Affinage

KCNA2

Potassium voltage-gated channel subfamily A member 2 · UniProt P16389

Length
499 aa
Mass
56.7 kDa
Annotated
2026-04-28
100 papers in source corpus 41 papers cited in narrative 41 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCNA2 encodes Kv1.2, a voltage-gated potassium channel that functions as a central regulator of neuronal excitability across diverse brain circuits, controlling presynaptic terminal firing fidelity, dendritic integration, intrinsic plasticity, dopaminergic neurotransmission, and sleep architecture. Structural studies reveal that independent voltage-sensing domains transduce membrane potential changes through S4–S5 linker helices to gate the pore, with gating charge contributed predominantly by the outermost S4 arginine and a unique bimodal (fast/slow) activation property conferred by residues in the S2–S3 linker (PMID:16002579, PMID:17766348, PMID:39945513). Channel surface expression is dynamically regulated by a convergent set of post-translational mechanisms—tyrosine phosphorylation (modulated by RPTPα and cortactin interaction with the cytoskeleton), PKA phosphorylation at Ser-449/Ser-440/Ser-441, N-glycosylation-dependent ER export, and interactions with Slc7a5 and sigma-1 receptor—that collectively tune Kv1.2-mediated K⁺ current amplitude through endocytic trafficking and gating modulation (PMID:9878055, PMID:12151401, PMID:18056633, PMID:19389710, PMID:30356053, PMID:23332758). De novo KCNA2 mutations cause epileptic encephalopathy through either loss-of-function (dominant-negative current reduction) or gain-of-function (constitutively open channels) mechanisms (PMID:25751627), and nerve injury–induced epigenetic silencing of Kcna2 by DNMT3a, DNMT1, G9a, MBD1, and a natural antisense lncRNA in dorsal root ganglion neurons reduces Kv1.2 current, increases excitability, and drives neuropathic pain (PMID:23792947, PMID:28270689, PMID:31182635).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1994 High

    Establishing where Kv1.2 protein resides in the nervous system was prerequisite to understanding its functional roles; immunolocalization revealed differential subcellular targeting—synaptic terminals, juxta-paranodes, dendrites—varying by neuronal type, implying participation in distinct heteromultimeric complexes at each site.

    Evidence Immunocytochemistry and subcellular fractionation across mouse and rat brain regions

    PMID:8046438 PMID:8158277

    Open questions at the time
    • Identity of heteromultimeric partners at each subcellular site was not determined
    • Mechanism directing polarized trafficking to specific compartments was unknown
  2. 1999 High

    The question of how GPCR signaling suppresses Kv1.2 was answered by showing that RPTPα directly binds Kv1.2, counteracts tyrosine-kinase-mediated phosphorylation and current suppression, and is recruited to Kv1.2 in an m1 muscarinic receptor–dependent manner, establishing a phosphorylation-based regulatory axis.

    Evidence Co-immunoprecipitation, in vitro binding, Xenopus oocyte electrophysiology

    PMID:9878055

    Open questions at the time
    • Identity of the tyrosine kinase phosphorylating Kv1.2 in this pathway was not established
    • Specific phosphorylated tyrosine residues on Kv1.2 were not mapped
  3. 2002 High

    Discovery that cortactin physically links Kv1.2 to the actin cytoskeleton—and that tyrosine phosphorylation disrupts this interaction—resolved how cytoskeletal association controls channel current magnitude and laid the groundwork for understanding phosphorylation-triggered endocytosis.

    Evidence Purified recombinant binding assays, co-immunoprecipitation, mutagenesis, electrophysiology in HEK293 cells; later confirmed by FRET, cortactin domain mutagenesis, and endocytosis assays

    PMID:12151401 PMID:17959782

    Open questions at the time
    • Structural basis of the cortactin–Kv1.2 interface was not determined
    • Role of Arp2/3-mediated actin remodeling versus simple anchoring in endocytosis was not fully separated
  4. 2003 High

    Selective toxin dissection at the calyx of Held and in striatal neurons demonstrated that Kv1.2 homomers carry the majority of low-threshold presynaptic K⁺ current and suppress terminal hyperexcitability, establishing a specific physiological function for Kv1.2 at defined synapses.

    Evidence Tityustoxin-Kα and DTX-K pharmacology combined with paired pre/postsynaptic recordings (calyx) and whole-cell recordings (striatal neurons)

    PMID:12777451 PMID:13679409

    Open questions at the time
    • Contribution of heteromeric Kv1.2-containing channels versus homomers at these synapses was only partially resolved
    • Mechanisms regulating Kv1.2 density at the presynaptic transition zone were unknown
  5. 2005 High

    The 2.9 Å crystal structure of Kv1.2 resolved a long-standing debate about voltage-sensor topology by showing voltage-sensing domains as modular peripheral units connected to the pore through S4–S5 linker helices, with conserved S4 arginines positioned at the protein–lipid interface.

    Evidence X-ray crystallography of full-length Kv1.2

    PMID:16002579

    Open questions at the time
    • Only the open-state structure was captured; closed- and inactivated-state conformations were unknown
    • Lipid interactions were modeled but not directly resolved
  6. 2007 High

    A cluster of discoveries defined how post-translational modifications control Kv1.2 trafficking: C-terminal phosphorylation at S440/S441 (identified by MS across three species) marks post-ER channels for surface delivery; N-glycosylation promotes ER exit and modulates gating; PKA and cAMP pathways bidirectionally regulate surface expression through endocytosis and turnover.

    Evidence Tandem MS phosphoproteomics, site-directed mutagenesis, cell-surface biotinylation, glycosylation-site mutagenesis, pharmacological dissection of cAMP/PKA pathways

    PMID:17324383 PMID:18003609 PMID:18056633

    Open questions at the time
    • The kinase responsible for S440/S441 phosphorylation was not identified
    • How glycosylation and phosphorylation signals are coordinated was not addressed
  7. 2007 High

    Identification of bimodal (fast/slow) activation gating unique to Kv1.2 and mapping of the gating-mode switch to a charge at T252 in the S2–S3 linker revealed an intrinsic regulatory mechanism modifiable by cytoplasmic factors, distinguishing Kv1.2 from other Kv1 channels.

