Affinage

KCND2

A-type voltage-gated potassium channel KCND2 · UniProt Q9NZV8

Length
630 aa
Mass
70.5 kDa
Annotated
2026-04-28
100 papers in source corpus 52 papers cited in narrative 52 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCND2 (Kv4.2) is the principal pore-forming α-subunit of rapidly inactivating, somatodendritic A-type potassium channels in neurons and the fast transient outward current (Ito,f) channel in ventricular cardiomyocytes, serving as a major regulator of dendritic excitability, action potential back-propagation, synaptic plasticity, and cardiac repolarization. Kv4.2 assembles into octameric macromolecular complexes with cytoplasmic KChIP (4:4 stoichiometry) and transmembrane DPP6/DPP10 auxiliary subunits, which together promote ER exit, surface trafficking, unitary conductance, and rapid recovery from inactivation that recapitulates native ISA gating (PMID:14623880, PMID:18364354, PMID:16123112, PMID:12829703). Channel availability is dynamically tuned by phosphorylation at multiple C-terminal sites—ERK (T602/T607/S616), PKA (T38/S552), PKC (S447/S537), CaMKII (S438/S459), and GSK3β (S616)—and by activity-dependent clathrin-mediated internalization requiring NMDA receptor activation and PKA phosphorylation at S552, as well as Pin1-catalyzed prolyl isomerization at pT607 that dissociates the DPP6 complex (PMID:11080179, PMID:10681507, PMID:18650329, PMID:32218435, PMID:32209671). De novo gain-of-function mutations in KCND2 (V404M, S447R) cause epilepsy with autism spectrum features and familial nocturnal paroxysmal atrial fibrillation, respectively (PMID:24501278, PMID:30571183).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1991 High

    Establishing the basic identity of KCND2 as an A-type K+ channel gene resolved which molecular entity produces rapidly inactivating, 4-AP-sensitive currents with cardiac Ito-like properties.

    Evidence Heterologous expression in Xenopus oocytes with two-electrode voltage clamp

    PMID:1722463

    Open questions at the time
    • Native subunit composition unknown
    • Physiological role in neurons vs. heart not yet distinguished
    • Inactivation mechanism (open vs. closed state) not resolved
  2. 1997 High

    Demonstration that Kv4.2 localizes to somatodendritic membranes and that dominant-negative Kv4.2 suppresses neuronal A-current and cardiac Ito established Kv4.2 as the molecular basis of these native currents in both tissues.

    Evidence Immunoelectron microscopy in neurons, adenoviral dominant-negative expression with patch-clamp in cerebellar granule neurons and ventricular myocytes

    PMID:9070739 PMID:9093524 PMID:9395498

    Open questions at the time
    • Auxiliary subunits not yet identified
    • Phosphorylation-dependent regulation unknown
    • Trafficking mechanisms undefined
  3. 2000 High

    Identification of ERK (T602/T607/S616) and PKA (T38/S552) phosphorylation sites, the filamin interaction, and quantitative mRNA–current correlation across neuron types established that Kv4.2 is a convergent signaling target whose expression level directly determines A-current amplitude.

    Evidence In vitro kinase assays, phosphopeptide mapping, phospho-selective antibodies, yeast two-hybrid, co-IP from brain, quantitative single-cell RT-PCR with voltage clamp

    PMID:10632587 PMID:10681507 PMID:11080179 PMID:11102480

    Open questions at the time
    • Functional consequences of each phosphorylation site on channel gating not yet resolved
    • Auxiliary subunit requirement for kinase modulation unknown
    • ER-to-surface trafficking mechanism undefined
  4. 2001 High

    Distinguishing N-terminal-dependent open-state inactivation from a separate closed-state inactivation pathway, and identifying KCNE2/MiRP1 as a modulatory β-subunit, revealed that Kv4.2 uses dual inactivation mechanisms and engages multiple types of auxiliary subunits.

    Evidence N-terminal deletion mutagenesis with kinetic modeling in HEK293 cells; co-IP and dose-dependent gating modulation by KCNE2 in oocytes

    PMID:11375270 PMID:11507158

    Open questions at the time
    • Structural basis of closed-state inactivation not defined
    • Relative contribution of KCNE2 vs. other β-subunits in native tissue unclear
  5. 2003 High

    Discovery that KChIPs form 4:4 octameric complexes with Kv4.2, mask an N-terminal ER-retention signal, and promote surface trafficking resolved how auxiliary subunits control channel biogenesis and established the native channel stoichiometry.

    Evidence Protein purification with amino acid analysis, electron microscopy, surface biotinylation with KChIP1-3 co-expression, N-terminal domain mapping

    PMID:12829703 PMID:14623880

    Open questions at the time
    • DPP stoichiometry and ternary complex architecture not yet determined
    • KChIP4a inhibitory mechanism not fully resolved
  6. 2005 High

    Reconstitution of ternary Kv4.2–KChIP–DPP complexes and genetic knockout studies demonstrated that DPP6/10 contributes the rapid recovery kinetics of native ISA, that Kv4.2 is essential for cardiac Ito,f, and that KChIP stability depends on Kv4.2 expression.

    Evidence Co-IP from brain, ternary co-expression electrophysiology matching native ISA, Kv4.2 KO mouse cardiac and neuronal recordings, KChIP protein quantification in KO

    PMID:16123112 PMID:16251476 PMID:16293790

    Open questions at the time
    • DPP6 stoichiometry in ternary complex not directly measured
    • Mechanism by which DPP accelerates recovery not structurally resolved
  7. 2006 High

    Kv4.2 KO elimination of dendritic A-current in CA1 neurons—with enhanced back-propagating action potentials, increased Ca2+ influx, and lowered LTP threshold—established Kv4.2 as the molecular gatekeeper of dendritic excitability and synaptic plasticity.

    Evidence Kv4.2 KO mice, dendritic patch-clamp, calcium imaging, theta-burst LTP in hippocampal slices

    PMID:17122039

    Open questions at the time
    • Compensatory mechanisms in KO not fully catalogued
    • Spine-specific vs. dendritic shaft contributions not separated
  8. 2007 High

    Discovery of activity-dependent, NMDA-receptor- and clathrin-dependent Kv4.2 internalization from spines during LTP, and SAP97/Kif17-dependent dendritic targeting, revealed that Kv4.2 surface levels are bidirectionally regulated to tune synaptic strength.

