Affinage

Showing KCNA2 — KV1.2 is a alias.

KCNA2

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

Length
499 aa
Mass
56.7 kDa
Annotated
2026-06-10
100 papers in source corpus 38 papers cited in narrative 38 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCNA2 encodes Kv1.2, a voltage-gated potassium channel that sets neuronal excitability across somatic, axonal, presynaptic, and dendritic compartments, where it suppresses hyperexcitability and tunes state transitions (PMID:8046438, PMID:12777451, PMID:13679409). Atomic-resolution crystal and multi-state cryo-EM structures establish that independent voltage-sensor domains perform mechanical work on the pore through the S4-S5 linker, that gating charge (~10 e0) is carried principally by the first S4 arginine, and that pore-blocking toxins occlude the extracellular pore mouth — α-dendrotoxin inserting a lysine into the selectivity filter and displacing the outermost ion site (PMID:16002579, PMID:25779871, PMID:39945513, PMID:8355670). Channel gating shows distinctive bimodal and use-dependent activation governed by the S2-S3 linker residue T252 and by cytoplasmic and extracellular redox-sensitive regulators (PMID:17766348, PMID:25716850, PMID:28831076). Surface expression and function are tuned by phosphorylation: PKA acts at Ser-449 and a C-terminal cluster (Ser-440/441) marks post-ER, surface channels and controls trafficking, while N-linked glycosylation promotes forward trafficking and stabilizes internalized channel (PMID:18056633, PMID:19389710, PMID:27377235). Kv1.2 activity is further set by a network of accessory and signaling partners — cortactin, which links the channel to actin and the endocytic machinery and is required for activity-dependent internalization; RPTPα, which opposes tyrosine-kinase-mediated current suppression downstream of muscarinic receptors; the amino acid transporter Slc7a5, which strongly hyperpolarizes activation and reduces channel protein; Kvβ subunits; and sigma-1 receptor (PMID:12151401, PMID:17959782, PMID:9878055, PMID:30356053, PMID:31222975). In neurons this regulation underlies intrinsic plasticity, as activity-dependent endocytosis of Kv1.2 from distal CA3 dendrites produces long-term potentiation of intrinsic excitability and heterosynaptic potentiation (PMID:23981714, PMID:26047212). After peripheral nerve injury, Kcna2 is epigenetically silenced in DRG neurons through promoter methylation by DNMT3a, DNMT1, the histone methyltransferase G9a, MBD1-recruited DNMT3a, and an antisense lncRNA, while the transcription factor EBF1 directly activates Kcna2 transcription; loss of channel expression increases neuronal excitability and drives neuropathic pain (PMID:28270689, PMID:31182635, PMID:27874088, PMID:30266739, PMID:23792947, PMID:37607607). De novo KCNA2 mutations cause epileptic encephalopathy through either dominant-negative loss-of-function or gain-of-function mechanisms (PMID:25751627).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1993 High

    Establishing how peptide toxins block Kv1.2 provided the pharmacological tools needed to isolate Kv1.2-mediated currents in native tissue.

    Evidence Competitive binding and patch-clamp with TsTX-Kα and α-dendrotoxin on B82 cells stably expressing Kv1.2

    PMID:8355670

    Open questions at the time
    • Did not resolve the structural basis of toxin occlusion
    • Did not address channel function in vivo
  2. 1994 High

    Mapping where Kv1.2 protein resides established that the channel occupies distinct neuronal compartments in a cell-type-specific manner, implying compartment-specific roles.

    Evidence Immunocytochemistry, in situ hybridization, and subcellular fractionation in mouse and rat brain

    PMID:8046438 PMID:8158277

    Open questions at the time
    • Mechanism of differential targeting unresolved
    • Functional consequence of each localization not tested
  3. 1999 High

    Identifying RPTPα as a Kv1.2-associated phosphatase explained how GPCR-driven tyrosine phosphorylation suppression of the channel is reversed.

    Evidence mAChR-dependent co-IP, in vitro binding, and Xenopus oocyte electrophysiology

    PMID:9878055

    Open questions at the time
    • Specific tyrosine residues targeted not fully defined here
    • Endogenous neuronal relevance not directly shown
  4. 2002 High

    Discovery of a direct cortactin-Kv1.2 interaction linked the channel to the actin cytoskeleton and to phosphorylation-dependent regulation of current.

    Evidence Purified recombinant protein binding, reciprocal co-IP, mutagenesis, and electrophysiology in HEK293 cells

    PMID:12151401

    Open questions at the time
    • Did not yet define cortactin's role in trafficking versus current
    • In vivo neuronal requirement not established
  5. 2003 High

    Functional dissection in presynaptic terminals and striatal neurons established Kv1.2 as a suppressor of hyperexcitability and a regulator of subthreshold state transitions.