    Evidence Chimeric channel construction, site-directed mutagenesis, excised-patch electrophysiology in HEK293 cells

    PMID:17766348

    Open questions at the time
    • The identity of the endogenous cytoplasmic regulator switching gating mode was not determined
    • Structural basis of the two gating conformations was not resolved
  8. 2009 High

    PKA phosphorylation of Kv1.2 was mapped to Ser-449 by mass spectrometry and mutagenesis, with functional electrophysiology showing this modification increases current amplitude, providing a molecular mechanism for vasodilatory agonist modulation of Kv1 channels.

    Evidence In vitro kinase assay, MALDI-TOF MS/MS, site-directed mutagenesis, whole-cell and inside-out patch clamp

    PMID:19389710

    Open questions at the time
    • Whether S449 phosphorylation operates in vascular smooth muscle in vivo was not confirmed
    • Cross-talk between S449 and the S440/S441 phosphorylation cluster was only partially explored
  9. 2011 High

    D2 dopamine autoreceptor activation was shown to increase Kv1.2 current via Gβγ signaling, with physical association between D2-AR and Kv1.2 in striatum; Kv1.2 KO attenuated D2-AR-mediated inhibition of dopamine overflow, establishing Kv1.2 as a downstream effector of presynaptic dopamine autoreceptor signaling.

    Evidence Fast-scan cyclic voltammetry in Kv1.2 KO mice, co-immunoprecipitation from striatal tissue, selective pharmacological blockade

    PMID:21233214

    Open questions at the time
    • Whether Gβγ directly binds Kv1.2 or acts through an intermediary was not resolved
    • Contribution of heteromeric Kv1.2 complexes versus homomers in dopamine terminals was not dissected
  10. 2013 High

    Two parallel discoveries connected Kv1.2 downregulation to neuropathic pain and synaptic plasticity: a nerve injury–induced antisense lncRNA (driven by MZF1) silences Kcna2 in DRG to increase excitability and produce pain; activity-dependent Kv1.2 endocytosis in CA3 dendrites mediates long-term potentiation of intrinsic excitability.

    Evidence ChIP, antisense RNA overexpression/knockdown, patch-clamp and behavioral pain testing (neuropathic pain); Kv1.2 KO mice, endocytosis inhibition, PTK blockade in hippocampal slices (LTP-IE)

    PMID:23792947 PMID:23981714

    Open questions at the time
    • Mechanism by which the antisense lncRNA degrades or silences Kcna2 mRNA at a molecular level was not fully elucidated
    • Whether LTP-IE-associated Kv1.2 endocytosis uses the same cortactin/tyrosine-phosphorylation pathway was not confirmed
  11. 2013 High

    Sigma-1 receptor was found to form a persistent protein complex with Kv1.2, promoting its redistribution to the plasma membrane and upregulating D-type K⁺ current in nucleus accumbens after cocaine exposure, establishing a Sig-1R–Kv1.2 axis in addiction-related neuronal hypoactivity.

    Evidence Co-immunoprecipitation, subcellular fractionation, ex vivo electrophysiology, behavioral studies in cocaine-exposed rats

    PMID:23332758

    Open questions at the time
    • The Sig-1R binding site on Kv1.2 was not mapped
    • Whether Kvβ subunits occlude Sig-1R interaction in vivo (as later suggested in heterologous cells) was not tested in native tissue
  12. 2015 High

    De novo KCNA2 mutations were shown to cause epileptic encephalopathy through two mechanistically opposite routes—loss-of-function (dominant-negative) and gain-of-function (constitutively open)—with distinct clinical presentations, establishing genotype-phenotype correlations for KCNA2 channelopathy.

    Evidence Next-generation sequencing of patient cohorts, Xenopus oocyte voltage-clamp functional characterization

    PMID:25751627

    Open questions at the time
    • Neuron-type-specific consequences of each mutation class were not characterized
    • Whether gain-of-function mutations alter Kv1.2 heteromultimerization was not tested
  13. 2017 High

    The epigenetic silencing pathway was extended: DNMT3a (recruited by Oct1 and MBD1) and later DNMT1 (activated by CREB) were shown to directly methylate the Kcna2 promoter in injured DRG neurons, suppressing Kv1.2 and driving neuropathic pain; G9a and HDAC2 also contribute to injury-induced Kcna2 repression.

    Evidence ChIP, bisulfite sequencing, reporter assays, viral overexpression/knockdown, siRNA, electrophysiology, behavioral pain testing in rodent models

    PMID:27874088 PMID:28270689 PMID:31022463 PMID:31182635

    Open questions at the time
    • Hierarchical ordering of DNMT3a, DNMT1, G9a, and HDAC2 contributions was not determined
    • Whether these epigenetic modifications are reversible after nerve regeneration was not addressed
  14. 2018 High

    Slc7a5 (LAT1) was identified as a novel Kv1.2 interactor that dramatically hyperpolarizes voltage-dependent activation by ~47 mV and reduces total protein levels, with Kvβ and Slc3a2 providing counterbalancing modulation; this interaction has pathophysiological relevance in diabetic neuropathic pain where BCAA deficiency upregulates LAT1.

    Evidence Mass spectrometry interactome, co-expression electrophysiology, mutagenesis in Xenopus oocytes; RNA-seq, proteomics, and pharmacological LAT1 inhibition in DRG and diabetic mouse models

    PMID:30356053 PMID:32311044 PMID:38946582

    Open questions at the time
    • Structural basis of the Slc7a5–Kv1.2 interaction is unknown
    • Stoichiometry of Slc7a5 modulation of native neuronal Kv1.2 complexes is uncharacterized
  15. 2025 High

    CryoEM structures in open, C-type inactivated, toxin-blocked, and Na⁺-bound states resolved how α-dendrotoxin blocks by inserting a lysine into the outermost selectivity filter site and showed the selectivity filter remains structurally intact in Na⁺ rather than collapsing, revising models of ion selectivity and C-type inactivation.