    Evidence Live EGFP-Kv4.2 imaging, mEPSC recordings, dominant-negative Kif17, co-IP for SAP97 and Kif17 from brain

    PMID:16257958 PMID:17582333 PMID:17635915

    Open questions at the time
    • Endocytic adaptor proteins linking Kv4.2 to clathrin not identified
    • Ubiquitination or degradation fate of internalized channels not determined
  9. 2008 High

    Identification of PKA-S552 as the required phosphorylation event for activity-driven internalization, determination of 4:4 Kv4.2:DPP6 stoichiometry, and gating-charge immobilization studies linked phosphorylation-controlled trafficking to a defined voltage-sensor desensitization mechanism for closed-state inactivation.

    Evidence S552A mutagenesis with live imaging, tandem-linked subunit electrophysiology and protein purification, gating current measurements in CTX-blocked channels

    PMID:18299396 PMID:18364354 PMID:18650329

    Open questions at the time
    • Structural rearrangement of voltage sensor during CSI not directly observed
    • Interplay between PKA-S552 and KChIP/DPP in internalization not dissected
  10. 2009 High

    PKC phosphorylation sites (S447, S537) were mapped and shown to regulate surface expression and prime ERK phosphorylation, while structure–function analysis of S4-S5 linker and S6 residues defined the electromechanical coupling underlying closed-state inactivation.

    Evidence In vitro kinase assays, sequential kinase cross-talk experiments, alanine-scanning mutagenesis with double-mutant thermodynamic cycles in oocytes, single-channel recordings in DPP6 KO neurons

    PMID:18795890 PMID:19171772 PMID:19279261

    Open questions at the time
    • Atomic-resolution structure of the inactivated state not available
    • PKC-ERK cross-talk not validated in native neurons
  11. 2014 High

    Identification of a de novo V404M mutation causing epilepsy and autism, with gain-of-function slowed inactivation, linked channel gating mechanisms to human neurodevelopmental disease.

    Evidence Whole-exome sequencing in affected twins, heterologous expression electrophysiology of V404M with auxiliary subunits

    PMID:24501278

    Open questions at the time
    • In vivo consequences of V404M in animal models not tested
    • Genotype–phenotype spectrum of KCND2 variants not established
  12. 2018 High

    The S447R gain-of-function mutation causing familial atrial fibrillation disrupts PKC-mediated attenuation of Kv4.2 surface expression, and detailed biophysical analysis of V404M revealed that channel closure is prerequisite for closed-state inactivation, unifying gating and disease mechanisms.

    Evidence Linkage analysis and whole-exome sequencing, oocyte electrophysiology with Kv4.2-Kv4.3 heteromers, detailed kinetic dissection of V404M CSI/OSI

    PMID:29581270 PMID:30571183

    Open questions at the time
    • Structural basis of V404M-induced gate obstruction not resolved at atomic level
    • Penetrance and expressivity of KCND2 cardiac variants in larger cohorts unknown
  13. 2020 High

    Pin1 prolyl isomerase was identified as a signal-dependent disassembly switch for the Kv4.2–DPP6 complex via ERK-phosphorylated T607, and GSK3β was shown to phosphorylate S616 to drive maladaptive plasticity in depression models, revealing kinase-specific channel modulation in behavioral circuits.

    Evidence Kv4.2-T607A knock-in mice with co-IP, electrophysiology, and behavioral testing; AAV-RNAi of GSK3β in nucleus accumbens with electrophysiology and biochemistry

    PMID:32209671 PMID:32218435

    Open questions at the time
    • Pin1-dependent complex disassembly not reconstituted in vitro with purified components
    • How GSK3β accesses Kv4.2 at the membrane is unclear
    • Whether Pin1 and GSK3β pathways interact on the same channel complex is untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • High-resolution structural determination of the full Kv4.2–KChIP–DPP ternary complex, the conformational basis of closed-state inactivation, and genotype-phenotype relationships across the expanding spectrum of KCND2 disease variants remain unresolved.
  • No cryo-EM or crystal structure of ternary Kv4.2–KChIP–DPP complex
  • Mechanism of clathrin adaptor recruitment to internalized Kv4.2 unknown
  • Full spectrum of KCND2 pathogenic variants and disease mechanisms incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5
Localization
GO:0005886 plasma membrane 5 GO:0005829 cytosol 2 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-112316 Neuronal System 4 R-HSA-382551 Transport of small molecules 4
Partners
DLG1DLG4DPP10DPP6FLNAKCNIP2KCNIP3KIF17
Complex memberships
Kv4.2-DPP6 octamer (4:4)Kv4.2-KChIP octamer (4:4)Kv4.2-KChIP-DPP ternary complex

