Affinage

KCNE3

Potassium voltage-gated channel subfamily E member 3 · UniProt Q9Y6H6

Length
103 aa
Mass
11.7 kDa
Annotated
2026-06-10
42 papers in source corpus 20 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCNE3 (MiRP2) is a single-transmembrane regulatory β-subunit that assembles with multiple voltage-gated K+ channel α-subunits to reshape their gating and set the electrical properties of epithelial, muscle, neuronal, and cardiac cells (PMID:11207363, PMID:20051516). Its best-defined action is on KCNQ1: the KCNE3 transmembrane domain alone is sufficient to assemble with and constitutively activate KCNQ1, with neither terminus required (PMID:15572349), and it does so by shifting the voltage dependence of S4 voltage-sensor movement to extreme hyperpolarized potentials so the channel conducts across the physiological range (PMID:26668384). This stabilization of the activated 'up' state of S4 is achieved through direct electrostatic and inter-helical contacts—the acidic KCNE3 residues D54/D55 engaging KCNQ1 S4 R228, contacts at both ends of the KCNE3 transmembrane domain with the voltage-sensing domain, and a precisely calibrated tight interface with the KCNQ1 S1 segment confirmed by compensatory mutagenesis (PMID:26668384, PMID:27626070, PMID:36331187). In epithelia, KCNQ1/KCNE3 heteromers reside in the basolateral membrane and provide the K+ recycling required for cAMP-stimulated transepithelial Cl- secretion; Kcne3 knockout abolishes this secretion without altering KCNQ1 abundance, and 17β-estradiol acutely dissociates the complex via PKCδ phosphorylation of KCNE3 S82 to produce sexually dimorphic colonic secretion (PMID:20051516, PMID:21911611). In skeletal muscle, KCNE3 assembles with Kv3.4 to form a subthreshold channel that sets resting membrane potential, an interaction dependent on PKC phosphorylation at S82 (PMID:11207363, PMID:16449802). KCNE3 also modulates cardiac currents through Kv4.3 and Kv12.2 and regulates neuronal Kv4.2, and timeline disease findings link KCNE3 variants to familial periodic paralysis, Brugada syndrome, long QT syndrome, and atrial fibrillation through gain- or loss-of-function effects on these partner channels (PMID:11207363, PMID:19122847, PMID:19306396, PMID:19623261).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2001 High

    Established KCNE3 as a functional β-subunit by showing it assembles with Kv3.4 to create a distinct subthreshold channel that sets skeletal muscle resting potential, and tied a KCNE3 variant to periodic paralysis.

    Evidence Patch-clamp, co-immunoprecipitation, heterologous expression and genetic segregation of R83H

    PMID:11207363

    Open questions at the time
    • R83H pathogenicity later disputed
    • structural basis of Kv3.4 modulation not resolved
  2. 2002 High

    Demonstrated that KCNE3 modulation of KCNQ1 has direct physiological consequence by showing ectopic KCNE3 accelerates current and shortens action potential and QT interval in vivo.

    Evidence Heterologous co-expression, adenoviral transduction in guinea pig ventricle, patch-clamp and ECG

    PMID:11956246

    Open questions at the time
    • ectopic rather than native cardiac context
    • mechanism of gating change not yet mapped to residues
  3. 2004 High

    Localized KCNQ1-activating function to the KCNE3 transmembrane domain, distinguishing it from the C-terminus-driven KCNE1 mechanism and defining a bipartite model.

    Evidence Truncation mutagenesis panel with whole-cell patch-clamp in heterologous cells

    PMID:15572349

    Open questions at the time
    • specific contact residues not identified
    • did not resolve voltage-sensor versus gate target
  4. 2006 High

    Identified S82 as the functional PKC phosphorylation site required for MiRP2-Kv3.4 function and showed R83H confers pathological pH sensitivity rather than blocking phosphorylation.

