Affinage

KCNE2

Potassium voltage-gated channel subfamily E member 2 · UniProt Q9Y6J6

Length
123 aa
Mass
14.5 kDa
Annotated
2026-06-10
78 papers in source corpus 44 papers cited in narrative 42 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

KCNE2 (MiRP1) is a single-transmembrane ancillary β subunit that promiscuously co-assembles with diverse voltage-gated cation channel α subunits to tune their gating, conductance, surface trafficking, and current density across cardiac, epithelial, neuronal, and endocrine tissues (PMID:10219239, PMID:18603586). Its founding role is in cardiac repolarization, where co-assembly with HERG (KCNH2) reconstitutes native-like IKr and where multiple missense mutations (e.g. V65M, T10M, M54T) reduce IKr by accelerating inactivation or altering gating, defining the long-QT (LQT6) phenotype (PMID:10219239, PMID:12185453, PMID:18006462), while the gain-of-function R27C variant acts through the KCNQ1-KCNE2 background current to cause familial atrial fibrillation (PMID:15368194). Beyond hERG, KCNE2 modulates an unusually broad partner set—HCN1-4 pacemaker channels (PMID:15292247, PMID:19429827, PMID:23631727), KCNQ1 (alone and within tripartite KCNQ1-KCNE1 IKs complexes) (PMID:15579540, PMID:17161791), Kv1.5, Kv2.1, and Kv4 family channels (PMID:18603586, PMID:19219384), and the L-type Ca2+ channel Cav1.2 (PMID:24681347)—through direct physical interaction at defined transmembrane and C-terminal contacts (PMID:12856183, PMID:24827085). A major function is regulation of channel biogenesis and surface delivery: KCNE2 retains N-type-inactivating Kv α subunits in the early secretory pathway as a composition checkpoint (PMID:21943416, PMID:21943417), requires a C-terminal KSKR motif for its own ER export (PMID:31679457), and suppresses KCNQ1 surface expression, with S98 phosphorylation accelerating hERG degradation as a post-translational brake on IKr (PMID:22180649). In native epithelia, the apical KCNQ1-KCNE2 channel is essential for gastric acid secretion in parietal cells (PMID:15579540, PMID:16754665), thyroid iodide uptake (PMID:22549510), and choroid plexus K+/Cl−/myo-inositol homeostasis via co-regulation with KCNA3 and the solute transporter SMIT1 (PMID:21859894, PMID:24595108); mouse Kcne2 loss further impairs pancreatic β-cell insulin secretion to cause type 2 diabetes (PMID:28280005) and disrupts pulmonary gas exchange (PMID:31162977). Cardiac-specific Kcne2 deletion produces dilated cardiomyopathy and heart failure (PMID:32584506), and reduced cardiac KCNE2 drives pathological hypertrophy through enhanced Cav1.2-mediated Ca2+ entry and calcineurin-NFAT signaling (PMID:28611128).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1999 High

    Established KCNE2's founding function—that a small accessory subunit converts HERG into native-like cardiac IKr and that its mutations cause long-QT syndrome—answering what MiRP1 contributes to a physiological current.

    Evidence Whole-cell and single-channel patch clamp of MiRP1+HERG co-expression and LQT-associated mutants in oocytes and mammalian cells

    PMID:10219239

    Open questions at the time
    • Stoichiometry and structural basis of the HERG-KCNE2 interface not resolved
    • Whether MiRP1 is the dominant native IKr β subunit in human heart not established here
  2. 2000 Medium

    Extended KCNE2 partner promiscuity beyond hERG to neuronal M-channel subunits, raising the question of how one β subunit modulates structurally distinct α subunits.

    Evidence Co-immunoprecipitation and whole-cell electrophysiology of KCNE2 with KCNQ2/KCNQ3 in COS cells

    PMID:11034315

    Open questions at the time
    • No native neuronal demonstration of KCNQ2/3-KCNE2 complexes
    • Physiological relevance to brain excitability untested
  3. 2001 Medium

    Distinguished which KCNE2-induced biophysical changes actually matter for repolarization and localized part of the HERG interaction to the cyclic nucleotide binding domain.

    Evidence HERG CNBD mutagenesis, co-expression electrophysiology, and computational action potential modeling

    PMID:11278781 PMID:11440975

    Open questions at the time
    • Direct structural contact within the CNBD not mapped
    • Modeling conclusions depend on assumed expression levels
  4. 2002 Medium

    Defined an additional gating mechanism (accelerated inactivation) by which a KCNE2 mutation reduces IKr, broadening the molecular spectrum of LQT6.

    Evidence Whole-cell patch clamp and co-localization of V65M mutant with HERG in CHO cells

    PMID:12185453

    Open questions at the time
    • Penetrance and in vivo arrhythmia link not addressed
    • Single mutant in a heterologous background
  5. 2003 Medium

    Identified HCN pacemaker channels as physical and functional KCNE2 partners, expanding its role into cardiac automaticity and identifying the C-terminal tail as the HCN4 interaction site.

    Evidence Two-electrode and patch clamp in oocytes/CHO cells plus yeast two-hybrid for HCN4; AP-clamp analysis of LQT6 mutants on HERG

    PMID:12856183 PMID:12923204

    Open questions at the time
    • Native HCN-KCNE2 association not yet shown
    • Stoichiometry of the interaction unknown
  6. 2004 High

    Confirmed native cardiac HCN2-KCNE2 complexes and discovered the gain-of-function R27C variant acting through the KCNQ1-KCNE2 background current, linking KCNE2 to atrial fibrillation as distinct from LQT.

    Evidence Co-IP of endogenous HCN2 and KCNE2 in neonatal rat myocytes; AF-kindred sequencing with electrophysiology testing R27C against multiple partners

    PMID:15292247 PMID:15368194

    Open questions at the time
    • How a single residue selectively affects KCNQ1 but not HERG/HCN currents not mechanistically explained
    • In vivo AF causation not demonstrated
  7. 2004 High

    Established the apical gastric KCNQ1-KCNE2 channel and its regulation by acid pH, PIP2, cAMP, and purinergic signaling, defining KCNE2's first epithelial physiological context.