Evidence

Reading pass · 52 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1991 Kv4.2 (RK5) encodes a rapidly inactivating A-type potassium current when expressed in Xenopus oocytes, with kinetics consistent with contribution to cardiac Ito current (activation rise time ~2.8 ms, midpoint ~-1 mV, rapid inactivation with tau 15 and 60 ms, sensitive to 4-AP but not TEA or dendrotoxins). Xenopus oocyte expression with two-electrode voltage clamp FEBS letters High 1722463
1996 4-aminopyridine blocks Kv4.2 exclusively from the closed (resting) state via an intracellular binding site, and channel inactivation and 4-AP binding are mutually exclusive, indicating that the 4-AP binding site is near cytoplasmic domains involved in inactivation. Two-electrode voltage clamp in Xenopus oocytes with pharmacological analysis The Journal of pharmacology and experimental therapeutics High 8930194
1997 Kv4.2 is localized to the somatodendritic membrane of neurons and is concentrated postsynaptically at synaptic contacts in rat supraoptic nucleus, as demonstrated by immunoelectron microscopy. Confocal and immunoelectron microscopy Neuroscience High 9070739
1997 A truncated dominant-negative Kv4.2 construct (Kv4.2ST) suppresses A-type currents in cerebellar granule neurons and Ito in ventricular myocytes when delivered by adenoviral gene transfer, establishing that Kv4 family subunits are the primary contributors to these currents. Dominant-negative adenoviral overexpression in neurons and cardiac myocytes with patch-clamp recording The Journal of biological chemistry High 9395498
1997 Kv4.2 electrophysiological and pharmacological properties (including flecainide sensitivity and rapid recovery from inactivation) closely match native cardiac Ito in rat myocytes, supporting Kv4.2 as a major molecular substrate of cardiac transient outward current. Stable expression in mouse L-cells, whole-cell voltage clamp, pharmacological profiling Cardiovascular research High 9093524
1998 Kv4.2 mRNA is co-expressed with Kv4.1 in neostriatal cholinergic interneurons and Kv4.2 protein is present in somatodendritic membranes; A-type current recovery kinetics match Kv4.2/Kv4.1 channels rather than Kv1.4, indicating Kv4.2-containing channels underlie somatodendritic A-current in these neurons. Single-cell RT-PCR, immunocytochemistry, whole-cell voltage clamp with kinetic analysis The Journal of neuroscience High 9547221
2000 Kv4.2 mRNA abundance is linearly correlated with A-type K+ current amplitude across four neuron types (neostriatal medium spiny neurons, cholinergic interneurons, globus pallidus neurons, basal forebrain cholinergic neurons), establishing Kv4.2 as the major determinant of somatodendritic A-current in these neurons. Quantitative single-cell RT-PCR combined with voltage-clamp analysis The Journal of neuroscience High 10632587
2000 ERK2 directly phosphorylates Kv4.2 at three C-terminal sites: Thr602, Thr607, and Ser616, as identified by in vitro kinase assay and phosphopeptide mapping; ERK-phosphorylated Kv4.2 was confirmed in rat hippocampus using phospho-site-selective antibodies. In vitro kinase assay with GST fusion proteins, phosphopeptide mapping, phospho-selective antibodies in native tissue Journal of neurochemistry High 11080179
2000 PKA directly phosphorylates Kv4.2 at Thr38 (N-terminus) and Ser552 (C-terminus), identified by in vitro kinase assay, phosphopeptide mapping, and confirmed in intact COS-7 cells and hippocampal CA1. In vitro kinase assay with GST-fusion proteins, phosphopeptide mapping, phospho-selective antisera, intact cell PKA stimulation The Journal of biological chemistry High 10681507
2000 Kv4.2 interacts directly with the actin-binding protein filamin via yeast two-hybrid and co-immunoprecipitation from brain; this interaction localizes Kv4.2 to filopodial roots and increases whole-cell current density ~2.7-fold in filamin-positive vs. filamin-negative cells. Yeast two-hybrid, co-immunoprecipitation from brain and in vitro, immunocytochemistry, whole-cell patch clamp in filamin+/- cells The Journal of neuroscience High 11102480
2000 Kv4.2 localizes predominantly to the transverse-axial tubular system (T-tubules) in rat ventricular myocytes, as demonstrated by immunofluorescence and immunogold electron microscopy. Immunofluorescence, immunoelectron microscopy with FluoroNanogold Journal of molecular and cellular cardiology High 10860776
2001 Kv4.2 channel inactivation occurs from both open and pre-open closed states; N-terminal deletion (residues 2-40) slows open-state inactivation components without affecting closed-state inactivation or recovery, indicating the N-terminus contributes to open-state but not closed-state inactivation. Whole-cell patch clamp in HEK293 cells with N-terminal deletion mutants, kinetic modeling The Journal of physiology High 11507158
2001 MiRP1 (KCNE2) co-immunoprecipitates with Kv4.2 and modulates its gating (slows activation and inactivation, shifts voltage dependence positive) in a dose-dependent manner in Xenopus oocytes, suggesting MiRP1 serves as a regulatory beta subunit of cardiac Ito channels. Xenopus oocyte expression, two-electrode voltage clamp, co-immunoprecipitation Circulation research High 11375270
2002 PSD-95 interacts with Kv4.2 via the C-terminal VSAL motif; co-expression of PSD-95 increases surface expression of Kv4.2 and causes its clustering; palmitoylation of PSD-95 is required for these effects. Co-immunoprecipitation in mammalian cells, mutation analysis of VSAL motif, deconvolution microscopy, surface biotinylation assay The Journal of biological chemistry High 11923279
2002 PKA phosphorylation of Kv4.2 alpha-subunit is necessary but not sufficient for channel modulation; association with the ancillary subunit KChIP3 is additionally required for PKA-dependent regulation of Kv4.2 channel properties. Electrophysiology in Xenopus oocytes, PKA stimulation, KChIP3 co-expression, site-directed mutagenesis The Journal of neuroscience High 12451113
2003 KChIP1-3 co-expression with Kv4.2 releases ER retention, promotes surface trafficking, increases steady-state expression, alters phosphorylation, and changes detergent solubility; these effects occur through masking of an N-terminal hydrophobic domain of Kv4.2. KChIP4a does not exert these effects and negatively modulates other KChIPs. Co-expression in heterologous cells, immunocytochemistry, surface biotinylation, biochemical fractionation, phosphorylation analysis The Journal of biological chemistry High 12829703
2003 Kv4.2 and KChIP2 form octameric complexes with 4:4 stoichiometry (4 Kv4.2 and 4 KChIP2 subunits), as determined by purification of native Ito complexes and direct amino acid analysis. Protein purification, electron microscopy, amino acid analysis The Journal of biological chemistry High 14623880
2003 PSD-95 recruits Kv1.4, but not Kv4.2, to lipid rafts via palmitoylation-dependent mechanism; a fraction of native Kv4.2 is found in lipid rafts in rat brain and hippocampal neurons via an alternative PSD-95-independent mechanism. Lipid raft fractionation, lipid raft patching, immunostaining, co-expression in heterologous cells, VSAL deletion mutants The Journal of biological chemistry Medium 14559911
2004 CaMKII directly phosphorylates Kv4.2 at Ser438 and Ser459 in vitro; CaMKII phosphorylation does not alter channel biophysics but increases Kv4.2 protein levels and surface expression, leading to increased A-current amplitude and decreased neuronal excitability in hippocampal neurons. In vitro kinase assay, site-directed mutagenesis, Xenopus oocyte expression, CaMKII overexpression in hippocampal neurons, whole-cell patch clamp The Journal of neuroscience High 15071113
