaling in MCF7 cells Biochemical and biophysical research communications Low 40157292
2010 siRNA-mediated inhibition of Kv3.4 expression in head and neck squamous cell carcinoma (HNSCC) cells leads to inhibition of cell proliferation via selective cell cycle arrest at G2/M phase without affecting apoptosis. siRNA knockdown, flow cytometry (cell cycle analysis), cell proliferation assay in HNSCC-derived cell lines The Journal of pathology Low 20593490

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis. Cell 240 11207363
2003 Kv3.4 subunits enhance the repolarizing efficiency of Kv3.1 channels in fast-spiking neurons. Nature neuroscience 118 12592408
2007 Up-regulation and increased activity of KV3.4 channels and their accessory subunit MinK-related peptide 2 induced by amyloid peptide are involved in apoptotic neuronal death. Molecular pharmacology 76 17495071
2004 Up-regulation of the Kv3.4 potassium channel subunit in early stages of Alzheimer's disease. Journal of neurochemistry 72 15485486
2015 Dysregulation of Kv3.4 channels in dorsal root ganglia following spinal cord injury. The Journal of neuroscience : the official journal of the Society for Neuroscience 54 25609640
2011 Modulation of Kv3.4 channel N-type inactivation by protein kinase C shapes the action potential in dorsal root ganglion neurons. The Journal of physiology 48 22063632
1992 Genomic organization, nucleotide sequence, and cellular distribution of a Shaw-related potassium channel gene, Kv3.3, and mapping of Kv3.3 and Kv3.4 to human chromosomes 19 and 1. Genomics 47 1740329
2008 Subacute hypoxia suppresses Kv3.4 channel expression and whole-cell K+ currents through endogenous 15-hydroxyeicosatetraenoic acid in pulmonary arterial smooth muscle cells. European journal of pharmacology 44 18430420
2006 Phosphorylation and protonation of neighboring MiRP2 sites: function and pathophysiology of MiRP2-Kv3.4 potassium channels in periodic paralysis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 41 16449802
2003 The increase of voltage-gated potassium channel Kv3.4 mRNA expression in oral squamous cell carcinoma. Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology 38 14632936
2005 Down regulation of Kv3.4 channels by chronic hypoxia increases acute oxygen sensitivity in rabbit carotid body. The Journal of physiology 34 15890707
2018 Kv3.1 and Kv3.4, Are Involved in Cancer Cell Migration and Invasion. International journal of molecular sciences 33 29614836
2004 Association of potassium channel Kv3.4 subunits with pre- and post-synaptic structures in brainstem and spinal cord. Neuroscience 32 15207333
1998 Expression of the potassium channel KV3.4 in mouse skeletal muscle parallels fiber type maturation and depends on excitation pattern. FEBS letters 32 9468318
2010 Expression and clinical significance of the Kv3.4 potassium channel subunit in the development and progression of head and neck squamous cell carcinomas. The Journal of pathology 30 20593490
2013 Kv3.4 potassium channel-mediated electrosignaling controls cell cycle and survival of irradiated leukemia cells. Pflugers Archiv : European journal of physiology 26 23443853
1995 Inactivation of the cloned potassium channel mouse Kv1.1 by the human Kv3.4 'ball' peptide and its chemical modification. The Journal of physiology 26 7602512
2010 Cell cycle-dependent expression of Kv3.4 channels modulates proliferation of human uterine artery smooth muscle cells. Cardiovascular research 25 20093253
2017 Kv3.4 is modulated by HIF-1α to protect SH-SY5Y cells against oxidative stress-induced neural cell death. Scientific reports 18 28522852
2004 Identification of a Kv3.4 channel in corneal epithelial cells. Investigative ophthalmology & visual science 18 15161842
2020 LINC01535 Promotes the Development of Osteosarcoma Through Modulating miR-214-3p/KCNC4 Axis. Cancer management and research 16 32753970
2019 HIF-1α Regulates Proliferation and Invasion of Oral Cancer Cells through Kv3.4 Channel. Annals of clinical and laboratory science 16 31471334
2018 β-Secretase BACE1 Promotes Surface Expression and Function of Kv3.4 at Hippocampal Mossy Fiber Synapses. The Journal of neuroscience : the official journal of the Society for Neuroscience 16 29507146
2022 Reducing voltage-dependent potassium channel Kv3.4 levels ameliorates synapse loss in a mouse model of Alzheimer's disease. Brain and neuroscience advances 14 35359460
2011 Selective underexpression of Kv3.2 and Kv3.4 channels in the cortex of rats exposed to ethanol during early postnatal life. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 14 21234782
2007 The MiRP2-Kv3.4 potassium channel: muscling in on Alzheimer's disease. Molecular pharmacology 11 17595326
2022 Tunable Action Potential Repolarization Governed by Kv3.4 Channels in Dorsal Root Ganglion Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 10 36198500
2016 Expression of the voltage-gated potassium channel Kv3.4 in oral leucoplakias and oral squamous cell carcinomas. Histopathology 10 26648458
2010 Chronic deficit in the expression of voltage-gated potassium channel Kv3.4 subunit in the hippocampus of pilocarpine-treated epileptic rats. Brain research 10 20971086
1996 Studies on the blocking action of human Kv3.4 inactivation peptide variants in the mouse cloned Kv1.1 K+ channel. The Journal of physiology 7 8910203
2024 Kv3.4 regulates cell migration and invasion through TGF-β-induced epithelial-mesenchymal transition in A549 cells. Scientific reports 6 38280903
2006 [Kv3.4 channel is involved in rat pulmonary vasoconstriction induced by 15-hydroxyeicosatetraenoic acid]. Sheng li xue bao : [Acta physiologica Sinica] 6 16489408
2021 PKCε associates with the Kv3.4 channel to promote its expression in a kinase activity-dependent manner. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 3 33368632
2025 Bisphenol A enhanced cell migration through Kv3.4 in MCF7 cells. Biochemical and biophysical research communications 2 40157292
2025 N-glycosylation modulates the inactivation kinetics of the Kv3.4 ion channel. iScience 1 40995118
2020 Inhibition of overexpressed Kv3.4 augments HPV in endotoxemic mice. BMC pulmonary medicine 1 33032555
2016 [Expression of voltage-gated potassium channel Kv3.4 in oral squamous cell carcinoma]. Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology 1 26980650

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