    Evidence In situ hybridization, confocal immunofluorescence, and patch clamp in parietal cells and COS cells

    PMID:15579540

    Open questions at the time
    • Direct coupling to H+,K+-ATPase activity not established
    • In vivo requirement not yet tested at this stage
  8. 2006 High

    Demonstrated in vivo that KCNE2 is essential for gastric acid secretion with a gene-dose effect, converting in vitro complex assembly into a defined organ-level physiological requirement.

    Evidence Targeted Kcne2 knockout mice with acid-secretion measurement, histology, and KCNQ1 immunolocalization

    PMID:16754665

    Open questions at the time
    • Secondary systemic consequences of achlorhydria not yet mapped
    • Mechanism of abnormal KCNQ1 distribution unclear
  9. 2006 Medium

    Showed KCNE2 participates in native cardiac IKs as a tripartite KCNQ1-KCNE1-KCNE2 complex and modulates Kv4.3 Ito, reinforcing multi-channel cardiac regulation.

    Evidence Co-IP and immunocytochemistry in adult rat ventricular myocytes; patch clamp of Kv4.3 in COS-7 cells

    PMID:17161791 PMID:17259113

    Open questions at the time
    • Stoichiometry within the tripartite complex unresolved
    • Kv4.3 modulation rests on single-method electrophysiology
  10. 2007 Medium

    Revealed KCNE2's distinctive trafficking behavior versus KCNE1 and provided the first gating mechanism for the reduced-penetrance T10M arrhythmia variant.

    Evidence Co-IP, surface labeling, Brefeldin A and ER-retention engineering for trafficking; whole-cell clamp of T10M in CHO cells

    PMID:17895974 PMID:18006462

    Open questions at the time
    • Functional significance of extracellular/vesicular KCNE2 pool unknown
    • Trafficking differences not linked to a defined sorting determinant yet
  11. 2008 High

    Identified Kv1.5 as a novel in vivo KCNE2 partner and showed KCNE2 controls Kv1.5 protein levels and intercalated-disc trafficking, while structural spectroscopy began defining MiRP1 domain architecture.

    Evidence Kcne2 knockout mice with myocyte electrophysiology and native co-IP; FTIR/CD spectroscopy of synthetic MiRP1 peptides; Kv4.3/KChIP2 complex electrophysiology

    PMID:18221016 PMID:18501111 PMID:18536731 PMID:18603586

    Open questions at the time
    • Mechanism by which KCNE2 stabilizes mature Kv1.5 protein not defined
    • Peptide spectroscopy does not represent the native folded protein
  12. 2009 Medium

    Consolidated KCNE2 as a broad single-channel-level modulator of all four HCN isoforms, Kv2.1, and Kv4.3, and showed it can dynamically substitute into IKs complexes and traffic independently of KCNQ1.

    Evidence Whole-cell and single-channel recordings, membrane fractionation, native-tissue co-IP (Kv2.1), pulse-chase and biotinylation trafficking assays, myocyte electrophysiology

    PMID:19219384 PMID:19372218 PMID:19429827 PMID:20042375

    Open questions at the time
    • Tissue-specific partner selection rules not established
    • How one β subunit produces opposite effects on different α subunits unexplained
  13. 2011 High

    Defined KCNE2 as a secretory-pathway checkpoint that retains N-type-inactivating Kv subunits and uncovered choroid plexus epithelial functions controlling CSF ion homeostasis.

    Evidence Electrophysiology, co-IP, immunofluorescence, Brefeldin A and dynamin-inhibitor dissection; Kcne2 KO with CPe patch clamp, pharmacology, and CSF ion measurement

    PMID:21859894 PMID:21943416 PMID:21943417

    Open questions at the time
    • Molecular machinery executing ER retention not identified
    • Link between altered CPe trafficking and CSF chloride change not fully mechanistic
  14. 2010 Medium

    Provided rigorous NMR backbone assignments and helical secondary-structure mapping of human MiRP1, establishing a structural framework for interpreting interaction studies.

    Evidence Solution NMR triple-resonance assignment and CD spectroscopy of E. coli-expressed MiRP1 in detergent micelles

    PMID:21087668

    Open questions at the time
    • No full tertiary structure or channel-bound conformation
    • No functional validation in this study
  15. 2012 High

    Extended the apical KCNQ1-KCNE2 channel's physiological role to thyroid iodide uptake and dissected which transport step requires it, and defined neuronal HCN dysfunction upon Kcne2 loss.

    Evidence In vivo PET iodide imaging, in vitro uptake assays, and Kcne2 KO/pharmacology for thyroid; KO brain-slice patch clamp and co-IP for thalamocortical HCN

    PMID:22549510 PMID:22880098

    Open questions at the time
    • Negative brain co-IP leaves the neuronal HCN mechanism likely indirect and undefined
    • Cell type mediating iodide retention not pinpointed
  16. 2011 Medium

    Identified S98 phosphorylation as a post-translational mechanism by which KCNE2 controls hERG protein stability and IKr amplitude.

    Evidence Phospho-specific antibody, adenoviral manipulation, Western blotting, and immunofluorescence in adult cardiac myocytes

    PMID:22180649

    Open questions at the time
    • Kinase responsible for S98 phosphorylation not identified
    • Degradation pathway targeting hERG not defined
  17. 2014 Medium

    Linked the KCNQ1-KCNE2 channel to solute-transporter regulation and mapped the precise transmembrane interaction residues distinguishing KCNE2 from KCNE1, and added Cav1.2 as a physical KCNE2 partner.

    Evidence Native-tissue co-IP, myo-inositol uptake assays, CSF metabolomics and seizure rescue; solution NMR plus electrophysiology of KCNE2-KCNQ1 contacts; Cav1.2 co-IP, domain deletion and patch clamp

    PMID:24595108 PMID:24681347 PMID:24827085

    Open questions at the time
    • How a constitutive K+ channel mechanistically inhibits a Na+-coupled transporter not fully resolved
    • Cav1.2 regulation mechanism beyond the N-terminal inhibitory module untested
  18. 2016 Medium

    Connected KCNE2 loss to altered cellular survival signaling and a hypoxia-dependent cytoskeletal interaction, broadening its role beyond channel gating.