2004 DPP10 co-immunoprecipitates with Kv4.2, enhances surface expression ~5-fold without changing protein levels, and remodels gating kinetics by accelerating inactivation and recovery and shifting conductance-voltage relationship ~19 mV hyperpolarized; the cytoplasmic N-terminal domain of DPP10 determines inactivation acceleration. Co-immunoprecipitation from Xenopus oocytes, two-electrode voltage clamp, domain deletion analysis Biophysical journal High 15454437
2005 Direct ERK/MAPK phosphorylation of Kv4.2 at Thr607 mimics ERK-induced rightward shift in activation and current reduction; this effect requires KChIP3 co-expression. Ser616 phosphorylation produces the opposite gating effect. Site-directed mutagenesis (phosphomimetic T607D, S616D), Xenopus oocyte electrophysiology, co-expression with KChIP3 American journal of physiology. Cell physiology High 16251476
2005 Kv4.2, KChIP3, and DPP10 form ternary macromolecular complexes in rat brain and heterologous cells (confirmed by co-immunoprecipitation); ternary complexes show greatly accelerated recovery from inactivation (~18-26 ms) that matches native ISA, distinct from binary Kv4.2+KChIP3 or Kv4.2+DPP10 channels. Co-immunoprecipitation from rat brain and oocytes, two-electrode voltage clamp in oocytes and CHO cells The Journal of physiology High 16123112
2005 Kv4.2 is transported to dendrites by the kinesin motor Kif17; dominant-negative Kif17 inhibits dendritic localization of endogenous and introduced Kv4.2, while Kv4.2 and Kif17 co-immunoprecipitate from brain and co-localize in cortical neuron dendrites. The interaction occurs through the extreme C-terminus of Kv4.2. Dominant-negative kinesin expression, co-immunoprecipitation from brain and COS cells, immunofluorescence co-localization in cortical neurons The Journal of biological chemistry High 16257958
2005 Targeted deletion of Kv4.2 eliminates fast transient outward current Ito,f in ventricular myocytes; Kv1.4 protein and Ito,s are upregulated compensatorily, while KChIP2 expression is markedly reduced, demonstrating that Kv4.2 is essential for Ito,f generation and that KChIP2 stability depends on Kv4.2. Kv4.2 knockout mice, voltage-clamp recordings from ventricular myocytes, Western blot Circulation research High 16293790
2005 KChIP N-terminus residues 11-23 form a primary interaction site with Kv4.2, the T1 domain provides a secondary site, and C-terminal deletions of Kv4.2 also reduce KChIP binding and functional modulation, revealing a C-terminal interaction site. Lysine-scanning and structure-based mutagenesis of Kv4.2, co-immunoprecipitation, whole-cell patch clamp in mammalian cells The Journal of physiology High 16096338
2006 GRK2 phosphorylates DREAM/KChIP3 at Ser95; the phosphomimetic S95D mutation blocks DREAM-mediated membrane expression of Kv4.2 without affecting channel tetramerization; calcineurin dephosphorylates GRK2-phosphorylated DREAM and its inhibition also blocks Kv4.2 trafficking, establishing a GRK2/calcineurin-dependent regulation of Kv4.2 surface expression via KChIP3. In vitro kinase assay, site-directed mutagenesis (S95D), calcineurin inhibitor treatment, cell surface expression assays The Journal of biological chemistry High 17102134
2006 Deletion of Kv4.2 eliminates dendritic A-type K+ current in CA1 pyramidal neurons nearly completely, increases backpropagating action potential amplitude and Ca2+ influx, and lowers the threshold for LTP induction with theta burst pairing, establishing Kv4.2 as the molecular substrate of dendritic A-current that regulates synaptic plasticity. Kv4.2 knockout mice, dendritic patch-clamp recordings, calcium imaging, LTP induction The Journal of neuroscience High 17122039
2006 In Kv4.2 knockout mice, KChIP expression is regionally and cell-specifically reduced in proportion to the normal Kv4.2 expression level, demonstrating reciprocal Kv4.2-dependent stabilization of KChIP auxiliary subunits. Immunohistochemistry in Kv4.2 KO vs. wild-type brains The Journal of neuroscience High 17122038
2007 Kv4.2 undergoes activity-dependent internalization in hippocampal spines and dendrites upon glutamate receptor stimulation; this internalization is clathrin-mediated, requires NMDA receptor activation and Ca2+ influx. LTP induction causes synaptic GluR1-AMPAR insertion concurrent with Kv4.2 internalization. Live imaging of EGFP-Kv4.2 in hippocampal neurons, electrophysiology (mEPSC recordings), LTP induction in slice cultures Neuron High 17582333
2007 SAP97 interacts with Kv4.2 via its PDZ domains and the intact C-terminus of Kv4.2; SAP97 directs Kv4.2 to dendritic spines (PSD fraction); CaMKII-dependent phosphorylation of SAP97 regulates this Kv4.2 targeting to spines. Co-immunoprecipitation, subcellular fractionation, lentiviral RNAi of SAP97, pharmacological SAP97 translocation in hippocampal neurons The Journal of biological chemistry High 17635915
2007 mGlu5 activation leads to ERK-mediated phosphorylation of Kv4.2 at Ser616, inhibiting A-type K+ currents and increasing dorsal horn neuronal excitability; Kv4.2 knockout mice show impaired nociceptive behavior after spinal group I mGluR activation, establishing Kv4.2 as a downstream effector of mGlu5-ERK signaling in nociception. Electrophysiology in dorsal horn neurons, site-directed mutagenesis of S616, Kv4.2 KO mice, behavioral nociception assays The Journal of neuroscience High 18045912
2008 PKA activation induces Kv4.2 internalization from dendritic spines; PKA inhibition prevents AMPA-induced internalization; a point mutation at the C-terminal PKA phosphorylation site S552A prevents AMPA-induced internalization of Kv4.2, establishing S552 as required for PKA-dependent activity-driven trafficking. Live imaging in hippocampal neurons, pharmacological PKA activation/inhibition, point mutation S552A The Journal of neuroscience High 18650329
2008 Kv4.2 deletion eliminates IA in cortical pyramidal neurons, accompanied by loss of KChIP3 protein (degraded without Kv4.2) and upregulation of IK and Iss densities (electrical remodeling), but without change in action potential waveform. Kv4.2 KO mice, whole-cell voltage clamp of cortical neurons, Western blot The Journal of physiology High 18187474
2008 Kv4.2 ISA channels are complexes of four Kv4.2 and four DPP6 subunits (4:4 stoichiometry), established by tandem-linked subunit biophysics and direct amino acid analysis of purified complexes. Tandem-linked subunit expression, electrophysiology, protein purification and amino acid analysis The Journal of biological chemistry High 18364354
2008 Ternary Kv4.2+KChIP1+DPPX-S channels reconstitute the voltage-dependent slowing of inactivation rate (characteristic of native ISA in cerebellar granule neurons) through a mechanism of preferential closed-state inactivation and weakly voltage-dependent opening, as shown by quantitative kinetic modeling. Whole-cell patch clamp in heterologous cells, native neuron recordings, global kinetic modeling The Journal of physiology High 18276729
2008 Gating charge (Q) immobilization in Kv4.2 occurs over hyperpolarized voltages that do not open channels, with kinetics and voltage dependence paralleling closed-state inactivation; Q-immobilization and closed-state inactivation are two manifestations of the same process involving desensitization of voltage sensors. Gating current measurements in CTX-blocked Kv4.2 channels in Xenopus oocytes, coupled state modeling The Journal of general physiology High 18299396