    Evidence Mutagenesis, PKC phosphorylation assays and patch-clamp

    PMID:16449802

    Open questions at the time
    • physiological trigger of S82 phosphorylation in muscle not defined
    • kinase identity in vivo not established
  5. 2008 Medium

    Extended KCNE3 partnerships to cardiac Kv4.3 and Kv11.1 and linked gain-of-function variants (R99H, V17M) to Brugada syndrome and atrial fibrillation.

    Evidence Co-IP from human atrial tissue and voltage-clamp of channel complexes in CHO and oocytes

    PMID:18209471 PMID:19122847

    Open questions at the time
    • single-method electrophysiology for V17M
    • in vivo arrhythmic mechanism not tested
  6. 2009 Medium

    Showed the same R99H variant reduces KCNQ1/KCNE3 current (long QT mechanism) and that KCNE3 suppresses Kv12.2 surface expression in native brain, revealing partner-dependent and additive regulation.

    Evidence Patch-clamp in CHO cells; siRNA knockdown, surface biotinylation and brain co-IP for Kv12.2

    PMID:19306396 PMID:19623261

    Open questions at the time
    • opposite directional effects of R99H across partners unreconciled
    • tripartite KCNE1/KCNE3/Kv12.2 stoichiometry not resolved
  7. 2010 High

    Proved in vivo that KCNE3 biophysical modulation of basolateral KCNQ1—not KCNQ1 abundance—is required for transepithelial Cl- secretion.

    Evidence Kcne3 knockout mice, Ussing chamber secretion assays, immunolocalization and membrane fractionation

    PMID:20051516

    Open questions at the time
    • upstream signaling controlling complex activity in epithelia not yet defined
  8. 2011 High

    Revealed dynamic, hormone-regulated control of the complex: estradiol dissociates KCNQ1:KCNE3 via PKCδ phosphorylation of S82, explaining sexual dimorphism in colonic secretion.

    Evidence Co-IP, patch-clamp, short-circuit current and S82A mutagenesis in crypts and CHO cells

    PMID:21911611

    Open questions at the time
    • estrogen receptor coupling to PKCδ not detailed
    • in vivo reversibility kinetics not measured
  9. 2013 High

    Uncovered an extracardiac arrhythmogenic mechanism whereby Kcne3 loss causes aldosterone-dependent adrenal pathology that impairs ventricular repolarization.

    Evidence Kcne3-/- mice with ECG, patch-clamp, histology, blood assays and ischemia-reperfusion

    PMID:24225147

    Open questions at the time
    • link between KCNE3 channel function and aldosterone regulation not molecularly defined
  10. 2014 High

    Showed KCNE3 shapes neuronal excitability by regulating Kv4.2 in spiral ganglion neurons independent of KChIP2.

    Evidence Kcne3-/- mice with patch-clamp and conductance analysis of spiral ganglion neurons

    PMID:24727472

    Open questions at the time
    • direct KCNE3-Kv4.2 binding not structurally mapped
    • behavioral/auditory consequence not assessed
  11. 2015 High

    Defined the gating mechanism: KCNE3 acts on KCNQ1 by hyperpolarizing S4 voltage-sensor movement via D54/D55–R228 electrostatics, affecting the gate only indirectly—mechanistically distinct from KCNE1.

    Evidence Voltage clamp fluorometry, mutagenesis, domain-swap and PIP2 depletion separating S4 movement from gating

    PMID:26668384 PMID:28808020

    Open questions at the time
    • full atomic stoichiometry of S4 contacts addressed separately by structural work
  12. 2016 High

    Built an integrative structural model of the contacts driving constitutive activation, identified an N-terminally extended isoform that tunes partner specificity, and mapped the aldosterone/Akt/Rab pathway underlying AF in knockouts.

    Evidence NMR-guided modeling with electrophysiology; oocyte electrophysiology of isoforms; Kcne3-/- mice with co-IP, Western blot and spironolactone rescue

    PMID:26985008 PMID:27162025 PMID:27626070

    Open questions at the time
    • isoform tissue distribution and abundance incompletely defined
    • high-resolution structure not yet available at this stage
  13. 2017 High

    Demonstrated KCNE3 is required for normal skeletal muscle contractile dynamics and controls Kv3.4/mERG subunit expression and fiber-type composition.