    Evidence Ischemia/reperfusion in Kcne2 KO mice with GSK-3β phospho-analysis and pharmacological epistasis; yeast two-hybrid and condition-dependent co-IP for filamin C

    PMID:26952045 PMID:26956495

    Open questions at the time
    • Mechanism linking KCNE2 to GSK-3β phosphorylation unknown
    • Filamin C interaction lacks functional electrophysiological readout
  19. 2017 High

    Established KCNE2's roles in β-cell insulin secretion and as a brake on Cav1.2-driven calcineurin-NFAT hypertrophic signaling, extending its physiology to metabolic and remodeling pathways.

    Evidence Kcne2 KO glucose tolerance, insulin assays and β-cell patch clamp; bidirectional KCNE2 manipulation with TAC model, calcineurin assays, and in vivo gene delivery

    PMID:28280005 PMID:28611128

    Open questions at the time
    • Channel partner mediating β-cell K+ current loss not defined
    • Direct vs indirect contribution of Cav1.2 modulation to hypertrophy not separated
  20. 2019 Medium

    Resolved isoform- and concentration-dependent KCNE2:HCN stoichiometry, defined the KSKR ER-export motif required for KCNE2 forward trafficking, and added pulmonary KCNQ1-KCNE2 complexes governing gas exchange.

    Evidence Single-molecule subunit counting; trafficking motif mutagenesis with biotinylation and electrophysiology; lung-tissue co-IP and Kcne2 KO blood-gas analysis

    PMID:31162977 PMID:31235733 PMID:31679457

    Open questions at the time
    • Functional consequence of variable stoichiometry in native tissue untested
    • Trafficking factors recognizing the KSKR motif unidentified
  21. 2020 Medium

    Demonstrated that cardiac-specific KCNE2 loss causes dilated cardiomyopathy and that its systemic loss reshapes the gut microbiome via achlorhydria, linking organ-level and microbial axes to heart failure progression.

    Evidence Cardiac-specific vs global Kcne2 KO with histology, microbiome profiling, PPI treatment, and survival analysis

    PMID:32584506

    Open questions at the time
    • Channel partner driving cardiomyopathy in cardiac-specific KO not pinpointed
    • Mechanism by which microbiome changes modulate cardiac survival unclear
  22. 2021 Low

    Identified testin as a C-terminal KCNE2 partner that selectively reverses KCNE2 modulation of Kv1.5 but not KCNQ1, revealing partner-specific regulatory layering.

    Evidence Yeast two-hybrid, co-IP, and whole-cell patch clamp in CHO cells

    PMID:33464998

    Open questions at the time
    • In vitro system only, no native-tissue confirmation
    • Physiological context of testin-KCNE2 regulation untested
  23. 2022 Medium

    Defined how KCNE2 imposes Ca2+/calmodulin dependence on the KCNQ1-KCNE2 complex, providing the mechanism by which KCNQ1 gain-of-function mutations cause disease through this complex.

    Evidence Whole-cell patch clamp with intracellular Ca2+ and calmodulin manipulation and KCNQ1 mutagenesis in heterologous cells

    PMID:36077086

    Open questions at the time
    • Structural basis of Ca2+/calmodulin gating within the complex not resolved
    • Tissue-specific relevance of this regulatory mode not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single small β subunit selects among many α-subunit partners in a tissue-specific manner, and the structural basis for its opposing effects on different channels, remains unresolved.
  • No high-resolution structure of any KCNE2-channel complex
  • Determinants of tissue-specific partner choice unknown
  • Rules governing gain- vs loss-of-function modulation across partners undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 6 GO:0005215 transporter activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 4 GO:0005783 endoplasmic reticulum 3
Pathway
R-HSA-382551 Transport of small molecules 3 R-HSA-112316 Neuronal System 2 R-HSA-397014 Muscle contraction 2 R-HSA-9609507 Protein localization 2
Partners
CACNA1CHCN2HCN4KCNA5KCNB1KCNH2KCNQ1TES
Complex memberships
HCN-KCNE2 pacemaker channelHERG(KCNH2)-KCNE2 (IKr) channelKCNQ1-KCNE1-KCNE2 (IKs) tripartite channelKCNQ1-KCNE2 channel