    Evidence Selective toxin pharmacology and paired/current-clamp recordings in calyx of Held and striatal slices

    PMID:12777451 PMID:13679409

    Open questions at the time
    • Heteromeric subunit composition only partially defined
    • Upstream signals controlling channel availability not addressed
  6. 2005 High

    The Kv1.2 crystal structure resolved the long-standing question of how voltage sensors mechanically couple to the pore.

    Evidence X-ray crystallography at 2.9 Å of the mammalian channel

    PMID:16002579

    Open questions at the time
    • Captured a single (open) conformation
    • Did not resolve inactivated or toxin-bound states
  7. 2007 High

    Identification of C-terminal phosphosites, gating-mode switches, and a glycosylation requirement showed that Kv1.2 surface expression and gating are post-translationally controlled.

    Evidence Tandem MS phosphosite mapping from brain, mutagenesis, surface assays, glycosidase treatment, and patch clamp including chimera/T252 analysis

    PMID:17324383 PMID:17766348 PMID:18056633

    Open questions at the time
    • Kinases and phosphatases for the C-terminal cluster not all identified
    • Cytoplasmic regulator of slow gating mode unidentified
  8. 2007 High

    cAMP/PKA signaling was shown to bidirectionally tune Kv1.2 surface levels through opposing trafficking pathways and endocytic machinery engaging cortactin.

    Evidence Surface biotinylation with PKA/endocytosis inhibitors and cortactin gene replacement with FRET and endocytosis assays

    PMID:17959782 PMID:18003609

    Open questions at the time
    • Molecular identity of PKA-independent pathway not defined
    • Link between specific phosphosites and endocytosis incomplete
  9. 2009 High

    Pinpointing Ser-449 as the functionally critical PKA site connected PKA signaling directly to a defined molecular event on the channel.

    Evidence In vitro/in situ phosphorylation, MS, S449A mutagenesis, and patch clamp

    PMID:19389710

    Open questions at the time
    • Whether Ser-449 acts through trafficking or gating in neurons not fully resolved
  10. 2010 High

    A spontaneous S6 mutation in mice demonstrated that reduced functional Kv1.2 in basket cell terminals causes motor incoordination, linking channel availability to circuit output.

    Evidence ENU-derived Pingu mouse, cerebellar slice patch clamp, immunochemistry, and transgenic complementation

    PMID:20696761

    Open questions at the time
    • Mechanism by which I402T reduces functional channel number unclear
    • Human relevance not addressed at the time
  11. 2013 High

    Activity-dependent Kv1.2 internalization was identified as a substrate for intrinsic plasticity, and sigma-1 receptor and D2 autoreceptor partnerships placed Kv1.2 in neuromodulatory signaling.

    Evidence Kv1.2 KO mice with endocytosis/PTK inhibitors and dendritic Ca2+ imaging; co-IP and electrophysiology for Sig-1R and D2-AR in striatal tissue

    PMID:21233214 PMID:23332758 PMID:23981714

    Open questions at the time
    • Precise endocytic adaptors recruiting Kv1.2 not fully defined
    • Direct versus indirect nature of Sig-1R association left open
  12. 2013 Medium

    Discovery of a Kcna2 antisense lncRNA established transcriptional/RNA-level silencing as a driver of injury-induced Kv1.2 loss and neuropathic pain.

    Evidence MZF1 promoter binding assays, expression manipulation, patch clamp, and behavioral pain assays in DRG

    PMID:23792947

    Open questions at the time
    • Single-lab characterization
    • Relationship to DNA-methylation silencing not integrated
  13. 2015 High

    Linking de novo KCNA2 mutations to epileptic encephalopathy via two opposite biophysical mechanisms established the channel as a Mendelian disease gene.

    Evidence Next-generation sequencing and two-electrode voltage-clamp functional characterization of mutant channels

    PMID:25751627

    Open questions at the time
    • Genotype-phenotype determinants beyond gain/loss dichotomy incomplete
    • In vivo consequences in neurons not directly modeled here
  14. 2015 High

    Use-dependent activation and dendritic Kv1.2 downregulation were shown to confer unique gating behavior and to mediate heterosynaptic potentiation, refining Kv1.2's role in dendritic computation.

    Evidence Patch clamp in HEK and hippocampal neurons; immunostaining, compartmental modeling, and TTX in slices

    PMID:25716850 PMID:25779871 PMID:26047212

    Open questions at the time
    • Molecular basis of use-dependent activation not fully resolved
    • Single-lab dendritic studies
  15. 2017 High

    DNA methyltransferases and histone methyltransferase G9a were identified as effectors silencing Kcna2 after nerve injury, defining an epigenetic axis driving neuropathic pain.