    Evidence Single-particle cryoEM at 2.5–3.2 Å resolution across four functional states

    PMID:39945513

    Open questions at the time
    • Resting/closed-state structure has not been captured
    • Lipid-dependent modulation of the selectivity filter in native membranes was not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of bimodal gating and its endogenous cytoplasmic regulator, the resting-state conformation of the voltage sensor, the hierarchical organization of multiple epigenetic silencing pathways converging on Kcna2, and how heteromultimeric assembly with other Kv1 subunits determines subcellular targeting and functional diversity.
  • No resting-state Kv1.2 structure exists
  • Identity of the cytoplasmic factor switching bimodal gating is unknown
  • Whether therapeutic reversal of Kcna2 epigenetic silencing can treat neuropathic pain is untested in humans

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 6 GO:0140299 molecular sensor activity 1
Localization
GO:0005886 plasma membrane 5 GO:0005783 endoplasmic reticulum 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-112316 Neuronal System 9 R-HSA-162582 Signal Transduction 5 R-HSA-382551 Transport of small molecules 5 R-HSA-9609507 Protein localization 5
Partners
CTTNDNMT3ADRD2MBD1PTPRASIGMAR1SLC7A5

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 X-ray crystal structure of Kv1.2 at 2.9 Å resolution revealed that voltage sensors are essentially independent domains inside the membrane, that mechanical work is performed on the pore through S4-S5 linker helices which constrict or dilate the S6 inner helices, and that in the open conformation two of four conserved Arg residues on S4 face lipid and two are buried in the voltage sensor. X-ray crystallography (crystal structure determination) Science High 16002579
1994 Kv1.2 protein is localized to multiple distinct subcellular compartments in neurons including synaptic terminals, juxta-paranodal regions of myelinated axons, unmyelinated axons, and proximal dendrites, with differential distribution compared to Kv1.1, suggesting it participates in distinct heteromultimeric complexes in different subcellular domains. Immunocytochemistry and subcellular fractionation in mouse brain The Journal of neuroscience High 8046438
1994 Kv1.2 shows complex differential subcellular distribution in neurons: concentrated in dendrites of hippocampal/cortical pyramidal and Purkinje cells, but predominantly in nerve terminals of cerebellar basket cells, suggesting Kv1.2-containing channels play diverse functional roles depending on neuronal cell type and subcellular compartment. Combined in situ hybridization and immunocytochemistry in rat brain The Journal of neuroscience High 8158277
2003 Kv1.2 homomers are responsible for two-thirds of presynaptic low-threshold K+ current at the calyx of Held, are located in the transition zone between axon and synaptic terminal, and suppress terminal hyperexcitability by limiting depolarizing after-potentials that would otherwise generate additional action potentials. Selective pharmacological blockade (tityustoxin-Kα and DTX-K) combined with current-clamp and paired pre/postsynaptic recordings in rat calyx of Held The Journal of physiology High 12777451
1999 Receptor protein tyrosine phosphatase alpha (RPTPalpha) co-immunoprecipitates with Kv1.2 in an m1 muscarinic receptor-dependent manner, directly binds N- and C-termini of Kv1.2 in vitro, and overexpression of RPTPalpha reverses tyrosine kinase-induced phosphorylation and suppression of Kv1.2 current, revealing a mechanism whereby GPCR-mediated Kv1.2 suppression depends on coordinate regulation of PTK and PTP activities. Co-immunoprecipitation, in vitro binding assays, Xenopus oocyte electrophysiology, biochemical phosphorylation analysis The EMBO journal High 9878055
2000 The Kv1.2 alpha-subunit mediates O2-sensitive K+ current in PC12 cells; anti-Kv1.2 antibody dialyzed intracellularly completely blocked the O2-sensitive current, and recombinant Kv1.2 expressed in Xenopus oocytes was inhibited by hypoxia, demonstrating Kv1.2 confers O2 sensitivity to this channel. Intracellular antibody blockade in patch clamp, Xenopus oocyte expression, Western blot The Journal of physiology High 10790158
2002 Kv1.2 associates with the actin-binding protein cortactin; the interaction maps to a 19-amino acid span in the Kv1.2 C-terminus; tyrosine phosphorylation of specific C-terminal tyrosines attenuates cortactin binding; M1 muscarinic receptor activation reduces cortactin-Kv1.2 interaction; and Kv1.2 mutants deficient in cortactin binding exhibit strongly attenuated ionic current, demonstrating a phosphorylation-dependent interaction with the actin cytoskeleton that regulates channel current. Co-immunoprecipitation, purified recombinant protein binding assays, immunocytochemistry, electrophysiology in HEK293 cells The Journal of biological chemistry High 12151401
2007 Cortactin directly regulates Kv1.2 endocytosis; pull-down assays confirmed direct Kv1.2-cortactin interaction that is reduced by tyrosine phosphorylation; FRET demonstrated in vivo interaction; cortactin's C-terminal tyrosines, fourth repeat actin-binding domain, and N-terminal Arp2/3-binding region are critical for Kv1.2 regulation, while cortactin's SH3 (dynamin-binding) domain is not required despite dynamin-dependent endocytosis. Recombinant pull-down, FRET, flow cytometry, cortactin gene replacement, site-directed mutagenesis Proceedings of the National Academy of Sciences High 17959782
2007 C-terminal phosphorylation of Kv1.2 at pS440/pS441 (identified by tandem MS from rat, human, and mouse brain) is present only on post-ER/cell surface Kv1.2, not on newly synthesized ER-localized protein; elimination of these phosphorylation sites reduces cell surface expression and functional Kv1.2 channel expression; S449 phosphorylation regulates phosphorylation at S440/S441 and also affects surface expression. Tandem mass spectrometry phosphoproteomics, site-directed mutagenesis, cell surface biotinylation, electrophysiology Proceedings of the National Academy of Sciences High 18056633
2007 Secretin decreases cell-surface Kv1.2 levels in cerebellar slices by modulating Kv1.2 endocytic trafficking via adenylate cyclase/PKA pathway; this effect is mimicked by forskolin and blocked by AC or PKA inhibitors; Kv1.2 endocytosis occurs in basket cell axon terminals and Purkinje cell dendrites; secretin or Kv1.2 inhibition enhances eyeblink conditioning acquisition. Cell-surface protein biotinylation, cerebellar slice pharmacology, behavioral testing (eyeblink conditioning) in rat The Journal of neuroscience High 22764231
2007 cAMP maintains Kv1.2 homeostasis through two distinct pathways: a PKA-dependent pathway that controls steady-state channel turnover (basal PKA inhibition elevates surface Kv1.2), and a PKA-independent pathway (elevated cAMP increases surface Kv1.2 by inhibiting endocytosis). Cell-surface biotinylation, pharmacological inhibitors of PKA and endocytosis, functional expression assays The Journal of biological chemistry Medium 18003609
2003 Kv1.2-containing channels underlie a slowly inactivating, low-threshold K+ current in striatal medium spiny neurons; toxin studies (alpha-DTX sensitive, but not DTX-K, agitoxin-2, or margatoxin) implicated Kv1.2 subunits; blockade of these channels reduced first-spike latency and increased discharge frequency from hyperpolarized membrane potentials, establishing a role in regulating state transitions and repetitive discharge. Pharmacological dissection with Kv1-selective toxins, whole-cell voltage/current clamp in acutely isolated neurons and slices, RT-PCR Journal of neurophysiology High 13679409