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 KCNE2 (MiRP1) assembles with HERG (KCNH2) to form IKr potassium channels. Co-expression of MiRP1 with HERG alters gating kinetics, unitary conductance, regulation by potassium, and biphasic inhibition by E-4031, making the complex resemble native cardiac IKr. Three KCNE2 missense mutations associated with LQT syndrome cause channels that open slowly and close rapidly, reducing potassium currents. Electrophysiology (whole-cell and single-channel patch clamp), heterologous expression in Xenopus oocytes and mammalian cells, functional characterization of LQT-associated mutants Cell High 10219239
2000 KCNE2 (MiRP1) co-assembles with KCNQ2 and/or KCNQ3 (M-type channel subunits expressed in brain) and accelerates their deactivation kinetics. KCNE2 mRNA is expressed in brain regions that also express KCNQ2/KCNQ3. Co-immunoprecipitation, heterologous expression in COS cells, whole-cell electrophysiology FEBS letters Medium 11034315
2001 The cyclic nucleotide binding domain (CNBD) of HERG may be involved in its interaction with KCNE2: co-expression of KCNE2 with CNBD-mutant HERG conferred a partially dominant current suppression not seen with wild-type HERG alone, indicating KCNE2 plays a role in determining phenotypic severity of some LQT2 mutations. Site-directed mutagenesis of HERG CNBD, heterologous co-expression, whole-cell electrophysiology The Journal of biological chemistry Medium 11278781
2001 KCNE2 co-expression with HERG alters both current kinetics and current density; incorporation of these effects into a quantitative action potential model showed that only changes in current density (not kinetics) significantly affect ventricular repolarization. Heterologous co-expression, whole-cell electrophysiology, computational action potential modeling Circulation research Medium 11440975
2002 A novel KCNE2 missense mutation V65M accelerates the inactivation time course of HERG/MiRP1 channels, thereby reducing IKr current density; mutant and wild-type MiRP1 co-localize with HERG subunits and form functional channels. Whole-cell patch clamp in CHO cells, single-strand conformation polymorphism analysis, direct sequencing, co-localization immunofluorescence Journal of molecular medicine Medium 12185453
2003 KCNE2 co-expression with HCN4 in Xenopus oocytes and CHO cells enhances HCN4 current amplitudes, slows activation kinetics, and shifts half-maximal activation voltage to more negative potentials. The C-terminal tail of KCNE2 (but not other KCNE subunits) interacts with the C-terminal tail of HCN4 in yeast two-hybrid assays. Two-electrode voltage clamp (Xenopus oocytes), patch clamp (CHO cells), yeast two-hybrid protein interaction assay Pflugers Archiv Medium 12856183
2003 Wild-type MiRP1 modulates HERG channel gating (more negative steady-state activation, altered inactivation), and three LQT6-associated MiRP1 mutants (T8A, Q9E, M54T) further alter HERG gating in distinct ways. During premature action potential clamp protocols, T8A and Q9E mutants augment HERG currents in early diastole, a potentially pro-arrhythmic mechanism. Whole-cell patch clamp in CHO cells at 37°C, action potential clamp protocols The Journal of physiology Medium 12923204
2004 KCNE2 (MiRP1) co-assembles with HCN2 in neonatal rat ventricular myocytes, as demonstrated by co-immunoprecipitation of both expressed and endogenous subunits. Co-expression of MiRP1 with HCN2 produces a 4-fold increase in pacemaker current maximal conductance and alters activation/deactivation kinetics at physiologically relevant voltages. Adenoviral overexpression in neonatal rat ventricular myocytes, co-immunoprecipitation (expressed and endogenous proteins), whole-cell patch clamp The Journal of biological chemistry High 15292247
2004 KCNE2 and KCNQ1 form a heteromeric K+ channel in the luminal membrane of gastric parietal cells. The KCNE2/KCNQ1 channel is activated by acidic pH, PIP2, cAMP, and purinergic receptor stimulation. KCNQ1 distribution in parietal cells does not substantially change during stimulation-induced H+,K+-ATPase trafficking. In situ hybridization, immunofluorescence, confocal microscopy in parietal cells and COS cells, patch clamp electrophysiology The Journal of physiology High 15579540
2004 KCNE2 R27C is a gain-of-function mutation affecting the KCNQ1-KCNE2 channel (responsible for a background potassium current) and is associated with familial atrial fibrillation. Unlike LQT-associated KCNE2 mutations, R27C does not alter HERG-KCNE2 current or HCN channel currents. Gene sequencing in AF kindreds, heterologous expression in Xenopus oocytes/mammalian cells, whole-cell electrophysiology American journal of human genetics Medium 15368194
2006 KCNE2 is essential for gastric acid secretion in vivo. Kcne2−/− mice have severe achlorhydria, abnormal parietal cell morphology, hypergastrinemia, and gastric glandular hyperplasia. KCNQ1 exhibited abnormal distribution in gastric glands from Kcne2−/− mice. Kcne2+/− mice showed reduced proton secretion (gene-dose effect), demonstrating that KCNE2 is required for normal gastric acid secretion. Targeted murine kcne2 gene disruption (knockout), gastric acid secretion measurement, histology, immunohistochemistry, Western blotting The Journal of biological chemistry High 16754665
2006 KCNE2 is co-localized with KCNQ1 and KCNE1 at the surface membrane and t-tubules of adult rat ventricular myocytes. Co-immunoprecipitation shows KCNQ1, KCNE1, and KCNE2 can form a tripartite complex. KCNE2 co-expression with KCNQ1 and KCNE1 decreases IKs current amplitude without altering its slow gating kinetics. Immunocytochemistry, co-immunoprecipitation in cardiomyocytes, patch clamp in oocytes and COS-7 cells Heart rhythm Medium 17161791
2006 KCNE2 modulates Kv4.3 (the major alpha subunit of cardiac Ito): co-expression in COS-7 cells reduces peak current density, slows inactivation kinetics, causes a positive shift of steady-state inactivation, and accelerates recovery from inactivation. Whole-cell patch clamp in COS-7 cells after transfection Journal of Southern Medical University Low 17259113
2007 KCNE2 has differential association with HERG compared to KCNE1: when forward trafficking is blocked (by Brefeldin A or ER-retention signals), KCNE2 abundance and association with HERG increase, while KCNE1 is preferentially retained in the ER. A significant fraction of KCNE2 is found extracellularly (soluble and vesicle-associated). HERG co-localizes more completely with KCNE1 at all membrane compartments. Co-immunoprecipitation, confocal immunofluorescence, surface labeling, Brefeldin A trafficking block, ER-retention signal engineering PloS one Medium 17895974
2007 A T10M mutation in MiRP1 (KCNE2) causes ≤80% reduction in hERG tail current, left-shifted steady-state inactivation, and 50% slower recovery from inactivation, providing a mechanism for reduced-penetrance inherited arrhythmia exacerbated by superimposed electrolyte disturbances. Whole-cell voltage clamp in transfected CHO cells Cardiovascular research Medium 18006462