    Evidence Methylation assays, reporter assays, siRNA/AAV manipulation, patch clamp, and behavioral assays in DRG (DNMT3a, DNMT1, G9a)

    PMID:27874088 PMID:28270689 PMID:31182635

    Open questions at the time
    • Hierarchy among DNMT3a, DNMT1, and G9a not fully ordered
    • Some studies single-lab and Medium confidence
  16. 2018 High

    Identification of Slc7a5 as a Kv1.2 complex partner revealed a powerful gating and protein-level regulator with direct relevance to epilepsy mutants.

    Evidence MS interactome, patch clamp, western blot, and co-expression with wild-type and disease-mutant channels (and Slc3a2)

    PMID:30356053

    Open questions at the time
    • Structural basis of the Kv1.2-Slc7a5 interaction unknown
    • Endogenous neuronal stoichiometry not defined
  17. 2018 Medium

    MBD1 was shown to recruit DNMT3a to the Kcna2 promoter, providing the reader/effector link in injury-induced epigenetic silencing.

    Evidence ChIP for DNMT3a recruitment, MBD1 KO mice, AAV overexpression, and pain behavior

    PMID:30266739

    Open questions at the time
    • Single-lab study
    • Direct effect on channel protein not measured
  18. 2019 Medium

    Demonstrating sigma-1 receptor modulation of bimodal Kv1.2 gating, including an ALS16 mutation that abolishes it, connected channel gating to a disease-relevant receptor.

    Evidence Patch clamp, co-transfection, Sig-1R ligands, and the E102Q dominant-negative mutation in HEK293 cells

    PMID:31222975

    Open questions at the time
    • Direct binding not demonstrated
    • Single-lab heterologous system
  19. 2020 Medium

    Showing convergent regulation of Kv1.2 by Slc7a5 and Kvβ1.2 clarified how accessory subunits jointly shape availability and inactivation.

    Evidence Whole-cell patch clamp and western blot with co-transfected subunit combinations in HEK cells

    PMID:32311044

    Open questions at the time
    • Single-lab
    • Native neuronal relevance of triple-partner regulation untested
  20. 2023 Medium

    Identifying EBF1 as a direct activator of Kcna2 transcription provided the positive regulatory counterpart to injury-induced silencing.

    Evidence ChIP, luciferase reporter, AAV overexpression/knockdown, and pain behavior in DRG

    PMID:37607607

    Open questions at the time
    • Single-lab
    • Interplay with repressive epigenetic machinery not resolved
  21. 2024 Medium

    Linking BCAA deficiency to ATF4-driven LAT1/Slc7a5 upregulation extended Slc7a5-mediated Kv1.2 suppression to diabetic neuropathic pain in vivo.

    Evidence RNA-seq, quantitative proteomics, patch clamp, membrane-localization imaging, and LAT1 inhibitor treatment in mice

    PMID:38946582

    Open questions at the time
    • Single-lab
    • Whether effect is purely via Slc7a5 not fully isolated
  22. 2025 High

    Multi-state cryo-EM structures resolved how Kv1.2 inactivates, conducts ions, and is blocked by dendrotoxin at atomic detail.

    Evidence Cryo-EM in open, C-type inactivated, dendrotoxin-blocked, and Na+-bound states

    PMID:39945513

    Open questions at the time
    • C-type inactivated W366F state only low-resolution
    • Structures of accessory-partner complexes not determined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many post-translational, accessory-protein, and transcriptional regulators of Kv1.2 are integrated in a single compartmentalized neuron, and the structural basis of partner interactions, remains unresolved.
  • No structure of Kv1.2 with Slc7a5, cortactin, or sigma-1 receptor
  • Integration of competing trafficking/silencing pathways in vivo not established
  • Mechanism of redox- and cytoplasm-dependent gating-mode switching unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5
Localization
GO:0005886 plasma membrane 5 GO:0005783 endoplasmic reticulum 3 GO:0005856 cytoskeleton 2
Pathway
R-HSA-112316 Neuronal System 4 R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-9609507 Protein localization 3
Partners
CTTNDRD2KCNA1KCNA5KCNAB2PTPRASIGMAR1SLC7A5