2013 Cocaine exposure triggers a sigma-1 receptor (Sig-1R)-dependent upregulation of D-type K+ current in nucleus accumbens neurons through a persistent protein-protein association between Sig-1R and Kv1.2 channels, accompanied by redistribution of both proteins from intracellular compartments to the plasma membrane, resulting in neuronal hypoactivity. Co-immunoprecipitation, ex vivo and in vitro electrophysiology, subcellular fractionation/trafficking assays, behavioral studies Cell High 23332758
2013 A lncRNA antisense to Kcna2 (Kcna2 antisense RNA) is induced by nerve injury in DRG via activation of myeloid zinc finger protein 1 (MZF1, which binds the antisense RNA gene promoter); this lncRNA silences Kcna2 expression by an antisense mechanism, reduces total voltage-gated K+ current, increases DRG neuron excitability, and produces neuropathic pain symptoms. Chromatin immunoprecipitation (ChIP), reporter assay, antisense RNA overexpression/knockdown, patch-clamp electrophysiology, behavioral pain testing in rats Nature neuroscience High 23792947
2015 De novo KCNA2 mutations cause epileptic encephalopathy through two opposite mechanisms: loss-of-function mutations (dominant-negative current amplitude reduction) produce focal seizures and multifocal epileptiform discharges, while gain-of-function mutations (permanently open channels with hyperpolarizing shift of voltage-dependent activation) produce more severe epilepsy and ataxia, establishing genotype-phenotype correlations. Next-generation sequencing, functional studies in Xenopus oocytes (two-microelectrode voltage clamp), site-directed mutagenesis Nature genetics High 25751627
2017 DNMT3a methylates the Kcna2 promoter region in injured DRG neurons (induced via activation of transcription factor Oct1), silencing Kcna2 expression; blocking DNMT3a prevents promoter methylation, rescues Kcna2 expression and Kv current, reduces neuronal excitability, and attenuates neuropathic pain. ChIP, bisulfite sequencing, reporter assays, DRG microinjection of virus expressing DNMT3a or shRNA, patch-clamp electrophysiology, behavioral pain testing Nature communications High 28270689
2016 G9a (euchromatic histone-lysine N-methyltransferase 2) contributes to nerve injury-induced downregulation of Kcna2 in DRG; blocking G9a increase rescues Kcna2 mRNA and protein expression; mimicking G9a increase reduces Kcna2, reduces Kv current, increases DRG neuron excitability, and produces neuropathic pain. Western blot, qRT-PCR, intrathecal siRNA injection, patch-clamp electrophysiology, behavioral pain testing in rats Scientific reports Medium 27874088
2019 DNMT1 acts as a de novo methyltransferase in injured DRG neurons (upregulated via CREB-mediated transcriptional activation of Dnmt1); it methylates the Kcna2 promoter and 5'-UTR, represses Kcna2 expression, increases neuronal excitability, and contributes to neuropathic pain genesis. ChIP, bisulfite sequencing, DRG microinjection of siRNA/AAV, patch-clamp electrophysiology, behavioral pain testing in mice The Journal of neuroscience High 31182635
2011 D2 dopamine autoreceptor (D2-AR) activation increases Kv1.2 currents through Gβγ subunit signaling; D2-AR and Kv1.2-containing channels physically associate (co-immunoprecipitation in striatal tissue); Kv1.2-specific blockade or Kv1.2 knockout attenuates D2-AR-mediated inhibition of axonal dopamine overflow, demonstrating Kv1.2 as a downstream effector of D2-AR in nigrostriatal DA release regulation. Fast scan cyclic voltammetry, Kv1.2 knockout mice, selective pharmacological blockade, co-immunoprecipitation, K+ current recordings in co-transfected cells The Journal of biological chemistry High 21233214
2009 PKA phosphorylates Kv1.2 specifically at Ser-449 (confirmed by in vitro phosphorylation, MALDI-TOF MS, MS/MS, and in situ phosphorylation in HEK293 cells); PKA-induced phosphorylation at Ser-449 increases Kv1.2 current amplitude, identified as a molecular mechanism for vasodilatory agonist modulation of Kv1 channels via PKA. In vitro phosphorylation, MALDI-TOF MS/MS, site-directed mutagenesis, whole-cell and inside-out patch clamp electrophysiology The Journal of biological chemistry High 19389710
2007 Glycosylation state of Kv1.2 affects trafficking, gating, and action potentials: preventing N-glycosylation decreases cell surface expression ~40% via increased ER retention (rescued by Kv1.4 but not Kvβ2); increasing glycosylation shifts V(1/2) negatively and increases activation kinetics; decreasing glycosylation has opposite effects consistent with a surface potential mechanism for activation but a conformational mechanism for deactivation. Site-directed mutagenesis to alter glycosylation sites, Western blot, immunocytochemistry, whole-cell patch clamp, computational action potential simulation Brain research Medium 17324383
2016 N-linked glycosylation of Kv1.2 is required for forward trafficking to the cell membrane; both wild-type and non-glycosylated Kv1.2 are internalized at comparable rates, but non-glycosylated channels are degraded faster after internalization; removal of sialic acids from cell-surface Kv1.2 also increases degradation of internalized channels. Site-directed mutagenesis, cell surface biotinylation, glycosidase treatment, pulse-chase experiments in COS-7 cells and hippocampal neurons The Journal of physiology Medium 27377235
2007 Kv1.2 activation gating is bimodal ('fast' and 'slow' modes); introduction of a positive charge at or around threonine 252 in the S2-S3 linker abolishes 'slow' activation gating; cytoplasm dialysis or patch excision switches gating from slow to fast, implicating cytoplasmic regulators in the gating mode switch. Chimeric channel construction, site-directed mutagenesis, whole-cell and excised patch-clamp electrophysiology in HEK293 cells Biophysical journal High 17766348
2013 A conditioning train of action potentials at 10 Hz causes long-term potentiation of intrinsic excitability (LTP-IE) in CA3 pyramidal cells mediated by internalization of Kv1.2 channels; LTP-IE was absent in Kv1.2 knockout mice, required intact distal apical dendrites, back-propagating APs, dendritic Ca2+ signaling, and protein tyrosine kinase activation; endocytosis inhibition blocked LTP-IE. Kv1.2 knockout mice, whole-cell patch clamp, endocytosis inhibition, PTK inhibition, dendritic ablation in hippocampal slices The Journal of physiology High 23981714
2015 Kv1.2 mediates MF-induced heterosynaptic LTP of perforant path inputs in CA3 pyramidal cells; Kv1.2 expression is polarized to distal apical dendrites; downregulation of Kv1.2 preferentially enhances distal PP-evoked EPSPs; this enhancement requires activation of dendritic Na+ channels, and its threshold is lowered by Kv1.2 downregulation. Whole-cell patch clamp in hippocampal slices, immunohistochemistry, compartmental simulation, tetrodotoxin pharmacology, Kv1.2 KO/knockdown The Journal of physiology Medium 26047212
2018 Slc7a5 (a neutral amino acid transporter) interacts with Kv1.2 (identified by mass spectrometry of Kv1.2 multi-protein complexes), reduces total Kv1.2 protein, and dramatically hyperpolarizes voltage-dependence of activation by -47 mV; Slc3a2 (binding partner of Slc7a5) attenuates these effects; neurodevelopmental delay-linked Slc7a5 mutations show localization defects and attenuated effects on Kv1.2. Mass spectrometry interactome, co-expression in Xenopus oocytes, two-electrode voltage clamp, site-directed mutagenesis, confocal imaging Nature communications High 30356053