2008 The secondary structure of MiRP1 (KCNE2) was characterized: the N-terminal extracellular domain is predominantly non-ordered in aqueous media but alpha-helical in lipid micelles; the transmembrane domain is predominantly alpha-helix/non-ordered; the C-terminal domain is predominantly alpha-helical when incorporated into lipid bilayers. Full-length MiRP1 contains ~34% alpha-helix, 23% beta-strand, and 43% non-ordered structure. FTIR and CD spectroscopy of synthetic MiRP1 peptides in various detergent/lipid environments Protein and peptide letters Low 18221016
2008 KCNE2 (MiRP1) modulates Kv4.3 Ito current when co-expressed as part of the Kv4.3/KChIP2/MiRP1 complex: it slows activation and inactivation kinetics and produces an 'overshoot' during recovery from inactivation. Co-expression of both KChIP2c and KCNE2 with Kv4.2 yields a current profile more similar to native cardiac Ito than either beta subunit alone. Whole-cell patch clamp in CHO cells stably expressing Kv4.3/KChIP2 or COS-7 cells transfected with Kv4.2/KChIP2c/KCNE2 Acta pharmacologica Sinica / British journal of pharmacology Low 18501111 18536731
2008 Targeted disruption of murine kcne2 prolonged ventricular action potential duration and reduced IK,slow1 by 50% (generated by Kv1.5, a novel in vivo partner for MiRP1) and Ito,f by ~25% (generated by Kv4 alpha subunits). Ventricular MiRP1 protein co-immunoprecipitated with native Kv1.5 and Kv4.2 but not Kv1.4 or Kv4.3. Kcne2 deletion also reduced mature Kv1.5 protein levels by 50% and disrupted Kv1.5 trafficking to intercalated discs. Targeted murine kcne2 gene disruption, whole-cell patch clamp in isolated ventricular myocytes, co-immunoprecipitation from native tissue, Western blotting, immunohistochemistry, in vivo QTc measurement FASEB journal High 18603586
2009 KCNE2 modulates all four cardiac HCN isoforms: co-expression increases current densities of HCN1, HCN2, and HCN4, accelerates activation kinetics, and increases single-channel amplitude and conductance. KCNE2 also increases HCN2 and HCN4 membrane protein expression (2.2-fold and 1.6-fold, respectively). These effects demonstrate direct functional interaction at the single-channel level. Whole-cell patch clamp and single-channel recordings in CHO cells, Western blotting of membrane fractions American journal of physiology. Heart and circulatory physiology Medium 19429827
2009 KCNE2 forms native cardiac complexes with Kv2.1, as shown by co-immunoprecipitation from rat heart tissue. KCNE2 (MiRP1) co-expression reduces Kv2.1 current density 2-fold and slows activation and deactivation kinetics. LQT-associated KCNE2 mutations M54T and I57T greatly alter Kv2.1 activation kinetics. Co-immunoprecipitation from rat heart tissue, whole-cell patch clamp in CHO cells The Journal of membrane biology Medium 19219384
2009 KCNE2 can substitute for KCNE1 in the KCNQ1-KCNE1 (IKs) channel complex due to dynamic KCNE1 turnover. KCNE2 independently traffics to the cell surface without requiring KCNQ1 co-assembly. In guinea pig ventricular myocytes, adenovirus-mediated KCNE2 expression co-localizes with native KCNQ1 and reduces native IKs current density. Pulse-chase experiments in COS-7 cells, biotinylation assays, vesicle injection in Xenopus oocytes, adenoviral gene delivery in adult cardiomyocytes, electrophysiology The Journal of biological chemistry Medium 19372218
2009 LQT6 KCNE2 M54T mutation modulates Kv4.3 (Ito alpha subunit): M54T and I57T variants significantly increase Ito current density, slow inactivation, and accelerate recovery from inactivation compared to wild-type KCNE2, suggesting a gain-of-function for Ito that may contribute to arrhythmogenesis. Whole-cell patch clamp in heterologous cell line co-expressing Kv4.3 and wild-type or mutant KCNE2 Heart rhythm Medium 20042375
2010 Solution NMR backbone assignments of human MiRP1 (KCNE2) were achieved in LMPG detergent micelles. CD spectroscopy revealed high alpha-helical content. Secondary structure analysis based on backbone chemical shifts showed multiple alpha-helical stretches along the primary sequence. Solution NMR (triple resonance backbone assignment), circular dichroism spectroscopy, protein expression and purification in E. coli Protein expression and purification Medium 21087668
2011 KCNE2 (along with KCNE1) retains homomeric N-type inactivating Kv alpha subunits (Kv1.4, Kv3.4) intracellularly early in the secretory pathway, suppressing their surface expression. This retention requires alpha-beta co-assembly, does not involve dynamin-dependent endocytosis, and acts as a checkpoint governing Kv channel alpha-subunit composition. Electrophysiology, co-immunoprecipitation, immunofluorescence, Brefeldin A treatment, dynamin inhibitor studies in mammalian cells Biophysical journal High 21943416 21943417
2011 In the choroid plexus epithelium (CPe), KCNE2 is enriched in the apical membrane where it co-localizes with KCNQ1 and KCNA3. Kcne2 deletion increases CPe outward K+ current 2-fold, alters KCNQ1 and KCNA3 trafficking polarity, hyperpolarizes the CPe membrane by 9 mV, and increases CSF [Cl−] by 14%. Immunofluorescence with Kcne2−/− negative control, whole-cell patch clamp in CPe cells, pharmacological dissection (XE991, margatoxin, dendrotoxin), ion concentration measurements FASEB journal High 21859894
2011 KCNE2 S98 phosphorylation modulates hERG/IKr amplitude by accelerating hERG protein degradation and reducing cell-surface hERG protein levels. S98 dephosphorylation leads to increased hERG/IKr amplitude. KCNE2 protein is more abundant in ventricles than atria in human and animal hearts. Adenovirus-mediated genetic manipulation in adult cardiac myocytes, phospho-specific antibody (Ab2), Western blotting, immunofluorescence American journal of physiology. Heart and circulatory physiology Medium 22180649
2012 KCNQ1-KCNE2 is required for adequate thyroid iodide (I−) uptake. Pharmacological blockade of KCNQ1 impairs thyroid I− uptake in vivo and in vitro. Kcne2 deletion doubles the rate of free I− efflux from the thyroid following ClO4− injection but does not affect Duox/TPO-mediated I− organification. Dynamic positron emission tomography in vivo, in vitro I− uptake assays, Kcne2 knockout mice, pharmacological inhibition with chromanol 293B FASEB journal High 22549510
2012 Kcne2 gene deletion impairs HCN channel function in thalamocortical neurons: it shifts the voltage-dependence of Ih activation to more hyperpolarized potentials, slows gating kinetics, decreases Ih density, and increases input resistance and burst firing. Whole-brain HCN1 and HCN2 (but not HCN4) expression is reduced. Co-immunoprecipitation from whole-brain lysates did not detect KCNE2 interaction with HCN1 or HCN2. Kcne2 knockout mice, whole-cell patch clamp in brain slices (VB thalamic and cortical layer 6 neurons), Western blotting, co-immunoprecipitation PloS one Medium 22880098