2009 PKC directly phosphorylates Kv4.2 at Ser447 and Ser537 on the C-terminus; mutation of both sites to alanine increases surface expression; PKC phosphorylation at Ser537 (within an ERK docking domain) enhances subsequent ERK phosphorylation of Kv4.2, establishing Kv4.2 as a locus for PKC-ERK cross-talk. In vitro kinase assay with GST fusion proteins, phospho-site antibody, surface biotinylation, electrophysiology, sequential kinase assay The Biochemical journal High 18795890
2009 S4-S5 linker and S6 residues Glu323 and Val404 are critical for both voltage-dependent gate opening and closed-state inactivation in Kv4.2 channels; double-mutant cycle analysis and redox modulation of cysteine double mutants confirm dynamic coupling between voltage sensor and cytoplasmic gate underlies closed-state inactivation. Alanine-scanning mutagenesis, double-mutant cycle analysis, cysteine-substitution redox modulation, two-electrode voltage clamp in Xenopus oocytes The Journal of general physiology High 19171772
2009 DPP6-S is necessary and sufficient to increase the unitary conductance of neuronal Kv4.2 channels from ~4 pS to ~7.5 pS (matching native CGN channels); CGN Kv4 channels from dpp6 KO mice show reduced conductance; two N-terminal acidic residues of DPP6-S mediate this effect via electrostatic interactions. Single-channel recordings from heterologous cells and CGNs, dpp6 KO mice, charge neutralization mutagenesis of DPP6-S The Journal of neuroscience High 19279261
2010 KChIP4a requires PKA phosphorylation of Kv4.2 at S552 to produce enhanced stabilization and membrane expression of Kv4.2, while other KChIP isoforms (KChIP1-3) enhance surface expression independently of S552 phosphorylation; A-kinase anchoring proteins (AKAPs) bind Kv4.2, enabling local PKA signaling. Co-expression in heterologous cells, surface biotinylation, S552A/D mutagenesis, co-immunoprecipitation for AKAP interaction Molecular and cellular neurosciences High 20045463
2010 CaV3.1 (T-type calcium channel) associates with the Kv4.2 complex (Kv4.2-KChIP3-DPP10c) and mediates calcium-dependent rightward shift in Kv4.2 inactivation voltage; this regulation is selective for CaV3 isoforms and not observed with CaV1.4, CaV2.1, or CaV2.3. Co-expression in heterologous cells, electrophysiology measuring inactivation voltage shift Channels Medium 20458163
2010 NR2B-containing (extrasynaptic) NMDA receptors mediate glutamate-induced reduction of total Kv4.2 protein and Kv4.2 clusters; Ca2+ influx is required; calpain proteolysis underlies Kv4.2 protein reduction, as calpain inhibitors prevent this effect. Pharmacological dissection with NR2B-selective antagonists and calpain inhibitors, immunocytochemistry, patch-clamp in cultured hippocampal neurons Neuroscience High 19857555
2012 DPP6 and DPP10 independently stabilize surface Kv4.2 protein without affecting DPP protein levels themselves; KChIP3 addition to DPP10+Kv4.2 further increases total and surface Kv4.2; DPP6/10 expression and localization are independent of Kv4 alpha-subunits. Heterologous co-expression, surface biotinylation, Kv4.2/Kv4.3 KO mouse brain Western blot, cell surface immunostaining The Journal of biological chemistry High 22311982
2014 A de novo missense mutation V404M (Val404Met) in KCND2 causes significantly slowed Kv4.2 inactivation (dominant effect) and impairs closed-state inactivation in the presence of auxiliary subunits, consistent with gain-of-function causing epilepsy and autism in affected twins. Whole-exome sequencing, heterologous expression electrophysiology of WT and mutant Kv4.2 in Xenopus oocytes, co-expression with auxiliary subunits Human molecular genetics High 24501278
2015 H2S inhibits Ito by targeting the Cys320/Cys529 disulfide bridge in Kv4.2; mutation of either cysteine blocks H2S-mediated inhibition; H2S breaks an existing disulfide bond without modifying single free cysteines. Mutagenesis of Cys320 and Cys529, whole-cell patch clamp in cardiomyocytes, H2S pharmacology Antioxidants & redox signaling High 25756524
2016 miR-324-5p directly binds KCND2 mRNA and inhibits Kv4.2 protein expression; antagonizing miR-324-5p is neuroprotective, seizure-suppressive, and blocks kainic-acid-induced Kv4.2 reduction in vitro and in vivo; these effects are absent in Kcnd2 KO mice, confirming specificity. RNA-induced silencing complex pulldown, miRNA mimic/antagonist transfection, luciferase reporter assay, in vivo miRNA antagonist injection, Kcnd2 KO mice Cell reports High 27681419
2018 The autism/epilepsy mutation V404M (Kv4.2) enhances closed-state inactivation (increases inactivated state stability) while dramatically impairing open-state inactivation by slowing channel closure; larger methionine volume is a key mechanistic factor; this reveals that channel closure is required for closed-state inactivation. Whole-cell patch clamp of WT and V404M Kv4.2 in heterologous cells, detailed kinetic analysis of CSI and OSI PNAS High 29581270
2018 A gain-of-function mutation S447R in KCND2 causes nocturnal paroxysmal atrial fibrillation; S447 is a PKC phosphorylation site that normally attenuates Kv4.2 membrane expression; the S447R mutant shows impaired response to PKC and augmented membrane expression; the mutation also exerts gain-of-function in Kv4.2-Kv4.3 heterotetramers. Xenopus oocyte electrophysiology, Kv4.2-Kv4.3 hybrid channel expression, linkage analysis, whole-exome sequencing Circulation. Genomic and precision medicine High 30571183
2020 Activity-induced ERK phosphorylation of Kv4.2 at pThr607-Pro triggers Pin1 binding and isomerization of Kv4.2, causing dissociation of the Kv4.2-DPP6 complex; Kv4.2-TA (T607A knock-in) mice show altered Kv4.2-DPP6 interaction, increased A-type K+ current, reduced hippocampal neuronal excitability, and improved reversal learning. Kv4.2-T607A knock-in mouse model, co-immunoprecipitation for Pin1 and DPP6 interaction, whole-cell patch clamp in CA1 neurons, behavioral testing Nature communications High 32218435
2020 GSK3β directly phosphorylates Kv4.2 at Ser616 in nucleus accumbens medium spiny neurons, inhibiting A-type K+ channel function and driving tLTP changes in a chronic stress depression model; GSK3β knockdown or Kv4.2-S616 phosphorylation blockade prevents maladaptive plasticity. In vivo AAV-RNAi knockdown of GSK3β, electrophysiology, immunohistochemistry, biochemistry, pharmacological Kv4.2 channel inhibition in mouse NAc PNAS High 32209671
2006 DPPX-S (DPP6) remodels gating charge dynamics in Kv4.2 channels by causing a -26 mV parallel shift in the Q-V relationship and accelerating both outward and return gating charge movements; this effect is absent in Shaker B channels, indicating DPPX-S specifically destabilizes resting and intermediate activation states in Kv4.2. Gating current measurements in CTX-blocked Kv4.2 channels in Xenopus oocytes, co-expression with DPPX-S The Journal of general physiology High 17130523
1999 Kvbeta1.2 co-expression with Kv4.2 in HEK293 cells confers oxygen/redox sensitivity to Kv4.2 channels (but not to Shaker), enabling inhibition by hypoxia, DTT, and DTDP; the O2 sensitivity is membrane-delimited and involves a hemoprotein O2 sensor. Heterologous co-expression in HEK293 cells, whole-cell patch clamp under hypoxia and redox agents, excised patch recordings The Journal of general physiology High 10352037