Evidence

Reading pass · 38 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 they perform mechanical work on the pore through the 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 are on a lipid-facing surface while two are buried in the voltage sensor. X-ray crystallography Science High 16002579
1994 Kv1.2 protein is localized to multiple subcellular compartments in mouse brain neurons including cell somata, juxta-paranodal regions of myelinated axons, synaptic terminals, unmyelinated axons, and proximal dendrites, with a differential pattern from Kv1.1 that depends on cell type. Immunocytochemistry / subcellular fractionation in mouse brain The Journal of neuroscience High 8046438
1994 In rat brain, Kv1.2 shows complex differential subcellular distribution: concentrated in dendrites of hippocampal/cortical pyramidal cells and Purkinje cells, but predominantly in nerve terminals of cerebellar basket cells. The authors hypothesize this arises from association with different heterologous subunits in different cell types. Combined in situ hybridization and immunocytochemistry in rat brain The Journal of neuroscience High 8158277
1999 Receptor protein tyrosine phosphatase alpha (RPTPalpha) co-immunoprecipitates with Kv1.2 in an m1 muscarinic acetylcholine receptor (mAChR)-dependent manner; N- and C-termini of Kv1.2 bind RPTPalpha in vitro; overexpression of RPTPalpha increases resting Kv1.2 current and reverses tyrosine kinase-induced phosphorylation and suppression of Kv1.2 current, establishing RPTPalpha as a phosphatase that opposes GPCR-mediated channel suppression. Co-immunoprecipitation, in vitro binding assay, Xenopus oocyte electrophysiology, biochemical phosphorylation analysis The EMBO journal High 9878055
2002 Kv1.2 associates with the actin-binding protein cortactin; this interaction is direct (shown with purified recombinant proteins), requires a 19-amino acid span in the Kv1.2 C-terminus, and is attenuated by tyrosine phosphorylation of specific C-terminal tyrosines. M1 muscarinic receptor activation reduces cortactin-Kv1.2 interaction, and mutant Kv1.2 channels deficient in cortactin binding exhibit strongly attenuated ionic current. Co-immunoprecipitation, purified recombinant protein binding assays, immunocytochemistry, electrophysiology in HEK293 cells The Journal of biological chemistry High 12151401
2007 Cortactin is required for Kv1.2 regulation: pull-down assays confirmed direct interaction reduced by tyrosine phosphorylation of Kv1.2; FRET demonstrated in vivo interaction; cortactin's fourth repeat actin-binding domain and N-terminal Arp2/3-binding region (but not the dynamin-binding SH3 domain) are critical for Kv1.2 endocytosis; manipulating the cortactin-binding site within Kv1.2 confirms cortactin proximity influences channel function. Pull-down with recombinant proteins, FRET, flow cytometry, cortactin gene replacement, endocytosis assays Proceedings of the National Academy of Sciences High 17959782
2007 A cluster of cytoplasmic C-terminal phosphorylation sites (pS434, pS440, pS441, pS449) on Kv1.2 regulates its trafficking. Phosphorylation at pS440/pS441 is present only on post-ER/cell-surface Kv1.2, not on newly synthesized ER-localized channel; elimination of these sites by mutation reduces cell-surface expression and functional expression. pS449 phosphorylation regulates pS440/pS441 phosphorylation. These mutations also suppress trafficking of Kv1.2/Kv1.4 heteromeric channels. Tandem MS of Kv1.2 purified from rat/human/mouse brain, site-directed mutagenesis, cell-surface expression assays Proceedings of the National Academy of Sciences High 18056633
2003 In the calyx of Held presynaptic terminal, Kv1.2 homomers are responsible for two-thirds of the presynaptic low-threshold K+ current, while Kv1.1/Kv1.2 heteromers contribute the remaining current. Kv1.2 channels are located in the transition zone between the axon and synaptic terminal. Blocking Kv1.2 (with TsTX-Kα) increases the depolarizing after-potential amplitude following each action potential, bringing the terminal closer to threshold and evoking additional EPSCs in postsynaptic cells, establishing Kv1.2 as a suppressor of presynaptic terminal hyperexcitability. Selective toxin pharmacology (TsTX-Kα, DTX-K), current-clamp and voltage-clamp recordings from calyx of Held, paired pre/postsynaptic recordings The Journal of physiology High 12777451
2000 The Kv1.2 α-subunit comprises the O2-sensitive K+ channel in PC12 cells: intracellularly dialyzed anti-Kv1.2 antibody completely blocked the O2-sensitive K+ current, whereas anti-Kv2.1 antibody had no effect; recombinant Kv1.2 expressed in Xenopus oocytes was inhibited by hypoxia, while Kv2.1 was not, establishing Kv1.2 as the molecular substrate of the hypoxic K+ current. Intracellular antibody dialysis, Xenopus oocyte expression, Western blot, whole-cell voltage clamp The Journal of physiology High 10790158
2007 N-glycosylation state of Kv1.2 affects its gating (V1/2 shifts, activation/deactivation kinetics, C-type inactivation) via a surface potential mechanism, and preventing N-glycosylation decreases cell-surface Kv1.2 expression by ~40% primarily through partial ER retention; this trafficking defect is rescued by co-expression with glycosylated Kv1.4 but not Kvβ2. Site-directed mutagenesis, whole-cell patch clamp, glycosidase treatment, confocal imaging, western blot Brain research Medium 17324383