2013 An LQT6 M54T MiRP1 mutation decreases HCN4 current density by 80% and slows HCN4 activation at physiologically relevant voltages in ventricular myocytes, causing sinus bradycardia through effects on pacemaker If. M54T effects on HCN4 are additive with its effects on hERG kinetics. Whole-cell patch clamp in neonatal rat ventricular myocytes transfected with human HCN4 or HCN2 ± wild-type or M54T MiRP1, computational simulation Journal of cardiovascular electrophysiology Medium 23631727
2014 KCNQ1, KCNE2, and Na+-coupled solute transporters (SMIT1, SGLT1) form reciprocally regulating complexes. KCNE2 and KCNQ1 co-localize and co-immunoprecipitate with SMIT1 in choroid plexus epithelium. The constitutively active KCNQ1-KCNE2 heteromeric channel inhibits myo-inositol transport by SMIT1. Kcne2−/− mice show reduced myo-inositol in CSF and increased seizure susceptibility corrected by myo-inositol injections. Co-immunoprecipitation from choroid plexus, heterologous co-expression with myo-inositol uptake assays, global metabolite profiling (Kcne2−/− mice), behavioral assays Science signaling High 24595108
2014 KCNE2 physically interacts with Cav1.2 (L-type Ca2+ channel alpha subunit) and modulates L-type Ca2+ current (ICa,L): KCNE2 overexpression decreases ICa,L amplitude and alters its voltage-dependence and inactivation kinetics; knockdown has opposite effects. Deletion of the N-terminal inhibitory module (NTI) of Cav1.2 abolishes KCNE2 regulation. The AF-associated R27C mutation enhances KCNE2 suppression of ICa,L. Co-immunoprecipitation and co-localization in cardiomyocytes and HEK293 cells, whole-cell patch clamp, adenoviral overexpression and RNA interference Journal of molecular and cellular cardiology Medium 24681347
2014 KCNE2 transmembrane domain residue Ile64 interacts with KCNQ1 residues Phe340 and Phe275 (different interaction mode from KCNE1). KCNE2 N-terminus decreases surface expression and activity of KCNQ1; KCNE2 C-terminus has minimal influence on KCNQ1 gating (unlike KCNE1 C-terminus). Electrophysiology, immunofluorescence, solution NMR and backbone flexibility analysis of transmembrane domains Scientific reports Medium 24827085
2016 Filamin C (FLNC) interacts with the C-terminal domain of KCNE2 specifically under hypoxic conditions (not normoxia), as demonstrated by yeast two-hybrid screening and co-immunoprecipitation/co-localization. Yeast two-hybrid screening of cardiac cDNA library, co-localization and co-immunoprecipitation under normoxic and hypoxic conditions Cardiovascular journal of Africa Low 26956495
2016 Kcne2 deletion attenuates acute myocardial infarction: Kcne2−/− mice show 40% lower infarct size and decreased apoptosis after ischemia/reperfusion injury. This is mechanistically linked to 2-fold increased GSK-3β phosphorylation (inactivation) in Kcne2−/− mice; GSK-3β inhibitor mimicked and did not further enhance cardioprotection in Kcne2−/−mice. Coronary ligation IRI model, infarct size quantification, Western blotting for GSK-3β phosphorylation, pharmacological GSK-3β inhibition (SB216763), Millar catheter cardiac function Cardiovascular research Medium 26952045
2017 Kcne2 deletion in mice impairs pancreatic β-cell insulin secretion up to 8-fold and diminishes β-cell peak outward K+ current, causing type 2 diabetes. Skeletal muscle insulin receptor β and insulin receptor substrate 1 are down-regulated 2-fold by Kcne2 deletion. Kcne2 knockout mice, glucose tolerance testing, in vitro insulin secretion assay, whole-cell patch clamp in pancreatic β-cells, Western blotting FASEB journal High 28280005
2017 Decreased cardiac KCNE2 expression contributes to pathological hypertrophy via activation of calcineurin-NFAT and MAPK pathways, mediated through enhanced L-type Ca2+ channel activity (increased intracellular Ca2+ transient). KCNE2 knockdown increased calcineurin activity and nuclear NFAT levels; inhibitors of L-type Ca2+ channel (nifedipine) or calcineurin (FK506) attenuated hypertrophy. KCNE2 overexpression by ultrasound-microbubble gene transfer suppressed TAC-induced hypertrophy in vivo. Adenoviral knockdown and overexpression in neonatal rat ventricular myocytes, TAC mouse model, pharmacological inhibition, calcineurin activity assay, Western blotting, ultrasound-microbubble gene delivery Circulation. Heart failure Medium 28611128
2019 The stoichiometry of KCNE2 subunits in complex with HCN channel pore-forming subunits differs by HCN isoform and is concentration-dependent. Disease-linked KCNE2 gene variants can alter this stoichiometry with functional implications. Single-molecule subunit counting (fluorescence) in heterologous expression Scientific reports Medium 31235733
2019 A conserved arginine/lysine-based motif (KSKR) in the KCNE2 proximal C-terminus is required for ER export of KCNE2 and its forward trafficking to the cell surface. This trafficking is essential for KCNE2-mediated suppression of KCNQ1 cell surface expression and current. The KCNE2 C-terminus does not appear to physically interact with KCNQ1 (C-terminus truncation did not reduce KCNE2-KCNQ1 apparent affinity), unlike KCNE1. Site-directed mutagenesis of the motif, biotinylation assays of surface expression, whole-cell electrophysiology in HEK293 cells Channels Medium 31679457
2019 Kcne2 deletion reduces pulmonary expression of Kcnq1 and Kcnb1. Kcne2 co-immunoprecipitates with Kcnq1 in mouse lungs, indicating pulmonary Kcnq1-Kcne2 channel complexes. Kcne2 deletion impairs gas exchange (reduced blood O2, increased CO2) and increases pulmonary inflammation and vascular leakage. Co-immunoprecipitation from lung tissue, Western blotting, blood gas analysis, bronchoalveolar lavage, Kcne2 knockout mice FASEB journal Medium 31162977
2020 Cardiac-specific Kcne2 deletion (Kcne2CS−/−) causes dilated cardiomyopathy and terminal heart failure (median survival 28 weeks). Global Kcne2 deletion reduces gut Bacteroidales species (through achlorhydria), which correlates with improved survival. Proton-pump inhibitor omeprazole similarly altered the microbiome and delayed heart failure in Kcne2CS−/− mice, extending survival 10-fold at 44 weeks. Cardiac-specific vs global Kcne2 knockout mice, cardiac histology, microbiome profiling, pharmacological PPI treatment, survival analysis FASEB journal Medium 32584506
2021 Testin (encoded by TES, a focal adhesion protein) interacts with the KCNE2 intracellular C-terminal domain, identified by yeast two-hybrid screening and confirmed by co-immunoprecipitation. Testin nullifies KCNE2 effects on Kv1.5 voltage dependence and activation kinetics without affecting KCNE2 regulation of KCNQ1. Yeast two-hybrid screening, co-immunoprecipitation in vitro, whole-cell patch clamp in CHO cells Channels Low 33464998
2022 KCNQ1 gain-of-function mutations (R116L, V185M, P369L) that cause gingival fibromatosis/pituitary hormone deficiency act by impairing Ca2+ sensitivity of the KCNQ1-KCNE2 channel complex; normally, KCNE2 limits resting Q1E2 conductance by requiring calcified calmodulin for effective channel opening. Whole-cell patch clamp with intracellular Ca2+ manipulation, calmodulin co-expression, KCNQ1 mutagenesis in heterologous cells International journal of molecular sciences Medium 36077086