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Regulation of dendritic excitability by activity-dependent trafficking of the A-type K+ channel subunit Kv4.2 in hippocampal neurons. Neuron 276 17582333
2006 Deletion of Kv4.2 gene eliminates dendritic A-type K+ current and enhances induction of long-term potentiation in hippocampal CA1 pyramidal neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 270 17122039
2012 Encephalitis and antibodies to dipeptidyl-peptidase-like protein-6, a subunit of Kv4.2 potassium channels. Annals of neurology 251 23225603
2003 A fundamental role for KChIPs in determining the molecular properties and trafficking of Kv4.2 potassium channels. The Journal of biological chemistry 217 12829703
2000 The A-type potassium channel Kv4.2 is a substrate for the mitogen-activated protein kinase ERK. Journal of neurochemistry 214 11080179
1998 Somatodendritic depolarization-activated potassium currents in rat neostriatal cholinergic interneurons are predominantly of the A type and attributable to coexpression of Kv4.2 and Kv4.1 subunits. The Journal of neuroscience : the official journal of the Society for Neuroscience 187 9547221
2005 ERK/MAPK regulates the Kv4.2 potassium channel by direct phosphorylation of the pore-forming subunit. American journal of physiology. Cell physiology 145 16251476
2001 minK-related peptide 1 associates with Kv4.2 and modulates its gating function: potential role as beta subunit of cardiac transient outward channel? Circulation research 144 11375270
1997 Suppression of neuronal and cardiac transient outward currents by viral gene transfer of dominant-negative Kv4.2 constructs. The Journal of biological chemistry 142 9395498
2000 Kv4.2 mRNA abundance and A-type K(+) current amplitude are linearly related in basal ganglia and basal forebrain neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 141 10632587
2004 Calcium-calmodulin-dependent kinase II modulates Kv4.2 channel expression and upregulates neuronal A-type potassium currents. The Journal of neuroscience : the official journal of the Society for Neuroscience 136 15071113
1999 Kvbeta1.2 subunit coexpression in HEK293 cells confers O2 sensitivity to kv4.2 but not to Shaker channels. The Journal of general physiology 129 10352037
2005 Targeted deletion of Kv4.2 eliminates I(to,f) and results in electrical and molecular remodeling, with no evidence of ventricular hypertrophy or myocardial dysfunction. Circulation research 128 16293790
2004 Modulation of Kv4.2 channel expression and gating by dipeptidyl peptidase 10 (DPP10). Biophysical journal 117 15454437
2005 Multiprotein assembly of Kv4.2, KChIP3 and DPP10 produces ternary channel complexes with ISA-like properties. The Journal of physiology 115 16123112
2000 Localization and enhanced current density of the Kv4.2 potassium channel by interaction with the actin-binding protein filamin. The Journal of neuroscience : the official journal of the Society for Neuroscience 115 11102480
2001 Kinetic analysis of open- and closed-state inactivation transitions in human Kv4.2 A-type potassium channels. The Journal of physiology 109 11507158
2000 Kv4.2 phosphorylation by cyclic AMP-dependent protein kinase. The Journal of biological chemistry 108 10681507
2007 Metabotropic glutamate receptor 5 modulates nociceptive plasticity via extracellular signal-regulated kinase-Kv4.2 signaling in spinal cord dorsal horn neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 100 18045912
2006 A Kv4.2 truncation mutation in a patient with temporal lobe epilepsy. Neurobiology of disease 98 16934482
2001 Hippocampal heterotopia lack functional Kv4.2 potassium channels in the methylazoxymethanol model of cortical malformations and epilepsy. The Journal of neuroscience : the official journal of the Society for Neuroscience 98 11517252
1997 Electrophysiological and pharmacological correspondence between Kv4.2 current and rat cardiac transient outward current. Cardiovascular research 92 9093524
2014 Exome sequencing identifies de novo gain of function missense mutation in KCND2 in identical twins with autism and seizures that slows potassium channel inactivation. Human molecular genetics 91 24501278
2003 Differential recruitment of Kv1.4 and Kv4.2 to lipid rafts by PSD-95. The Journal of biological chemistry 90 14559911
1997 Decreased expression of Kv4.2 and novel Kv4.3 K+ channel subunit mRNAs in ventricles of renovascular hypertensive rats. Circulation research 90 9314834
1999 Regional contributions of Kv1.4, Kv4.2, and Kv4.3 to transient outward K+ current in rat ventricle. The American journal of physiology 88 10330244
1997 Clustering of KV4.2 potassium channels in postsynaptic membrane of rat supraoptic neurons: an ultrastructural study. Neuroscience 88 9070739
2005 A role for Kif17 in transport of Kv4.2. The Journal of biological chemistry 85 16257958
2002 PKA modulation of Kv4.2-encoded A-type potassium channels requires formation of a supramolecular complex. The Journal of neuroscience : the official journal of the Society for Neuroscience 81 12451113
2008 Electrical remodelling maintains firing properties in cortical pyramidal neurons lacking KCND2-encoded A-type K+ currents. The Journal of physiology 76 18187474
2008 Protein kinase a mediates activity-dependent Kv4.2 channel trafficking. The Journal of neuroscience : the official journal of the Society for Neuroscience 74 18650329
2016 MicroRNA-Mediated Downregulation of the Potassium Channel Kv4.2 Contributes to Seizure Onset. Cell reports 73 27681419
2008 Ternary Kv4.2 channels recapitulate voltage-dependent inactivation kinetics of A-type K+ channels in cerebellar granule neurons. The Journal of physiology 70 18276729