2015 Kv1.2 exhibits use-dependent activation during trains of brief depolarizations (enabled by prepulse potentiation); this property is unique to Kv1.2 among Kv1 channels and is conferred even by a single Kv1.2 subunit in heteromeric channel complexes; use-dependent activation is observed in both mammalian cell lines and primary hippocampal neurons. Voltage-clamp electrophysiology in mammalian cells, primary hippocampal neuron cultures, heteromeric channel co-expression The Journal of neuroscience Medium 25716850
2019 Sigma-1 receptor (Sig-1R) interacts with Kv1.2 at baseline to influence bimodal activation gating; ligand activation of Sig-1R modulates Kv1.2 current amplitude; these effects are abolished by auxiliary subunit Kvβ2 (which occludes the Sig-1R interaction site) and by ALS16-linked Sig-1R mutation E102Q. Co-expression in HEK293 cells, whole-cell patch clamp, site-directed mutagenesis, pharmacological Sig-1R ligand activation Physiological reports Medium 31222975
2001 Kv1.2 and Kv1.5 form heteromultimeric channels in rabbit portal vein myocytes; 4-AP block of native vascular K(DR) shows voltage-dependent characteristics matching Kv1.2 homomers and Kv1.2/Kv1.5 heterotetramers but not Kv1.5 homomers; charybdotoxin insensitivity of native channels distinguishes them from Kv1.2 homotetramers. Patch clamp electrophysiology, tandem-linked subunit expression in mammalian cells, pharmacological characterization Circulation research Medium 11717161
2007 Molecular dynamics simulations of Kv1.2 in lipid membrane show the voltage-sensing domains undergo important lateral fluctuations consistent with their modular nature; S4 arginines R294 and R297 adopt interfacial positions interacting with water and lipid headgroups, while R300 and R303 interact predominantly with water and E226 in S2; the transmembrane potential is focused over the outer half of the membrane in the arginine-rich region of S4. All-atom molecular dynamics simulation with continuum electrostatic computations Biophysical journal Medium 17704179
2008 Kv1.2 and the paddle chimera channel (with Kv2.1 voltage sensor paddle transferred to Kv1.2) produced in Pichia yeast are functional in planar lipid bilayers with properties qualitatively similar to Shaker K+ channel; several functional properties of Kv1.2 are distinct from previously reported Kv1.2 in other systems. Planar lipid bilayer electrophysiology, yeast expression system Journal of molecular biology Medium 18638484
2025 CryoEM structures of Kv1.2 in open (3.2 Å), C-type inactivated (2.5 Å), α-dendrotoxin-blocked (3.2 Å), and Na+-bound (2.9 Å) states reveal: toxin lysine penetrates the selectivity filter disrupting the outermost ion-binding site; in Na+ solution the selectivity filter remains intact with ion density at each binding site rather than collapsing; C-type inactivated W366F in Na+ shows highly variable protein conformation. Single-particle cryoEM structure determination at near-atomic resolution eLife High 39945513
2015 Kv1.2 gating charge measured directly is ~10 elementary charges, ~25% less than Shaker; neutralization of R1 in Kv1.2 S4 decreases voltage sensitivity to ~50% of wild-type, whereas subsequent arginines have much smaller effects (contrasting with Shaker), suggesting the voltage-sensing domain aqueous crevice septum in Kv1.2 may be thicker than in Shaker. Two-electrode voltage clamp in Xenopus oocytes, site-directed mutagenesis of S4 arginines, gating current measurement The Journal of general physiology Medium 25779871
2018 MBD1 (methyl-CpG-binding domain protein 1) represses Kcna2 gene expression in DRG neurons by recruiting DNMT3a to the Kcna2 promoter; DRG MBD1 deficiency blunts nerve injury-induced pain hypersensitivity and reduces acute pain responses; DRG overexpression of MBD1 produces pain hypersensitivity and restores acute pain in MBD1-deficient mice. ChIP for MBD1 and DNMT3a at Kcna2 promoter, DRG-specific knockout/overexpression, behavioral pain testing in mice The Journal of neuroscience Medium 30266739
2023 Transcription factor EBF1 directly binds the Kcna2 gene promoter and activates its transcriptional activity in DRG neurons; nerve injury reduces EBF1 binding to the Kcna2 promoter; EBF1 overexpression reverses CCI-induced Kv1.2 downregulation; EBF1 knockdown reduces Kv1.2 expression and produces pain hypersensitivity. ChIP, reporter assay (Kcna2 promoter-luciferase), AAV-mediated DRG overexpression/knockdown, behavioral pain testing in mice Translational research Medium 37607607
2020 Slc7a5-induced suppression of Kv1.2 current and protein expression is attenuated by Kvβ1.2 co-transfection; however, gating effects of Slc7a5 (disinhibition and hyperpolarizing shift in activation) persist alongside Kvβ-mediated inactivation; Slc7a5 modifies Kvβ-induced inactivation including accelerated inactivation, hyperpolarizing shift of steady-state inactivation, and delayed recovery from inactivation. Co-transfection in Xenopus oocytes, two-electrode voltage clamp, Kv1.2/Kvβ/Slc7a5 triple co-expression The Journal of general physiology Medium 32311044
2007 Kv1.2 knockout mice have significantly less NREM sleep (-23%) and more waking (+21%) than wild-type littermates at P17, with increased number of waking episodes but no change in REM sleep, establishing that Kv1.2 regulates NREM sleep in mammals. EEG/EMG continuous recording, video monitoring, sleep scoring in Kcna2 knockout mice BMC biology Medium 17925011
2008 Kv1.2 is expressed in microglia; blockade of Kv1.2 with tityustoxin-Kα partially recovers intracellular K+ concentration and reduces IL-1β and TNF-α mRNA/protein expression and intracellular ROS production in hypoxia/LPS/ATP-treated microglia, suggesting Kv1.2 regulates microglial proinflammatory cytokine production by modulating intracellular K+ concentration. Pharmacological blockade, quantitative RT-PCR, Western blot, immunofluorescence, intracellular K+ measurement in rat brain and primary microglia Journal of neurochemistry Medium 18627436
1999 Kv1.2 is resistant to acidic pH while Kv1.5 shows enhanced C-type inactivation at acidic pH; a histidine residue in the third extracellular loop of Kv1.5 (H452) accounts for this difference; mutation of H452 to glutamine in Kv1.5 abolishes pH-dependent inactivation, revealing H452 as a pH sensor for C-type inactivation. Two-electrode voltage clamp and cell-attached patch clamp in Xenopus oocytes, site-directed mutagenesis Molecular pharmacology Medium 10220559
2024 BCAA deficiency activates LAT1 (L-type amino acid transporter 1, i.e. Slc7a5) expression through ATF4, and upregulated LAT1 reduces Kv1.2 localization to the cell membrane, inhibiting Kv1.2 channels and increasing DRG neuronal excitability to cause neuropathic pain in diabetic models. RNA sequencing, label-free quantitative proteomics, western blot, patch-clamp electrophysiology, pharmacological LAT1 inhibition in mouse DRG and HFD/STZ and db/db mouse models Advanced science Medium 38946582
2017 HDAC2, but not HDAC1, regulates Kv1.2 expression in DRG neurons; Kv1.2 co-localizes with HDAC2 in NF200-positive large neurons; HDAC2 siRNA relieves mechanical/thermal hypersensitivity in CCI rats and upregulates Kv1.2, whereas HDAC1 siRNA has no effect on Kv1.2; HDAC2 siRNA in PC12 cells also upregulates Kv1.2. Double-label immunofluorescence, intrathecal siRNA injection, HDAC inhibitor treatment, western blot, qRT-PCR in CCI rats Neuroscience Medium 31022463