2007 cAMP regulates Kv1.2 surface levels through two opposing trafficking pathways: a PKA-dependent pathway controlling steady-state channel turnover (basal PKA activity promotes endocytosis), and a PKA-independent pathway that elevates surface Kv1.2 by inhibiting endocytosis when cAMP is elevated above basal. Surface biotinylation, pharmacological inhibitors of PKA, endocytosis inhibitors, immunofluorescence The Journal of biological chemistry Medium 18003609
2009 PKA phosphorylates Kv1.2 specifically at Ser-449 in the C-terminus; in vitro and in situ phosphorylation at this site were confirmed by MS; PKA-induced increase in Kv1.2 current amplitude is abolished by the S449A mutation, establishing Ser-449 as the functionally critical PKA phosphorylation site for channel regulation. In vitro phosphorylation, MALDI-TOF MS, MS/MS, site-directed mutagenesis, whole-cell and inside-out patch clamp The Journal of biological chemistry High 19389710
2013 Cocaine exposure triggers a sigma-1 receptor (Sig-1R)-dependent upregulation of D-type K+ current in nucleus accumbens neurons, caused by persistent protein-protein association between Sig-1Rs and Kv1.2 channels, associated with redistribution of both proteins from intracellular compartments to the plasma membrane. Co-immunoprecipitation in striatal tissue, ex vivo and in vitro electrophysiology, subcellular fractionation, behavioral cocaine response assays Cell High 23332758
2011 Kv1.2 contributes to D2 dopamine autoreceptor (D2-AR) regulation of axonal dopamine overflow: selective Kv1.2 blockade and Kv1.2 knockout both attenuate D2-AR-mediated inhibition of DA overflow; D2-AR activation increases Kv1.2 currents in co-transfected cells via Gβγ subunit signaling; D2-AR and Kv1.2 physically associate in striatal tissue by immunoprecipitation. Fast-scan cyclic voltammetry in striatal slices, Kv1.2 KO mice, selective toxin blockade, electrophysiology, immunoprecipitation The Journal of biological chemistry High 21233214
2013 Activity-dependent downregulation of Kv1.2 in hippocampal CA3 pyramidal cells underlies long-term potentiation of intrinsic excitability (LTP-IE): a conditioning train of 20 APs at 10 Hz causes persistent reduction in D-type K+ current; LTP-IE is abolished by inhibition of endocytosis or protein tyrosine kinase, and is absent in Kv1.2 knockout mice, indicating it is mediated by internalization of Kv1.2 from distal apical dendrites triggered by back-propagating AP-induced dendritic Ca2+ signaling. Whole-cell patch clamp, endocytosis inhibitors, PTK inhibitors, Kv1.2 KO mice, dendritic Ca2+ imaging The Journal of physiology High 23981714
2012 Secretin decreases cell-surface Kv1.2 levels in rat cerebellar slices by modulating Kv1.2 endocytic trafficking; this effect is mimicked by adenylate cyclase activation (forskolin) and blocked by pharmacological inhibitors of AC or PKA, localizing the effect to basket cell axon terminals and Purkinje cell dendrites. Intra-cerebellar infusion of a Kv1.2 inhibitor or secretin both enhance acquisition of eyeblink conditioning. Cell-surface protein biotinylation, pharmacological inhibitors, cerebellar slice imaging, behavioral eyeblink conditioning The Journal of neuroscience Medium 22764231
2015 De novo mutations in KCNA2 cause epileptic encephalopathy through two distinct mechanisms: dominant-negative loss-of-function (almost complete current reduction) causing multifocal epileptiform discharges and focal seizures, or gain-of-function (permanently open channels with drastic negative shift in activation) causing a more severe encephalopathy with generalized seizures, as established by functional electrophysiology of the mutant channels. Xenopus oocyte two-electrode voltage clamp, next-generation sequencing, functional expression of mutant channels Nature genetics High 25751627
2017 DNA methyltransferase DNMT3a represses Kcna2 expression by methylating the Kcna2 promoter region in DRG neurons after nerve injury; blocking DNMT3a prevents nerve injury-induced methylation of the Kcna2 promoter, rescues Kcna2 expression and Kv current, and attenuates neuropathic pain. Mimicking DNMT3a upregulation reduces Kcna2 promoter activity, Kcna2 expression, and Kv current and causes neuropathic pain symptoms. Chromatin methylation assay, luciferase reporter assay, siRNA knockdown, AAV overexpression, patch clamp, behavioral pain assays Nature communications High 28270689
2016 G9a (euchromatic histone-lysine N-methyltransferase 2) epigenetically silences Kcna2 in injured DRG neurons: blocking nerve injury-induced G9a increase rescues Kcna2 mRNA and protein expression; mimicking the increase decreases Kcna2 expression, reduces Kv current, and increases DRG neuronal excitability. G9a mRNA is co-localized with Kcna2 mRNA in DRG neurons. siRNA, AAV-mediated overexpression, western blot, qPCR, patch clamp, immunofluorescence Scientific reports Medium 27874088