2006 Differential expression of I(A) channel subunits Kv4.2 and Kv4.3 in mouse visual cortical neurons and synapses. The Journal of neuroscience : the official journal of the Society for Neuroscience 69 17122053
2000 Input-specific immunolocalization of differentially phosphorylated Kv4.2 in the mouse brain. Learning & memory (Cold Spring Harbor, N.Y.) 67 11040264
2008 Altered phosphorylation and localization of the A-type channel, Kv4.2 in status epilepticus. Journal of neurochemistry 65 18513371
2002 Cell surface targeting and clustering interactions between heterologously expressed PSD-95 and the Shal voltage-gated potassium channel, Kv4.2. The Journal of biological chemistry 64 11923279
2009 Kv4.2 knockout mice demonstrate increased susceptibility to convulsant stimulation. Epilepsia 62 19453702
2006 Unanticipated region- and cell-specific downregulation of individual KChIP auxiliary subunit isotypes in Kv4.2 knock-out mouse brain. The Journal of neuroscience : the official journal of the Society for Neuroscience 62 17122038
1991 Functional characterization of RK5, a voltage-gated K+ channel cloned from the rat cardiovascular system. FEBS letters 61 1722463
2010 Molecular dissection of I(A) in cortical pyramidal neurons reveals three distinct components encoded by Kv4.2, Kv4.3, and Kv1.4 alpha-subunits. The Journal of neuroscience : the official journal of the Society for Neuroscience 57 20371829
2016 MiR-223-3p as a Novel MicroRNA Regulator of Expression of Voltage-Gated K+ Channel Kv4.2 in Acute Myocardial Infarction. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 53 27322747
2003 Ito channels are octomeric complexes with four subunits of each Kv4.2 and K+ channel-interacting protein 2. The Journal of biological chemistry 53 14623880
2006 G protein-coupled receptor kinase 2-mediated phosphorylation of downstream regulatory element antagonist modulator regulates membrane trafficking of Kv4.2 potassium channel. The Journal of biological chemistry 52 17102134
2005 Contribution of N- and C-terminal Kv4.2 channel domains to KChIP interaction [corrected]. The Journal of physiology 52 16096338
2012 Kv4.2 knockout mice have hippocampal-dependent learning and memory deficits. Learning & memory (Cold Spring Harbor, N.Y.) 50 22505720
2002 Prevention of hypertrophy by overexpression of Kv4.2 in cultured neonatal cardiomyocytes. Circulation 50 12403671
2012 Neuritin activates insulin receptor pathway to up-regulate Kv4.2-mediated transient outward K+ current in rat cerebellar granule neurons. The Journal of biological chemistry 49 23066017
2006 Differential modulation of Kv4.2 and Kv4.3 channels by calmodulin-dependent protein kinase II in rat cardiac myocytes. American journal of physiology. Heart and circulatory physiology 49 16648177
1999 Characterization of human Kv4.2 mediating a rapidly-inactivating transient voltage-sensitive K+ current. Receptors & channels 47 10551270
1996 Reverse use dependence of Kv4.2 blockade by 4-aminopyridine. The Journal of pharmacology and experimental therapeutics 47 8930194
2009 Dynamic coupling of voltage sensor and gate involved in closed-state inactivation of kv4.2 channels. The Journal of general physiology 46 19171772
2009 The dipeptidyl-peptidase-like protein DPP6 determines the unitary conductance of neuronal Kv4.2 channels. The Journal of neuroscience : the official journal of the Society for Neuroscience 44 19279261
2014 Evaluation of genes encoding for the transient outward current (Ito) identifies the KCND2 gene as a cause of J-wave syndrome associated with sudden cardiac death. Circulation. Cardiovascular genetics 43 25214526
2013 MicroRNA-301a mediated regulation of Kv4.2 in diabetes: identification of key modulators. PloS one 43 23573265
2012 Differential dorso-ventral distributions of Kv4.2 and HCN proteins confer distinct integrative properties to hippocampal CA1 pyramidal cell distal dendrites. The Journal of biological chemistry 42 22511771
2006 Calcineurin increases cardiac transient outward K+ currents via transcriptional up-regulation of Kv4.2 channel subunits. The Journal of biological chemistry 42 17060317
2011 Unique somato-dendritic distribution pattern of Kv4.2 channels on hippocampal CA1 pyramidal cells. The European journal of neuroscience 41 22098631
2007 SAP97 directs the localization of Kv4.2 to spines in hippocampal neurons: regulation by CaMKII. The Journal of biological chemistry 41 17635915
2008 Gating charge immobilization in Kv4.2 channels: the basis of closed-state inactivation. The Journal of general physiology 39 18299396
2000 Voltage-gated K(+)Channel, Kv4.2, localizes predominantly to the transverse-axial tubular system of the rat myocyte. Journal of molecular and cellular cardiology 39 10860776
1998 Regulation of Kv4.2 and Kv1.4 K+ channel expression by myocardial hypertrophic factors in cultured newborn rat ventricular cells. Journal of molecular and cellular cardiology 39 9710812
2018 Kv4.2 autism and epilepsy mutation enhances inactivation of closed channels but impairs access to inactivated state after opening. Proceedings of the National Academy of Sciences of the United States of America 38 29581270
2010 KChIP4a regulates Kv4.2 channel trafficking through PKA phosphorylation. Molecular and cellular neurosciences 37 20045463
2020 Activity-dependent isomerization of Kv4.2 by Pin1 regulates cognitive flexibility. Nature communications 36 32218435
2011 Metabotropic glutamate receptor 5 regulates excitability and Kv4.2-containing K⁺ channels primarily in excitatory neurons of the spinal dorsal horn. Journal of neurophysiology 36 21451053
2010 Regulation of the KV4.2 complex by CaV3.1 calcium channels. Channels (Austin, Tex.) 36 20458163