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Voltage sensor of Kv1.2: structural basis of electromechanical coupling. Science (New York, N.Y.) 806 16002579
1994 Localization of Kv1.1 and Kv1.2, two K channel proteins, to synaptic terminals, somata, and dendrites in the mouse brain. The Journal of neuroscience : the official journal of the Society for Neuroscience 337 8046438
2013 A long noncoding RNA contributes to neuropathic pain by silencing Kcna2 in primary afferent neurons. Nature neuroscience 321 23792947
2015 De novo loss- or gain-of-function mutations in KCNA2 cause epileptic encephalopathy. Nature genetics 211 25751627
2013 Dynamic interaction between sigma-1 receptor and Kv1.2 shapes neuronal and behavioral responses to cocaine. Cell 176 23332758
2017 DNA methyltransferase DNMT3a contributes to neuropathic pain by repressing Kcna2 in primary afferent neurons. Nature communications 164 28270689
1994 Contrasting subcellular localization of the Kv1.2 K+ channel subunit in different neurons of rat brain. The Journal of neuroscience : the official journal of the Society for Neuroscience 153 8158277
2001 Characterization of hK4 (prostase), a prostate-specific serine protease: activation of the precursor of prostate specific antigen (pro-PSA) and single-chain urokinase-type plasminogen activator and degradation of prostatic acid phosphatase. Biochemistry 137 11735417
2003 Presynaptic rat Kv1.2 channels suppress synaptic terminal hyperexcitability following action potential invasion. The Journal of physiology 133 12777451
2017 Clinical spectrum and genotype-phenotype associations of KCNA2-related encephalopathies. Brain : a journal of neurology 126 29050392
2005 Kallikrein 4 (hK4) and prostate-specific antigen (PSA) are associated with the loss of E-cadherin and an epithelial-mesenchymal transition (EMT)-like effect in prostate cancer cells. Endocrine-related cancer 123 16172196
2007 Dynamics of the Kv1.2 voltage-gated K+ channel in a membrane environment. Biophysical journal 115 17704179
2003 Kv1.2-containing K+ channels regulate subthreshold excitability of striatal medium spiny neurons. Journal of neurophysiology 101 13679409
2002 Potassium channels Kv1.1, Kv1.2 and Kv1.6 influence excitability of rat visceral sensory neurons. The Journal of physiology 98 12042352
2009 Conformational changes and slow dynamics through microsecond polarized atomistic molecular simulation of an integral Kv1.2 ion channel. PLoS computational biology 94 19229308
2012 Kv1.1 and Kv1.2: similar channels, different seizure models. Epilepsia 92 22612818
2007 Sleep in Kcna2 knockout mice. BMC biology 85 17925011
1999 Receptor protein tyrosine phosphatase alpha participates in the m1 muscarinic acetylcholine receptor-dependent regulation of Kv1.2 channel activity. The EMBO journal 85 9878055
2000 O2-sensitive K+ channels: role of the Kv1.2 -subunit in mediating the hypoxic response. The Journal of physiology 81 10790158
2014 Impaired neuropathic pain and preserved acute pain in rats overexpressing voltage-gated potassium channel subunit Kv1.2 in primary afferent neurons. Molecular pain 80 24472174
2010 A new Kv1.2 channelopathy underlying cerebellar ataxia. The Journal of biological chemistry 78 20696761
2006 Environment of the gating charges in the Kv1.2 Shaker potassium channel. Biophysical journal 77 16533847
2000 Abnormal axonal physiology is associated with altered expression and distribution of Kv1.1 and Kv1.2 K+ channels after chronic spinal cord injury. The European journal of neuroscience 77 10712629
2016 G9a participates in nerve injury-induced Kcna2 downregulation in primary sensory neurons. Scientific reports 76 27874088
2016 Dominant KCNA2 mutation causes episodic ataxia and pharmacoresponsive epilepsy. Neurology 74 27733563
2001 Heteromultimeric Kv1.2-Kv1.5 channels underlie 4-aminopyridine-sensitive delayed rectifier K(+) current of rabbit vascular myocytes. Circulation research 74 11717161
2019 Contribution of DNMT1 to Neuropathic Pain Genesis Partially through Epigenetically Repressing Kcna2 in Primary Afferent Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 72 31182635
1993 Cloning and expression of a Kv1.2 class delayed rectifier K+ channel from canine colonic smooth muscle. Proceedings of the National Academy of Sciences of the United States of America 72 8415758
1992 Effects of the level of mRNA expression on biophysical properties, sensitivity to neurotoxins, and regulation of the brain delayed-rectifier K+ channels Kv1.2. Biochemistry 70 1281425
2015 Ataxia and myoclonic epilepsy due to a heterozygous new mutation in KCNA2: proposal for a new channelopathy. Clinical genetics 69 25477152
1999 Differential sensitivity of voltage-gated potassium channels Kv1.5 and Kv1.2 to acidic pH and molecular identification of pH sensor. Molecular pharmacology 69 10220559
2007 Trafficking-dependent phosphorylation of Kv1.2 regulates voltage-gated potassium channel cell surface expression. Proceedings of the National Academy of Sciences of the United States of America 68 18056633
2007 The glycosylation state of Kv1.2 potassium channels affects trafficking, gating, and simulated action potentials. Brain research 63 17324383
2002 Tyrosine phosphorylation of Kv1.2 modulates its interaction with the actin-binding protein cortactin. The Journal of biological chemistry 58 12151401
1993 Tityustoxin-K alpha, a structurally novel and highly potent K+ channel peptide toxin, interacts with the alpha-dendrotoxin binding site on the cloned Kv1.2 K+ channel. Molecular pharmacology 57 8355670