2019 DNMT1, acting as a de novo methyltransferase, represses Kcna2 expression by increasing DNA methylation within the promoter and 5'-UTR of the Kcna2 gene in injured DRG, downstream of CREB-mediated Dnmt1 transcriptional activation; blocking DNMT1 upregulation prevents Kcna2 methylation, rescues Kv current and reduces DRG neuronal hyperexcitability. CREB knockout/overexpression, DNMT1 siRNA, bisulfite sequencing of Kcna2 promoter, patch clamp, behavioral assays The Journal of neuroscience Medium 31182635
2007 Kv1.2 channels exhibit two distinct activation gating modes ('fast' and 'slow') switchable by a prepulse; the S2-S3 linker threonine residue (T252) acts as a switch between these modes — introduction of a positive charge at this position abolishes 'slow' activation gating; cytoplasm dialysis or patch excision also switches gating from slow to fast, implicating cytoplasmic regulators. Whole-cell and inside-out patch clamp, chimera construction between Kv1.2 and Kv1.5, point mutagenesis, cytoplasm dialysis Biophysical journal High 17766348
2001 The dominant form of vascular delayed rectifier K+ channel in rabbit portal vein myocytes involves heteromultimeric association of Kv1.2 and Kv1.5 subunits: native K(DR) properties including 4-AP-induced positive shift in voltage dependence of activation are reproduced by Kv1.5/Kv1.2 heteromers or tandem constructs but not by Kv1.5 homotetramers alone; native K(DR) was insensitive to charybdotoxin (which blocks Kv1.2 homomers), consistent with heteromeric composition. Patch clamp, expression of heteromeric and tandem-linked channel constructs in mammalian cells, pharmacological profiling Circulation research Medium 11717161
2018 Slc7a5, a neutral amino acid transporter, forms a multi-protein complex with Kv1.2 (identified by mass spectrometry), dramatically hyperpolarizes Kv1.2 voltage-dependence of activation by -47 mV, reduces total Kv1.2 protein, and accelerates inactivation causing channels to accumulate in a non-conducting state. Slc3a2 (a known Slc7a5 binding partner) attenuates these effects. Epilepsy-linked gain-of-function Kv1.2 mutants show enhanced sensitivity to Slc7a5. Mass spectrometry interactome screen followed by patch clamp, western blot, co-expression with wild-type and disease mutant channels Nature communications High 30356053
2020 Slc7a5 regulates Kv1.2 in the presence of Kvβ1.2: Slc7a5-induced suppression of Kv1.2 current and protein is attenuated by Kvβ1.2 co-expression, but gating effects of Slc7a5 (disinhibition, hyperpolarizing shift) persist alongside Kvβ-mediated inactivation. Slc7a5 also accelerates Kvβ-induced inactivation, shifts steady-state inactivation, and delays recovery, indicating convergent regulation by both accessory proteins. Whole-cell patch clamp, western blot, co-transfection in HEK cells The Journal of general physiology Medium 32311044
2015 Kv1.2 exhibits unique use-dependent activation during trains of brief depolarizations (arising from prepulse potentiation); this property is not shared by other Kv1 subtypes but is conferred in heteromeric channel complexes containing even a single Kv1.2 subunit; use-dependent activation is observed in mammalian cell lines and primary hippocampal neurons. Whole-cell patch clamp in HEK cells and primary hippocampal neuron cultures, heteromeric channel co-expression The Journal of neuroscience Medium 25716850
2017 Extracellular redox environment regulates Kv1.2 gating mode: reducing agents promote a shift to an 'inhibited' gating mode that resists opening and causes pronounced use-dependent activation; this redox sensitivity is absent in other Kv1 channels but is apparent in heteromeric channels containing Kv1.2 subunits; mutagenesis of candidate cysteines fails to abolish redox sensitivity, suggesting an extrinsic redox-sensitive binding partner. Whole-cell patch clamp, reducing agent application, site-directed mutagenesis of cysteine residues, heteromeric channel expression Scientific reports Medium 28831076
2003 Kv1.2-containing channels in striatal medium spiny neurons activate rapidly near resting potential (~-60 mV), inactivate slowly, and account for ~50% of subthreshold K+ current; pharmacological blockade (by tityustoxin-Kα but not by toxins lacking high Kv1.2 affinity) reduces first-spike latency and increases discharge frequency from hyperpolarized membrane potentials, establishing Kv1.2 as a regulator of state transitions in these neurons. Whole-cell patch clamp, selective toxin pharmacology, current-clamp in acute slices, RT-PCR Journal of neurophysiology High 13679409
2013 The lncRNA Kcna2 antisense RNA silences Kcna2 expression in DRG primary afferent neurons; its increase after peripheral nerve injury (via activation of transcription factor MZF1 binding to the antisense RNA gene promoter) downregulates Kcna2 mRNA and protein, reduces total voltage-gated K+ current, increases DRG neuron excitability, and produces neuropathic pain. Blocking the antisense RNA increase reverses these effects. Promoter binding assay (ChIP/EMSA for MZF1), siRNA/overexpression, patch clamp, behavioral pain assays Nature neuroscience Medium 23792947