    Evidence Kcne3-/- mice with muscle force measurements, myoblast patch-clamp, microarray and fiber-type immunofluorescence

    PMID:28356343

    Open questions at the time
    • transcriptional mechanism controlling Kv3.4/KCNH2 expression not defined
  14. 2022 High

    Confirmed that a precisely calibrated tight S1–KCNE3 transmembrane interface is required for constitutive activity, using compensatory mutant rescue to prove direct physical contact.

    Evidence Volume-scanning and compensatory mutagenesis with electrophysiology guided by the KCNQ1-KCNE3-calmodulin structure

    PMID:36331187

    Open questions at the time
    • energetics of the interface not quantified
    • how S1 contact integrates with S4 stabilization not unified
  15. 2025 Medium

    Cryo-EM reassessment identified a second KCNE3-dependent PIP2-binding site, recasting KCNE3 as converting KCNQ1 into a voltage-insensitive, PIP2- and GPCR-gated channel.

    Evidence Cryo-EM, electrophysiology and PIP2 site mutagenesis (preprint)

    Open questions at the time
    • preprint not peer-reviewed
    • GPCR signaling coupling demonstrated only inferentially
    • functional contribution of second PIP2 site in native epithelia not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How KCNE3 selects among its many partner α-subunits in different tissues, and how upstream signaling (PKC, estrogen, aldosterone, PIP2/GPCR) is integrated to dynamically gate these complexes in vivo, remains incompletely resolved.
  • no unified model of partner selection across tissues
  • in vivo signaling integration not reconstituted
  • stoichiometry of multi-KCNE/multi-α complexes uncertain

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0008289 lipid binding 1
Localization
GO:0005886 plasma membrane 2
Partners
CALM1KCNC4KCND2KCND3KCNH2KCNH3KCNQ1
Complex memberships
KCNQ1/KCNE3 channelMiRP2-Kv3.4 channel