2006 Remyelination of dorsal column axons by endogenous Schwann cells restores the normal pattern of Nav1.6 and Kv1.2 at nodes of Ranvier. Brain : a journal of neurology 55 16537565
2003 Enhancement of ischemia-induced tyrosine phosphorylation of Kv1.2 by vascular endothelial growth factor via activation of phosphatidylinositol 3-kinase. Journal of neurochemistry 55 14713306
2002 Contributions of Kv1.2, Kv1.5 and Kv2.1 subunits to the native delayed rectifier K(+) current in rat mesenteric artery smooth muscle cells. Life sciences 53 12127166
2018 MBD1 Contributes to the Genesis of Acute Pain and Neuropathic Pain by Epigenetic Silencing of Oprm1 and Kcna2 Genes in Primary Sensory Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 50 30266739
2020 Epigenetic restoration of voltage-gated potassium channel Kv1.2 alleviates nerve injury-induced neuropathic pain. Journal of neurochemistry 48 32621322
2011 Contribution of Kv1.2 voltage-gated potassium channel to D2 autoreceptor regulation of axonal dopamine overflow. The Journal of biological chemistry 47 21233214
2008 Molecular basis of inhibitory peptide maurotoxin recognizing Kv1.2 channel explored by ZDOCK and molecular dynamic simulations. Proteins 46 17729277
2007 An essential role for cortactin in the modulation of the potassium channel Kv1.2. Proceedings of the National Academy of Sciences of the United States of America 46 17959782
2016 A recurrent mutation in KCNA2 as a novel cause of hereditary spastic paraplegia and ataxia. Annals of neurology 45 27543892
2005 Compartmentalized expression of kallikrein 4 (KLK4/hK4) isoforms in prostate cancer: nuclear, cytoplasmic and secreted forms. Endocrine-related cancer 45 16322328
2019 TET1 Overexpression Mitigates Neuropathic Pain Through Rescuing the Expression of μ-Opioid Receptor and Kv1.2 in the Primary Sensory Neurons. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 44 30515739
2006 Interplay of human tissue kallikrein 4 (hK4) with the plasminogen activation system: hK4 regulates the structure and functions of the urokinase-type plasminogen activator receptor (uPAR). Biological chemistry 44 16497155
2008 Functional analysis of Kv1.2 and paddle chimera Kv channels in planar lipid bilayers. Journal of molecular biology 43 18638484
1992 Charybdotoxin, dendrotoxin and mast cell degranulating peptide block the voltage-activated K+ current of fibroblast cells stably transfected with NGK1 (Kv1.2) K+ channel complementary DNA. Neuroscience 43 1280351
2010 Effect of sensor domain mutations on the properties of voltage-gated ion channels: molecular dynamics studies of the potassium channel Kv1.2. Biophysical journal 42 21044565
2016 Rett-like phenotypes: expanding the genetic heterogeneity to the KCNA2 gene and first familial case of CDKL5-related disease. Clinical genetics 41 27062609
2019 HDAC2, but not HDAC1, regulates Kv1.2 expression to mediate neuropathic pain in CCI rats. Neuroscience 40 31022463
2017 Long Noncoding RNA Kcna2 Antisense RNA Contributes to Ventricular Arrhythmias via Silencing Kcna2 in Rats With Congestive Heart Failure. Journal of the American Heart Association 40 29263036
2015 Voltage-dependent gating and gating charge measurements in the Kv1.2 potassium channel. The Journal of general physiology 38 25779871
2012 Molecular dynamics investigation of the ω-current in the Kv1.2 voltage sensor domains. Biophysical journal 37 22339862
2013 Activity-dependent downregulation of D-type K+ channel subunit Kv1.2 in rat hippocampal CA3 pyramidal neurons. The Journal of physiology 36 23981714
2012 Cellular mechanisms and behavioral consequences of Kv1.2 regulation in the rat cerebellum. The Journal of neuroscience : the official journal of the Society for Neuroscience 33 22764231
2007 An activation gating switch in Kv1.2 is localized to a threonine residue in the S2-S3 linker. Biophysical journal 32 17766348
1995 Antiarrhythmic and bradycardic drugs inhibit currents of cloned K+ channels, KV1.2 and KV1.4. European journal of pharmacology 32 7589202
2018 Slc7a5 regulates Kv1.2 channels and modifies functional outcomes of epilepsy-linked channel mutations. Nature communications 31 30356053
2003 Allowed N-glycosylation sites on the Kv1.2 potassium channel S1-S2 linker: implications for linker secondary structure and the glycosylation effect on channel function. The Biochemical journal 31 12911333
2018 De novo KCNA1 variants in the PVP motif cause infantile epileptic encephalopathy and cognitive impairment similar to recurrent KCNA2 variants. American journal of medical genetics. Part A 30 30055040
2017 DNMT3a contributes to the development and maintenance of bone cancer pain by silencing Kv1.2 expression in spinal cord dorsal horn. Molecular pain 30 29056068
2016 Severe early-onset epileptic encephalopathy due to mutations in the KCNA2 gene: Expansion of the genotypic and phenotypic spectrum. European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society 30 27117551
2007 Homeostatic regulation of Kv1.2 potassium channel trafficking by cyclic AMP. The Journal of biological chemistry 29 18003609
2020 Eukaryotic initiation factor 4 gamma 2 contributes to neuropathic pain through down-regulation of Kv1.2 and the mu opioid receptor in mouse primary sensory neurones. British journal of anaesthesia 28 33303185
2020 Genome analysis reveals probiotic propensities of Paenibacillus polymyxa HK4. Genomics 27 33096257