2015 Kv1.2 gating charge is ~10 elementary charges, approximately 25% less than Shaker; neutralization of R1 in the S4 segment decreases voltage sensitivity to ~50% of wild-type, while subsequent arginines have much smaller effects — in contrast to Shaker where the first four basic residues contribute roughly equally, suggesting the VSD septum separating aqueous crevices in Kv1.2 may be thicker than in Shaker. Two-electrode voltage clamp in Xenopus oocytes, gating current measurements, S4 arginine neutralization mutagenesis The Journal of general physiology High 25779871
2016 N-linked glycosylation of Kv1.2 at the conserved S1-S2 linker site facilitates forward trafficking to the cell membrane and enhances stability of internalized channels by reducing their degradation rate; removal of sialic acids from surface Kv1.2 accelerates degradation of internalized channels. Glycosidase treatment, N-glycosylation mutants, surface biotinylation, protein half-life assays in COS-7 cells and hippocampal neurons The Journal of physiology Medium 27377235
2025 CryoEM structures of Kv1.2 at near-atomic resolution 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: (1) dendrotoxin lysine penetrates into the selectivity filter coordinated by carbonyls, displacing the outermost ion-binding site with only two (not three) ion densities remaining; (2) in Na+ solution the selectivity filter remains intact with ion density in each binding site rather than collapsing; (3) the C-type inactivated W366F channel in Na+ shows highly variable conformation and only low-resolution structure. Cryo-EM structure determination in multiple functional states eLife High 39945513
2019 Sigma-1 receptor (Sig-1R) interacts with Kv1.2 in baseline conditions in HEK293 cells to influence bimodal activation gating; ligand activation of Sig-1R modulates Kv1.2 current amplitude; Kvβ2 occludes the Sig-1R–Kv1.2 interaction; the ALS16-associated Sig-1R-E102Q mutation abolishes Sig-1R modulation of Kv1.2, implicating E102 as critical for the interaction. Patch clamp electrophysiology, co-transfection in HEK293 cells, pharmacological Sig-1R ligands, dominant-negative mutation Physiological reports Medium 31222975
2018 MBD1 represses Kcna2 gene expression by recruiting DNA methyltransferase DNMT3a to the Kcna2 promoter in DRG neurons; MBD1-deficient mice show blunted nerve injury-induced pain hypersensitivity and DRG overexpression of MBD1 produces pain hypersensitivity; DRG MBD1 deficiency reduces acute pain responses. ChIP assay for DNMT3a recruitment to Kcna2 promoter, MBD1 knockout mice, AAV overexpression, behavioral pain assays The Journal of neuroscience Medium 30266739
2023 Transcription factor EBF1 directly binds the Kcna2 gene promoter and activates its transcription in DRG neurons; CCI-induced EBF1 downregulation decreases EBF1 binding to the Kcna2 promoter and reduces Kv1.2 expression; AAV-mediated EBF1 rescue restores Kv1.2 expression and attenuates neuropathic pain, while EBF1 knockdown reduces Kv1.2 and causes pain hypersensitivity. ChIP assay, luciferase reporter assay, AAV overexpression/knockdown, western blot, behavioral pain assays Translational research Medium 37607607
2024 BCAA deficiency activates expression of L-type amino acid transporter 1 (LAT1/Slc7a5) through ATF4 in DRG neurons; abnormally upregulated LAT1 reduces Kv1.2 localization to the cell membrane and inhibits Kv1.2 channels, increasing neuronal excitability and causing diabetic neuropathic pain symptoms; LAT1 inhibition alleviates these symptoms. RNA sequencing, label-free quantitative proteomics, patch clamp, immunostaining for membrane localization, LAT1 inhibitor treatment in mice Advanced science Medium 38946582
2010 A missense mutation I402T in the S6 segment of Kv1.2 (in Pingu mice) dramatically decreases the amount of functional Kv1 channels in cerebellar basket cell terminals without major changes in biophysical properties; this results in increased frequency and amplitude of spontaneous GABAergic IPSCs and reduced Purkinje cell firing, causing motor incoordination, which is partially rescued by acetazolamide or Kcna2 transgenic complementation. ENU mutagenesis screen, patch clamp in cerebellar slices, immunochemistry, CHO cell expression, transgenic complementation The Journal of biological chemistry High 20696761
1993 TsTX-Kα and α-dendrotoxin competitively block Kv1.2 K+ channels by binding to the same or closely related extracellular sites; TsTX-Kα blocks with Kd ~0.21 nM (10-fold more potent than DTX at 2.8 nM); TsTX-Kα does not affect kinetics or voltage dependence of activation; 4-AP blockade is unaffected by TsTX-Kα, indicating a distinct binding site for 4-AP. Whole-cell and patch-clamp recordings from B82 fibroblasts stably expressing Kv1.2, competitive binding analysis Molecular pharmacology High 8355670
2015 Kv1.2 downregulation in distal apical dendrites of CA3 pyramidal cells mediates mossy fiber-induced heterosynaptic LTP of perforant path (PP) EPSPs: Kv1.2 is polarized to distal apical dendrites; its downregulation specifically enhances PP-evoked EPSPs by facilitating activation of dendritic Na+ channels at distal dendrites; partial block of dendritic Na+ channels reverses the enhanced PP-EPSPs. Patch clamp, immunostaining for subcellular Kv1.2 distribution, compartmental simulations, TTX application in hippocampal slices The Journal of physiology Medium 26047212