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 KCNE3 (MiRP2) assembles with the pore-forming subunit Kv3.4 in skeletal muscle to form a subthreshold, voltage-gated potassium channel complex. MiRP2-Kv3.4 channels differ from Kv3.4 alone in unitary conductance, voltage-dependent activation, recovery from inactivation, steady-state open probability, and block by peptide toxin, and set resting membrane potential without producing afterhyperpolarization or cumulative inactivation. Electrophysiology (patch-clamp), co-immunoprecipitation, heterologous expression Cell High 11207363
2001 A missense mutation R83H in KCNE3 reduces current density of MiRP2-Kv3.4 complexes and diminishes their capacity to set resting membrane potential, segregating with familial periodic paralysis. Electrophysiology (patch-clamp), genetic segregation analysis Cell Medium 11207363
2006 KCNE3 (MiRP2) has a single functional PKC phosphorylation site at serine 82, and normal MiRP2-Kv3.4 function requires phosphorylation of this site. The R83H variant does not prevent PKC phosphorylation of S82 but endows MiRP2-Kv3.4 channels with sensitivity to intracellular pH changes across the physiological range (pKa ~7.3, consistent with histidine protonation), reducing single-channel current as internal pH is lowered. Electrophysiology (patch-clamp), mutagenesis, PKC phosphorylation assays FASEB journal High 16449802
2004 The KCNE3 transmembrane domain alone is sufficient for assembly with and constitutive activation (basal activation) of KCNQ1 channels; neither the N-terminal nor C-terminal regions are required for this modulation. This contrasts with KCNE1, where the transmembrane domain is passive and the C-terminus drives modulation, revealing a bipartite model of KCNQ1 modulation. Truncation mutagenesis, heterologous expression, whole-cell patch-clamp The Journal of general physiology High 15572349
2008 KCNE3 physically interacts with Kv4.3 in human atrial tissue, demonstrated by co-immunoprecipitation. A missense mutation R99H in KCNE3 significantly increases Ito current density when co-expressed with KCND3 (Kv4.3), establishing a gain-of-function role in Brugada syndrome pathogenesis. Co-immunoprecipitation from human atrial tissue, whole-cell patch-clamp in CHO cells, heterologous co-transfection Circulation. Arrhythmia and electrophysiology High 19122847
2008 KCNE3 V17M mutation increases activity of Kv4.3/KCNE3 and Kv11.1/KCNE3 channels in Xenopus oocytes, consistent with gain-of-function on multiple cardiac currents and susceptibility to atrial fibrillation. Two-electrode voltage-clamp in Xenopus laevis oocytes, heterologous expression Cellular physiology and biochemistry Medium 18209471
2009 KCNE3 mutation R99H reduces outward current through KCNQ1/KCNE3 complexes in CHO cells, representing a loss-of-function mechanism linked to long QT syndrome (LQTS). Mutation T4A showed no statistically significant change in current density. Whole-cell patch-clamp in CHO cells stably expressing KCNQ1, heterologous co-expression Human mutation Medium 19306396
2010 KCNQ1/KCNE3 heteromers are present in basolateral membranes of intestinal and tracheal epithelial cells. Kcne3 knockout mice show drastically reduced cAMP-stimulated electrogenic Cl- secretion across tracheal and intestinal epithelia, demonstrating that KCNE3 modification of KCNQ1 biophysical properties (not KCNQ1 abundance or localization) is essential for K+ recycling and transepithelial Cl- secretion. Kcne3 knockout mouse model, Ussing chamber Cl- secretion measurements, immunolocalization, membrane fractionation The Journal of biological chemistry High 20051516