2006 A dipeptidyl aminopeptidase-like protein remodels gating charge dynamics in Kv4.2 channels. The Journal of general physiology 36 17130523
2009 Kv4.2 is a locus for PKC and ERK/MAPK cross-talk. The Biochemical journal 35 18795890
2003 GATA and FOG2 transcription factors differentially regulate the promoter for Kv4.2 K(+) channel gene in cardiac myocytes and PC12 cells. Cardiovascular research 35 14613857
2001 Different effects of the Ca(2+)-binding protein, KChIP1, on two Kv4 subfamily members, Kv4.1 and Kv4.2. FEBS letters 34 11423117
1999 Expression of Kv3.1 and Kv4.2 genes in developing cerebellar granule cells. Developmental neuroscience 34 10449980
2020 Chronic mild stress alters synaptic plasticity in the nucleus accumbens through GSK3β-dependent modulation of Kv4.2 channels. Proceedings of the National Academy of Sciences of the United States of America 33 32209671
2003 Dihydropyridine Ca2+ channel antagonists and agonists block Kv4.2, Kv4.3 and Kv1.4 K+ channels expressed in HEK293 cells. British journal of pharmacology 33 12788813
2009 Expression and localization of voltage dependent potassium channel Kv4.2 in epilepsy associated focal lesions. Neurobiology of disease 32 19596445
2008 I SA channel complexes include four subunits each of DPP6 and Kv4.2. The Journal of biological chemistry 32 18364354
2016 Neuritin Up-regulates Kv4.2 α-Subunit of Potassium Channel Expression and Affects Neuronal Excitability by Regulating the Calcium-Calcineurin-NFATc4 Signaling Pathway. The Journal of biological chemistry 31 27307045
2008 Interaction between transcription factors Iroquois proteins 4 and 5 controls cardiac potassium channel Kv4.2 gene transcription. Cardiovascular research 31 18815185
1997 Kainic acid-induced generalized seizures alter the regional hippocampal expression of the rat Kv4.2 potassium channel gene. Neuroscience letters 31 9302094
2019 Expression, Cellular and Subcellular Localisation of Kv4.2 and Kv4.3 Channels in the Rodent Hippocampus. International journal of molecular sciences 29 30634540
2013 Neuregulin-1/ErbB4 signaling regulates Kv4.2-mediated transient outward K+ current through the Akt/mTOR pathway. American journal of physiology. Cell physiology 29 23703525
2004 Mossy fibre contact triggers the targeting of Kv4.2 potassium channels to dendrites and synapses in developing cerebellar granule neurons. Journal of neurochemistry 29 15140189
2003 Quantitative relationship between Kv4.2 mRNA and A-type K+ current in rat striatal cholinergic interneurons during development. Journal of neurophysiology 29 12843309
2018 Basal Ganglia Neuromodulation Over Multiple Temporal and Structural Scales-Simulations of Direct Pathway MSNs Investigate the Fast Onset of Dopaminergic Effects and Predict the Role of Kv4.2. Frontiers in neural circuits 28 29467627
2012 Augmentation of Kv4.2-encoded currents by accessory dipeptidyl peptidase 6 and 10 subunits reflects selective cell surface Kv4.2 protein stabilization. The Journal of biological chemistry 28 22311982
2009 Arachidonic acid potently inhibits both postsynaptic-type Kv4.2 and presynaptic-type Kv1.4 IA potassium channels. The European journal of neuroscience 28 19453640
2010 Downregulation of Kv4.2 channels mediated by NR2B-containing NMDA receptors in cultured hippocampal neurons. Neuroscience 27 19857555
2015 Convergent phosphomodulation of the major neuronal dendritic potassium channel Kv4.2 by pituitary adenylate cyclase-activating polypeptide. Neuropharmacology 26 26456351
2014 Type 2 diabetes induces subendocardium-predominant reduction in transient outward K+ current with downregulation of Kv4.2 and KChIP2. American journal of physiology. Heart and circulatory physiology 26 24486512
2010 High-mobility group box 1 (HMGB1) downregulates cardiac transient outward potassium current (Ito) through downregulation of Kv4.2 and Kv4.3 channel transcripts and proteins. Journal of molecular and cellular cardiology 26 20483361
2006 Pituitary adenylate cyclase activating polypeptide reduces expression of Kv1.4 and Kv4.2 subunits underlying A-type K(+) current in adult mouse olfactory neuroepithelia. Neuroscience 26 16426762
2004 Modulation of Kv4.2 channels by a peptide isolated from the venom of the giant bird-eating tarantula Theraphosa leblondi. Toxicon : official journal of the International Society on Toxinology 26 15208026
2018 Nocturnal Atrial Fibrillation Caused by Mutation in KCND2, Encoding Pore-Forming (α) Subunit of the Cardiac Kv4.2 Potassium Channel. Circulation. Genomic and precision medicine 25 30571183
2015 Hydrogen Sulfide Targets the Cys320/Cys529 Motif in Kv4.2 to Inhibit the Ito Potassium Channels in Cardiomyocytes and Regularizes Fatal Arrhythmia in Myocardial Infarction. Antioxidants & redox signaling 25 25756524
2008 Regulation of Kv4.2 channels by glutamate in cultured hippocampal neurons. Journal of neurochemistry 25 18363830
2009 Convergent modulation of Kv4.2 channel alpha subunits by structurally distinct DPPX and KChIP auxiliary subunits. Biochemistry 24 19441798
2021 Long noncoding RNA FAM66C promotes tumor progression and glycolysis in intrahepatic cholangiocarcinoma by regulating hsa-miR-23b-3p/KCND2 axis. Environmental toxicology 23 34418280
2018 Saikosaponin A modulates remodeling of Kv4.2-mediated A-type voltage-gated potassium currents in rat chronic temporal lobe epilepsy. Drug design, development and therapy 23 30254424
2007 Role of N-terminal domain and accessory subunits in controlling deactivation-inactivation coupling of Kv4.2 channels. Biophysical journal 23 17981906
2003 Increased focal Kv4.2 channel expression at the plasma membrane is the result of actin depolymerization. American journal of physiology. Heart and circulatory physiology 23 14551056