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.) 807 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 323 23792947
2015 De novo loss- or gain-of-function mutations in KCNA2 cause epileptic encephalopathy. Nature genetics 214 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 167 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
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 129 29050392
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 102 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 93 22612818
2007 Sleep in Kcna2 knockout mice. BMC biology 86 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 82 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 79 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 64 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 51 30266739
2020 Epigenetic restoration of voltage-gated potassium channel Kv1.2 alleviates nerve injury-induced neuropathic pain. Journal of neurochemistry 49 32621322
2011 Contribution of Kv1.2 voltage-gated potassium channel to D2 autoreceptor regulation of axonal dopamine overflow. The Journal of biological chemistry 48 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
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
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 43 21044565
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
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
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 29 33303185
2007 Homeostatic regulation of Kv1.2 potassium channel trafficking by cyclic AMP. The Journal of biological chemistry 29 18003609
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
2017 Extracellular redox sensitivity of Kv1.2 potassium channels. Scientific reports 22 28831076
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
2020 LncRNA KCNA2-AS regulates spinal astrocyte activation through STAT3 to affect postherpetic neuralgia. Molecular medicine (Cambridge, Mass.) 21 33225882
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 20 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 17 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
2025 CryoEM structures of Kv1.2 potassium channels, conducting and non-conducting. eLife 15 39945513
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
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 15 28544933
2001 Age-related changes in the distribution of Kv1.1 and Kv1.2 channel subunits in the rat cerebellum. Brain research 15 11282376
2024 Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology. Molecular neurobiology 14 38517617
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
2024 Branched-Chain Amino Acids Deficiency Promotes Diabetic Neuropathic Pain Through Upregulating LAT1 and Inhibiting Kv1.2 Channel. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 13 38946582
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
1996 Quinidine enhances and suppresses Kv1.2 from outside and inside the cell, respectively. The Journal of pharmacology and experimental therapeutics 12 8930192
2006 Glycosylation and cell surface expression of Kv1.2 potassium channel are regulated by determinants in the pore region. Neurochemical research 11 16770729
2021 Gradual decorrelation of CA3 ensembles associated with contextual discrimination learning is impaired by Kv1.2 insufficiency. Hippocampus 10 34964210
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
1994 Alaproclate effects on voltage-dependent K+ channels and NMDA receptors: studies in cultured rat hippocampal neurons and fibroblast cells transformed with Kv1.2 K+ channel cDNA. Neuropharmacology 10 7936117
2023 Two epilepsy-associated variants in KCNA2 (KV 1.2) at position H310 oppositely affect channel functional expression. The Journal of physiology 9 37883018
2020 Stereotactically Injected Kv1.2 and CASPR2 Antisera Cause Differential Effects on CA1 Synaptic and Cellular Excitability, but Both Enhance the Vulnerability to Pro-epileptic Conditions. Frontiers in synaptic neuroscience 9 32269520
2019 Quantum Calculation of Proton and Other Charge Transfer Steps in Voltage Sensing in the Kv1.2 Channel. The journal of physical chemistry. B 9 31441655
2008 Molecular dynamic simulation of the Kv1.2 voltage-gated potassium channel in open and closed state conformations. The journal of physical chemistry. B 9 19093881
2019 Establishment of a human induced pluripotent stem cell (iPSC) line (HIHDNEi002-A) from a patient with developmental and epileptic encephalopathy carrying a KCNA2 (p.Arg297Gln) mutation. Stem cell research 8 31075689

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