2011 KCNQ1 and KCNE3 co-associate in colonic crypts and 17β-estradiol (E2) rapidly (<15 min) dissociates KCNQ1:KCNE3 complexes specifically in female crypts. This dissociation underlies the sexual dimorphism in colonic Cl- secretion. KCNE3-S82A mutation (abolishing PKCδ phosphorylation site) causes rapid run-down and insensitivity to E2, implicating phosphorylation at S82 in estrogen-regulated channel dissociation. Co-immunoprecipitation, whole-cell patch-clamp, short-circuit current recording, co-expression in CHO cells The Journal of physiology High 21911611
2012 KCNE3 T4A mutation increases Ito reconstituted by co-expressing Kv4.3 + KChIP2b + KCNE3 in CHO cells, representing a gain-of-function mechanism associated with Brugada-pattern ECG. Whole-cell patch-clamp in CHO cells, heterologous co-expression Circulation journal Medium 22987075
2013 Kcne3 deletion in mice causes secondary hyperaldosteronism associated with adrenal-specific lymphocyte infiltration, which in turn impairs ventricular repolarization (QTc prolongation) and predisposes to post-ischemia ventricular tachycardia. This establishes an extracardiac, aldosterone-dependent arrhythmogenic mechanism for KCNE3 loss. Kcne3-/- mouse model, ECG, patch-clamp, qPCR, microarray, coronary artery ligation/reperfusion, blood analysis, histology FASEB journal High 24225147
2014 KCNE3 null deletion abolishes characteristic wide variations in resting membrane potential of spiral ganglion neurons and causes age-dependent alterations in action potential and firing properties. KCNE3 regulates activity of Kv4.2 channels in spiral ganglion neurons, with null mutation resulting in enhanced outward K+ currents. Kcne3-/- mouse model, patch-clamp of spiral ganglion neurons, conductance analysis The Journal of biological chemistry High 24727472
2015 KCNE3 acts primarily by shifting the voltage dependence of S4 (voltage sensor) movement to extreme hyperpolarized potentials, making KCNQ1/KCNE3 channels constitutively conducting within the physiological voltage range. Two negatively charged residues D54 and D55 in KCNE3 are essential for this effect, exerting electrostatic interaction with R228 in the KCNQ1 S4 segment. KCNE3 directly affects voltage sensor movement and only indirectly affects the gate. Voltage clamp fluorometry, mutagenesis, PIP2 depletion, separation of S4 movement and gate opening Proceedings of the National Academy of Sciences of the United States of America High 26668384
2015 KCNE1 and KCNE3 affect KCNQ1 gating by different mechanisms: KCNE1 affects both S4 movement and the gate, whereas KCNE3 affects S4 movement and only affects the gate if intact S4-to-gate coupling is present. A triple mutation in the middle of the KCNE3 transmembrane segment introduces KCNE1-like effects on the second S4 movement and the gate. Differences in two residues at the external end of KCNE transmembrane segments underlie differences in effects on the first S4 movement and voltage sensor-to-gate coupling. Voltage clamp fluorometry, mutagenesis (triple TM mutation), PIP2 depletion, separation of S4 movement and gate opening Proceedings of the National Academy of Sciences of the United States of America High 28808020
2016 An integrative structural model of the KCNE3-KCNQ1 complex, built from NMR, computational, and electrophysiological data, shows that KCNE3 residues at both ends of its transmembrane domain directly interact with residues on the intra- and extracellular ends of the KCNQ1 voltage-sensing domain S4 helix, stabilizing the activated 'up' state of S4 and thereby inducing constitutive activation of the channel gate. Solution NMR structure, computational modeling, electrophysiology, mutagenesis Science advances High 27626070