Source papers

Stage 0 corpus · 78 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia. Cell 1032 10219239
2000 Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Circulation 962 10973849
2004 Identification of a KCNE2 gain-of-function mutation in patients with familial atrial fibrillation. American journal of human genetics 311 15368194
2002 A comparison of currents carried by HERG, with and without coexpression of MiRP1, and the native rapid delayed rectifier current. Is MiRP1 the missing link? The Journal of physiology 151 11927665
2006 The KCNE2 potassium channel ancillary subunit is essential for gastric acid secretion. The Journal of biological chemistry 121 16754665
2004 Heteromeric KCNE2/KCNQ1 potassium channels in the luminal membrane of gastric parietal cells. The Journal of physiology 110 15579540
2004 MiRP1 modulates HCN2 channel expression and gating in cardiac myocytes. The Journal of biological chemistry 104 15292247
2008 Targeted deletion of kcne2 impairs ventricular repolarization via disruption of I(K,slow1) and I(to,f). FASEB journal : official publication of the Federation of American Societies for Experimental Biology 89 18603586
2003 KCNE2 modulates current amplitudes and activation kinetics of HCN4: influence of KCNE family members on HCN4 currents. Pflugers Archiv : European journal of physiology 85 12856183
2001 Analysis of the cyclic nucleotide binding domain of the HERG potassium channel and interactions with KCNE2. The Journal of biological chemistry 81 11278781
2001 Molecular interactions between two long-QT syndrome gene products, HERG and KCNE2, rationalized by in vitro and in silico analysis. Circulation research 80 11440975
2000 M-type KCNQ2-KCNQ3 potassium channels are modulated by the KCNE2 subunit. FEBS letters 74 11034315
2004 KCNE2 protein is expressed in ventricles of different species, and changes in its expression contribute to electrical remodeling in diseased hearts. Circulation 67 15066947
2010 Targeted deletion of Kcne2 causes gastritis cystica profunda and gastric neoplasia. PloS one 65 20625512
2001 Screening for mutations and polymorphisms in the genes KCNH2 and KCNE2 encoding the cardiac HERG/MiRP1 ion channel: implications for acquired and congenital long Q-T syndrome. Clinical chemistry 65 11468227
2014 KCNQ1, KCNE2, and Na+-coupled solute transporters form reciprocally regulating complexes that affect neuronal excitability. Science signaling 62 24595108
2003 Canine ventricular KCNE2 expression resides predominantly in Purkinje fibers. Circulation research 53 12842918
2002 Identification and functional characterization of a novel KCNE2 (MiRP1) mutation that alters HERG channel kinetics. Journal of molecular medicine (Berlin, Germany) 53 12185453
2009 Regulation of the Kv2.1 potassium channel by MinK and MiRP1. The Journal of membrane biology 50 19219384
2009 Dynamic partnership between KCNQ1 and KCNE1 and influence on cardiac IKs current amplitude by KCNE2. The Journal of biological chemistry 48 19372218
2012 The KCNQ1-KCNE2 K⁺ channel is required for adequate thyroid I⁻ uptake. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 46 22549510
2015 The KCNE2 K⁺ channel regulatory subunit: Ubiquitous influence, complex pathobiology. Gene 43 26123744
2011 KCNE2 forms potassium channels with KCNA3 and KCNQ1 in the choroid plexus epithelium. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 43 21859894
2014 Kcne2 deletion creates a multisystem syndrome predisposing to sudden cardiac death. Circulation. Cardiovascular genetics 42 24403551
2006 KCNE2 is colocalized with KCNQ1 and KCNE1 in cardiac myocytes and may function as a negative modulator of I(Ks) current amplitude in the heart. Heart rhythm 41 17161791
2003 Mutant MiRP1 subunits modulate HERG K+ channel gating: a mechanism for pro-arrhythmia in long QT syndrome type 6. The Journal of physiology 41 12923204
2006 KCNE2, a down-regulated gene identified by in silico analysis, suppressed proliferation of gastric cancer cells. Cancer letters 38 16677757
2011 KCNE1 and KCNE2 inhibit forward trafficking of homomeric N-type voltage-gated potassium channels. Biophysical journal 37 21943416
2004 Local anaesthetic sensitivities of cloned HERG channels from human heart: comparison with HERG/MiRP1 and HERG/MiRP1 T8A. British journal of anaesthesia 36 14665560
2007 Differential association between HERG and KCNE1 or KCNE2. PloS one 35 17895974
2017 Loss-of-Function KCNE2 Variants: True Monogenic Culprits of Long-QT Syndrome or Proarrhythmic Variants Requiring Secondary Provocation? Circulation. Arrhythmia and electrophysiology 33 28794082
2016 Kcne2 deletion attenuates acute post-ischaemia/reperfusion myocardial infarction. Cardiovascular research 33 26952045
2009 Effects of KCNE2 on HCN isoforms: distinct modulation of membrane expression and single channel properties. American journal of physiology. Heart and circulatory physiology 31 19429827
2013 An LQTS6 MiRP1 mutation suppresses pacemaker current and is associated with sinus bradycardia. Journal of cardiovascular electrophysiology 30 23631727
2007 A KCNE2 mutation in a patient with cardiac arrhythmia induced by auditory stimuli and serum electrolyte imbalance. Cardiovascular research 29 18006462
2019 miR-584-5p regulates hepatocellular carcinoma cell migration and invasion through targeting KCNE2. Molecular genetics & genomic medicine 27 31044566
2006 Genetic polymorphisms in KCNQ1, HERG, KCNE1 and KCNE2 genes in the Chinese, Malay and Indian populations of Singapore. British journal of clinical pharmacology 26 16487223
2017 Kcne2 deletion impairs insulin secretion and causes type 2 diabetes mellitus. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 25 28280005
2013 Postmortem molecular analysis of KCNQ1, KCNH2, KCNE1 and KCNE2 genes in sudden unexplained nocturnal death syndrome in the Chinese Han population. Forensic science international 25 23890619