2012 Structural basis of the selective block of Kv1.2 by maurotoxin from computer simulations. PloS one 27 23071772
2008 Expression of Kv1.2 in microglia and its putative roles in modulating production of proinflammatory cytokines and reactive oxygen species. Journal of neurochemistry 26 18627436
2003 Developmental change in expression and subcellular localization of two shaker-related potassium channel proteins (Kv1.1 and Kv1.2) in the chick tangential vestibular nucleus. The Journal of comparative neurology 26 12746863
2013 Pharmacological characteristics of Kv1.1- and Kv1.2-containing channels are influenced by the stoichiometry and positioning of their α subunits. The Biochemical journal 23 23725331
2009 Identification and functional characterization of protein kinase A-catalyzed phosphorylation of potassium channel Kv1.2 at serine 449. The Journal of biological chemistry 22 19389710
2021 Genomics assisted functional characterization of Paenibacillus polymyxa HK4 as a biocontrol and plant growth promoting bacterium. Microbiological research 21 33690069
2020 LncRNA KCNA2-AS regulates spinal astrocyte activation through STAT3 to affect postherpetic neuralgia. Molecular medicine (Cambridge, Mass.) 21 33225882
2017 Extracellular redox sensitivity of Kv1.2 potassium channels. Scientific reports 21 28831076
2021 A Novel KCNA2 Variant in a Patient with Non-Progressive Congenital Ataxia and Epilepsy: Functional Characterization and Sensitivity to 4-Aminopyridine. International journal of molecular sciences 19 34576077
2015 Use-dependent activation of neuronal Kv1.2 channel complexes. The Journal of neuroscience : the official journal of the Society for Neuroscience 19 25716850
2013 Activation of lysophosphatidic acid receptor by gintonin inhibits Kv1.2 channel activity: involvement of tyrosine kinase and receptor protein tyrosine phosphatase α. Neuroscience letters 18 23769686
2017 Novel clinical manifestations in patients with KCNA2 mutations. Seizure 16 28806589
2016 N-linked glycosylation of Kv1.2 voltage-gated potassium channel facilitates cell surface expression and enhances the stability of internalized channels. The Journal of physiology 16 27377235
2015 Kv1.2 mediates heterosynaptic modulation of direct cortical synaptic inputs in CA3 pyramidal cells. The Journal of physiology 16 26047212
2012 Interaction of C70 fullerene with the Kv1.2 potassium channel. Physical chemistry chemical physics : PCCP 16 23087916
2006 Structure-based secondary structure-independent approach to design protein ligands: Application to the design of Kv1.2 potassium channel blockers. Journal of the American Chemical Society 16 17165772
2019 The sigma-1 receptor behaves as an atypical auxiliary subunit to modulate the functional characteristics of Kv1.2 channels expressed in HEK293 cells. Physiological reports 15 31222975
2001 Age-related changes in the distribution of Kv1.1 and Kv1.2 channel subunits in the rat cerebellum. Brain research 15 11282376
2025 CryoEM structures of Kv1.2 potassium channels, conducting and non-conducting. eLife 14 39945513
2022 Cm28, a scorpion toxin having a unique primary structure, inhibits KV1.2 and KV1.3 with high affinity. The Journal of general physiology 14 35699659
2017 Cardiotoxic effect of levofloxacin and ciprofloxacin in rats with/without acute myocardial infarction: Impact on cardiac rhythm and cardiac expression of Kv4.3, Kv1.2 and Nav1.5 channels. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 14 28544933
2024 KCNA2 IgG autoimmunity in neuropsychiatric diseases. Brain, behavior, and immunity 12 38309639
2023 Transcription factor EBF1 mitigates neuropathic pain by rescuing Kv1.2 expression in primary sensory neurons. Translational research : the journal of laboratory and clinical medicine 12 37607607
2015 The Role of Kv1.2 Channel in Electrotaxis Cell Migration. Journal of cellular physiology 12 26580832
2013 Fine-tuning of voltage sensitivity of the Kv1.2 potassium channel by interhelix loop dynamics. The Journal of biological chemistry 12 23413033
2012 Experimental validation of in silico predicted KCNA1, KCNA2, KCNA6 and KCNQ2 genes for association studies of peripheral nerve hyperexcitability syndrome in Jack Russell Terriers. Neuromuscular disorders : NMD 12 22342001
1999 Biotin production under limiting growth conditions by Agrobacterium/Rhizobium HK4 transformed with a modified Escherichia coli bio operon. Journal of industrial microbiology & biotechnology 12 10455485
1996 Quinidine enhances and suppresses Kv1.2 from outside and inside the cell, respectively. The Journal of pharmacology and experimental therapeutics 12 8930192
2024 Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology. Molecular neurobiology 11 38517617
2024 Branched-Chain Amino Acids Deficiency Promotes Diabetic Neuropathic Pain Through Upregulating LAT1 and Inhibiting Kv1.2 Channel. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 11 38946582
2006 Glycosylation and cell surface expression of Kv1.2 potassium channel are regulated by determinants in the pore region. Neurochemical research 11 16770729
2020 Slc7a5 alters Kvβ-mediated regulation of Kv1.2. The Journal of general physiology 10 32311044
2020 Beneficial effect of walnuts on vascular tone is associated with Akt signalling, voltage-dependent calcium channel LTCC and ATP-sensitive potassium channel Kv1.2. International journal of food sciences and nutrition 10 32693647