2016 Novel N-terminally extended (full-length) KCNE3 isoform, encoded by a previously undiscovered exon 1 protein-coding region adding 44 residues to the extracellular domain, preserves KCNQ1 constitutive activation but prevents KCNE3 inhibition of Kv4.2 and KCNQ4. This indicates the additional N-terminal segment modulates partner-channel specificity. Two-electrode voltage-clamp in Xenopus laevis oocytes, heterologous expression, RT-PCR/Western blot for tissue expression FASEB journal Medium 27162025
2016 In Kcne3-/- mice, AF predisposition arises from increased aldosterone-dependent recycling of Kv1.5 channels to the Z-disc/T-tubulus region and lateral membrane via activation of the Akt/AS160 pathway and Rab4, -5, and -9 GTPases, leading to reduced atrial effective refractory period. Spironolactone treatment normalized these effects, confirming aldosterone dependence. Kcne3-/- mouse model, electrophysiology (invasive), co-immunoprecipitation, Western blot for Akt/AS160 phosphorylation, pharmacological rescue with spironolactone FASEB journal High 26985008
2009 KCNE1 and KCNE3 both regulate Kv12.2 (KCNH3) channel surface expression and gating: siRNA knockdown of KCNE1 or KCNE3 increases macroscopic Kv12.2 currents ~4-fold by increasing membrane surface expression (not total protein). Co-expression of both siRNAs produces ~9-fold increase (additive). Native co-immunoprecipitation from mouse brain membranes shows KCNE1 and KCNE3 interact with Kv12.2 simultaneously, suggesting tripartite complexes in vivo. siRNA knockdown in Xenopus oocytes, surface biotinylation assay, co-immunoprecipitation from mouse brain, electrophysiology PloS one High 19623261
2017 KCNE3 deletion in mice impairs skeletal muscle function: Kcne3-/- mice show abnormal hindlimb clasping, loss of biphasic contractile force decline with repetitive stimulation in vivo and in vitro, and myoblasts from Kcne3-/- mice have faster-inactivating and smaller sustained outward K+ currents. Kcne3 deletion also specifically down-regulates KCNC4 (Kv3.4) and KCNH2 (mERG) alpha subunit expression and shifts muscle fiber type toward type IIa fast-twitch oxidative fibers. Kcne3-/- mouse model, in vivo/in vitro muscle force measurements, patch-clamp of myoblasts, microarray, immunofluorescence FASEB journal High 28356343
2002 Ectopic expression of KCNE3 in cardiac myocytes (via adenoviral delivery) interacts with KCNQ1 to increase outward current and accelerate activation, reducing action potential duration >3-fold in transduced cells and abbreviating QT interval by ~10% in guinea pigs. Heterologous co-expression (CHO), adenoviral transduction in guinea pig ventricle, patch-clamp, ECG recording The Journal of clinical investigation High 11956246
2022 Optimized tight binding between the S1 segment of KCNQ1 and the transmembrane domain of KCNE3 is required for constitutive channel activity. Volume scanning mutagenesis of interacting residues at the S1-KCNE3 interface shows the inter-helical distance is precisely calibrated; two pairs of compensatory KCNQ1/KCNE3 mutants partially restore constitutive activity when co-expressed, confirming a direct physical interaction. Volume scanning mutagenesis, compensatory mutagenesis, electrophysiology, based on KCNQ1-KCNE3-calmodulin complex structure eLife High 36331187
2025 Cryo-EM structures of KCNQ1-KCNE1 and reassessed KCNQ1-KCNE3 structures reveal two PIP2-binding sites in both complexes. KCNE3 contributes to a second, previously uncharacterized PIP2-binding site involving residues critical for voltage sensor-pore domain coupling. Through this site, KCNE3 converts KCNQ1 into a voltage-insensitive, PIP2-gated channel governed by GPCR signaling, maintaining ion homeostasis in non-excitable epithelial cells. Cryo-EM structure determination, electrophysiology, PIP2 binding site mutagenesis bioRxivpreprint Medium