2012 Targeted deletion of Kcne2 impairs HCN channel function in mouse thalamocortical circuits. PloS one 25 22880098
2011 KCNE1 and KCNE2 provide a checkpoint governing voltage-gated potassium channel α-subunit composition. Biophysical journal 25 21943417
2010 Dynamic changes in HCN2, HCN4, KCNE1, and KCNE2 expression in ventricular cells from acute myocardial infarction rat hearts. Biochemical and biophysical research communications 25 20381460
2009 KCNE2 modulation of Kv4.3 current and its potential role in fatal rhythm disorders. Heart rhythm 24 20042375
2006 Modulation of functional properties of KCNQ1 channel by association of KCNE1 and KCNE2. Biochemical and biophysical research communications 24 16631607
2008 Effects of MiRP1 and DPP6 beta-subunits on the blockade induced by flecainide of Kv4.3/KChIP2 channels. British journal of pharmacology 23 18536731
2014 KCNE2 modulates cardiac L-type Ca(2+) channel. Journal of molecular and cellular cardiology 21 24681347
2013 Gastric adenocarcinoma arising in gastritis cystica profunda presenting with selective loss of KCNE2 expression. World journal of gastroenterology 21 23483772
2015 Molecular Cloning and Functional Expression of the Equine K+ Channel KV11.1 (Ether à Go-Go-Related/KCNH2 Gene) and the Regulatory Subunit KCNE2 from Equine Myocardium. PloS one 20 26376488
2004 Expression of the IKr components KCNH2 (rERG) and KCNE2 (rMiRP1) during late rat heart development. Experimental & molecular medicine 20 15365256
2011 The voltage-gated channel accessory protein KCNE2: multiple ion channel partners, multiple ways to long QT syndrome. Expert reviews in molecular medicine 19 22166675
2011 KCNE2 protein is more abundant in ventricles than in atria and can accelerate hERG protein degradation in a phosphorylation-dependent manner. American journal of physiology. Heart and circulatory physiology 19 22180649
2019 Disease-linked mutations alter the stoichiometries of HCN-KCNE2 complexes. Scientific reports 14 31235733
2014 Differential modulations of KCNQ1 by auxiliary proteins KCNE1 and KCNE2. Scientific reports 14 24827085
2009 The transmembrane beta-subunits KCNE1, KCNE2, and DPP6 modify pharmacological effects of the antiarrhythmic agent tedisamil on the transient outward current Ito. Naunyn-Schmiedeberg's archives of pharmacology 13 19153714
2016 Electrophysiological Characteristics of the LQT2 Syndrome Mutation KCNH2-G572S and Regulation by Accessory Protein KCNE2. Frontiers in physiology 12 28082916
2019 The KCNE2 potassium channel β subunit is required for normal lung function and resilience to ischemia and reperfusion injury. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 9 31162977
2016 Filamin C: a novel component of the KCNE2 interactome during hypoxia. Cardiovascular journal of Africa 8 26956495
2015 Manipulation of KCNE2 expression modulates action potential duration and Ito and IK in rat and mouse ventricular myocytes. American journal of physiology. Heart and circulatory physiology 8 26297229
2019 AKT and ERK1/2 activation via remote ischemic preconditioning prevents Kcne2-dependent sudden cardiac death. Physiological reports 7 30737904
2008 Co-expression of KCNE2 and KChIP2c modulates the electrophysiological properties of Kv4.2 current in COS-7 cells. Acta pharmacologica Sinica 7 18501111
2021 The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity. Channels (Austin, Tex.) 6 33464998
2020 Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 5 32584506
2019 A conserved arginine/lysine-based motif promotes ER export of KCNE1 and KCNE2 to regulate KCNQ1 channel activity. Channels (Austin, Tex.) 5 31679457
2010 Expression, purification, detergent screening and solution NMR backbone assignment of the human potassium channel accessory subunit MiRP1. Protein expression and purification 5 21087668
2007 Mutation screening in KCNQ1, HERG, KCNE1, KCNE2 and SCN5A genes in a long QT syndrome family. Annals of the Academy of Medicine, Singapore 5 17597962
2006 [KCNE2 modulates the function of Kv4.3 channel]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 5 17259113
2022 Modulation of KV4.3-KChIP2 Channels by IQM-266: Role of DPP6 and KCNE2. International journal of molecular sciences 4 36012438
2020 Expression and Localization of Kcne2 in the Vertebrate Retina. Investigative ophthalmology & visual science 4 32191288
2017 Decreased KCNE2 Expression Participates in the Development of Cardiac Hypertrophy by Regulation of Calcineurin-NFAT (Nuclear Factor of Activated T Cells) and Mitogen-Activated Protein Kinase Pathways. Circulation. Heart failure 4 28611128
2021 KCNE2 gene mutation and Brugada syndrome. Journal of electrocardiology 3 33626434
2022 Clinically Relevant KCNQ1 Variants Causing KCNQ1-KCNE2 Gain-of-Function Affect the Ca2+ Sensitivity of the Channel. International journal of molecular sciences 2 36077086
2008 Secondary structure of the MiRP1 (KCNE2) potassium channel ancillary subunit. Protein and peptide letters 2 18221016
2012 [KCNQ1, KCNH2, KCNE1 and KCNE2 potassium channels gene variants in sudden manhood death syndrome]. Fa yi xue za zhi 1 23213782
2009 The stoichiometric relationship between KCNH-2 and KCNE-2 in I(Kr) channel formation. International journal of cardiology 1 19913309
2007 Mutation analysis of KCNQ1, KCNH2, SCN5A, KCNE1 and KCNE2 genes in Chinese patients with long QT syndrome. Frontiers of medicine in China 1 24573873
2024 The Multifunctional Role of KCNE2: From Cardiac Arrhythmia to Multisystem Disorders. Cells 0 39272981
2018 Screening for germline KCNQ1 and KCNE2 mutations in a set of somatotropinoma patients. Endocrine connections 0 29703730
2007 [KCNE2 protein S98 phosphorylation in heart of old SHR rats detected by point mutagenesis]. Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 0 17717828

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