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis. Cell 240 11207363
2008 Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome. Circulation. Arrhythmia and electrophysiology 232 19122847
2010 Disruption of the K+ channel beta-subunit KCNE3 reveals an important role in intestinal and tracheal Cl- transport. The Journal of biological chemistry 92 20051516
2008 KCNE3 mutation V17M identified in a patient with lone atrial fibrillation. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 80 18209471
2002 A mutation in the KCNE3 potassium channel gene is associated with susceptibility to thyrotoxic hypokalemic periodic paralysis. The Journal of clinical endocrinology and metabolism 79 12414843
2015 KCNE1 and KCNE3: The yin and yang of voltage-gated K(+) channel regulation. Gene 71 26410412
2002 Ectopic expression of KCNE3 accelerates cardiac repolarization and abbreviates the QT interval. The Journal of clinical investigation 57 11956246
2017 KCNE1 and KCNE3 modulate KCNQ1 channels by affecting different gating transitions. Proceedings of the National Academy of Sciences of the United States of America 47 28808020
2016 Structural basis for KCNE3 modulation of potassium recycling in epithelia. Science advances 46 27626070
2005 Ménière's disease is associated with single nucleotide polymorphisms in the human potassium channel genes, KCNE1 and KCNE3. ORL; journal for oto-rhino-laryngology and its related specialties 46 16374062
2006 Phosphorylation and protonation of neighboring MiRP2 sites: function and pathophysiology of MiRP2-Kv3.4 potassium channels in periodic paralysis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 41 16449802
2004 KCNE3 truncation mutants reveal a bipartite modulation of KCNQ1 K+ channels. The Journal of general physiology 41 15572349
2011 Sexual dimorphism and oestrogen regulation of KCNE3 expression modulates the functional properties of KCNQ1 K⁺ channels. The Journal of physiology 37 21911611
2004 Periodic paralysis mutation MiRP2-R83H in controls: Interpretations and general recommendation. Neurology 37 15037716
2003 Lack of association of the potassium channel-associated peptide MiRP2-R83H variant with periodic paralysis. Neurology 35 14504341
2015 KCNE3 acts by promoting voltage sensor activation in KCNQ1. Proceedings of the National Academy of Sciences of the United States of America 34 26668384
2009 Novel KCNE3 mutation reduces repolarizing potassium current and associated with long QT syndrome. Human mutation 31 19306396
2012 KCNE3 T4A as the genetic basis of Brugada-pattern electrocardiogram. Circulation journal : official journal of the Japanese Circulation Society 29 22987075
2019 The potassium channel Kcne3 is a VEGFA-inducible gene selectively expressed by vascular endothelial tip cells. Angiogenesis 22 31754927
2014 Functional significance of K+ channel β-subunit KCNE3 in auditory neurons. The Journal of biological chemistry 21 24727472
2013 Kcne3 deletion initiates extracardiac arrhythmogenesis in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 21 24225147
2004 No mutation in the KCNE3 potassium channel gene in Chinese thyrotoxic hypokalaemic periodic paralysis patients. Clinical endocrinology 21 15212652
2011 Deep resequencing of the voltage-gated potassium channel subunit KCNE3 gene in chronic tinnitus. Behavioral and brain functions : BBF 19 21899751
2009 KCNE1 and KCNE3 beta-subunits regulate membrane surface expression of Kv12.2 K(+) channels in vitro and form a tripartite complex in vivo. PloS one 18 19623261
2006 Protein distribution of Kcnq1, Kcnh2, and Kcne3 potassium channel subunits during mouse embryonic development. The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology 16 16463373
2016 Novel exon 1 protein-coding regions N-terminally extend human KCNE3 and KCNE4. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 14 27162025
2015 Upregulation of basolateral small conductance potassium channels (KCNQ1/KCNE3) in ulcerative colitis. Biochemical and biophysical research communications 14 26718405
2020 Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition. Scientific reports 13 32144311
2022 Comparing the structural dynamics of the human KCNE3 in reconstituted micelle and lipid bilayered vesicle environments. Biochimica et biophysica acta. Biomembranes 12 35716725
2022 Optimized tight binding between the S1 segment and KCNE3 is required for the constitutively open nature of the KCNQ1-KCNE3 channel complex. eLife 12 36331187
2016 Regulation of human cardiac potassium channels by full-length KCNE3 and KCNE4. Scientific reports 12 27922120
2007 The MiRP2-Kv3.4 potassium channel: muscling in on Alzheimer's disease. Molecular pharmacology 11 17595326
2016 Increased aldosterone-dependent Kv1.5 recycling predisposes to pacing-induced atrial fibrillation in Kcne3-/- mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 9 26985008
2016 Variants in the KCNE1 or KCNE3 gene and risk of Ménière's disease: A meta-analysis. Journal of vestibular research : equilibrium & orientation 8 26890422
2022 Investigating Structural Dynamics of KCNE3 in Different Membrane Environments Using Molecular Dynamics Simulations. Membranes 5 35629795
2017 Targeted deletion of Kcne3 impairs skeletal muscle function in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 4 28356343
2025 KCNE3 Facilitates M1 Macrophage Polarization by Suppressing the Wnt/β-Catenin Pathway, Inhibiting Glioma Proliferation, Migration, and Invasion. Molecular carcinogenesis 3 40146943
2024 Studying Conformational Properties of Transmembrane Domain of KCNE3 in a Lipid Bilayer Membrane Using Molecular Dynamics Simulations. Membranes 3 38392672
2023 Electron paramagnetic resonance spectroscopic characterization of the human KCNE3 protein in lipodisq nanoparticles for structural dynamics of membrane proteins. Biophysical chemistry 2 37531799
2009 Bacterial synthesis, purification, and solubilization of membrane protein KCNE3, a regulator of voltage-gated potassium channels. Biochemistry. Biokhimiia 2 19961415
2025 Structural Dynamics and Topology of Human KCNE3 in Lipid Bilayers Studied by Site-Directed Spin Labeling and Electron Paramagnetic Resonance Spectroscopy. The journal of physical chemistry. B 1 40981745
2019 NMR resonance assignments and secondary structure of a mutant form of the human KCNE1 channel accessory protein that exhibits KCNE3-like function. Biomolecular NMR assignments 1 30603955

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