Affinage

KCNT2

Potassium channel subfamily T member 2 · UniProt Q6UVM3

Length
1135 aa
Mass
130.5 kDa
Annotated
2026-06-10
57 papers in source corpus 29 papers cited in narrative 30 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCNT2 (Slick/Slo2.1) encodes a high-conductance, weakly voltage-dependent K+ channel that links intracellular ionic and metabolic state to electrical excitability, sensing intracellular Na+ and Cl- to set background K+ conductance (PMID:14684870). The intracellular Na+ sensor is a single C-terminal residue, Asp757 (PMID:25903137), and the channel is additionally gated by fenamates, cell volume, and PIP2 acting through Lys306 (PMID:20176855, PMID:25347289, PMID:22728883). Its activation gate resides at the selectivity filter rather than the S6 bundle crossing, with dynamic coupling between pore-helix Phe240 and hydrophobic S5/S6 contacts (notably Leu209) stabilizing the closed state (PMID:24166878, PMID:26724206). Slick co-assembles with Slack (KCNT1) into heteromeric KNa channels with distinct conductance, kinetics, and trafficking, a process requiring the Slack-B N-terminal domain, and confers graded cell-volume sensitivity proportional to Slick subunit number (PMID:19403831, PMID:28222129). Channel activity is inhibited by Gαq-coupled receptor signaling through PKC — engaged by muscarinic, metabotropic glutamate, and oxytocin receptors — and by TNF-α via p38 MAPK, while expression is transcriptionally driven by NF-κB under hypoxic stress (PMID:16687497, PMID:30334255, PMID:28579824, PMID:26100633). Functionally, Slick limits excitability in nociceptors and spinal interneurons, including coupling to Na+ entry through TRPM3, and shapes thermal pain and itch (PMID:39744124, PMID:35303056, PMID:28943756); in myometrial smooth muscle it forms a functional Na+-K+ relay with NALCN to control contractility (PMID:34746693, PMID:30334255); and it mediates anesthetic preconditioning and post-infarction fibrogenesis via SOCE in cardiac fibroblasts (PMID:26845140, PMID:41842949). De novo KCNT2 variants produce both gain- and loss-of-function effects underlying early-onset epileptic encephalopathy, with the Phe240Leu variant reversing ion selectivity and driving neuronal hyperexcitability (PMID:29069600, PMID:32038177, PMID:37062836).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2003 High

    Established KCNT2/Slick as a Na+- and Cl--activated K+ channel that integrates intracellular ionic signals to regulate excitability, defining the channel's core gating logic.

    Evidence Heterologous expression with patch-clamp and ATP-site mutagenesis

    PMID:14684870

    Open questions at the time
    • The proposed ATP inhibition was later contradicted
    • Native cellular roles not yet defined
  2. 2005 Medium

    Mapped Slick protein distribution across the CNS, showing overlapping but distinct expression from Slack and implicating it in spike-frequency adaptation.

    Evidence In situ hybridization, immunohistochemistry, computational simulation in rat brain

    PMID:15717307

    Open questions at the time
    • Localization does not establish functional contribution in vivo
    • Single-lab antibody specificity
  3. 2006 High

    Showed that Gαq receptor signaling via PKC inhibits Slo2.1, opposite to its effect on Slack, revealing receptor-driven modulation as a key regulatory axis.

    Evidence Xenopus co-expression with GqPCRs, PMA, chimera domain mapping

    PMID:16687497

    Open questions at the time
    • Direct PKC phosphorylation site not identified
    • Distal C-terminal determinant not resolved to residues
  4. 2009 High

    Demonstrated that Slick and Slack co-assemble into heteromers with unique properties and trafficking, establishing the physiological channel as a heteromeric entity.

    Evidence Reciprocal co-IP, single-channel recording, domain deletion analysis

    PMID:19403831

    Open questions at the time
    • Native stoichiometry not directly measured
    • Trafficking machinery downstream of Slack-B N-terminus unknown
  5. 2013 High

    Localized the activation gate to the selectivity filter rather than the S6 bundle crossing, redefining the structural mechanism of gating.

    Evidence Ala-scanning mutagenesis, intragenic rescue, homology modeling, verapamil pharmacology in oocytes

    PMID:24166878

    Open questions at the time
    • No experimental structure to confirm filter gating
    • Coupling to ligand sensors not structurally resolved
  6. 2014 High

    Overturned the original ATP-inhibition model with multiple negative experiments, refining the channel's metabolic sensing to Na+/Cl- rather than direct ATP.

    Evidence Inside-out patches, metabolic depletion, ATP-site mutagenesis in HEK293

    PMID:25214519

    Open questions at the time
    • Reconciliation with original report across constructs/species unresolved
  7. 2015 High

    Identified Asp757 as the single intracellular Na+ sensor and NF-κB as the hypoxia-driven transcriptional regulator, linking channel function and expression to molecular determinants.

    Evidence Site-directed mutagenesis with electrophysiology; ChIP, luciferase reporter, hypoxia in neurons

    PMID:25903137 PMID:26100633

    Open questions at the time
    • How Na+ binding at D757 couples to the filter gate not defined
    • NF-κB regulation not tested in disease-relevant tissues
  8. 2016 High

    Defined a cardioprotective role for Slick in anesthetic preconditioning, showing the channel mediates volatile-anesthetic-stimulated K+ transport in the heart.

    Evidence Slo2.1, Slo2.2, and double KO mice in ischemia-reperfusion and K+ flux assays

    PMID:26845140

    Open questions at the time
    • Subcellular site (mitochondrial vs plasma membrane) of action not definitively resolved
    • Molecular coupling to anesthetics unknown
  9. 2017 High

    Connected KCNT2 to disease and to sensory and pain circuits, showing a selectivity-altering de novo variant causes neuronal hyperexcitability and that Slick shapes nociceptor excitability and DAPs.

    Evidence Exome sequencing with patch-clamp; Slick KO mice, DRG electrophysiology, LDCV localization

    PMID:18664322 PMID:28943756 PMID:29069600

    Open questions at the time
    • Genotype-phenotype range not yet systematically mapped
    • Mechanism of channel translocation from LDCVs unknown
  10. 2018 High

    Established Slick as a regulator of myometrial excitability inhibited by oxytocin via Gαq/PKC, extending receptor modulation to smooth muscle contractility.

    Evidence Myometrial smooth muscle cell electrophysiology, pharmacology, Ca2+ imaging

    PMID:30334255

    Open questions at the time
    • In vivo contribution to parturition not tested
    • PKC target residue not identified
  11. 2021 Medium

    Revealed a NALCN-Slick functional relay in myometrium where NALCN-mediated Na+ entry activates Slick, defining a Na+-K+ feedback circuit controlling membrane potential.

    Evidence Proximity assay, electrophysiology, Ca2+ imaging in human MSMCs

    PMID:34746693

    Open questions at the time
    • Direct physical interaction not confirmed by co-IP
    • Stoichiometry and nanodomain organization unknown
  12. 2024 High

    Demonstrated functional coupling between TRPM3 and Slick, where TRPM3-mediated Na+ entry activates Slick to limit noxious heat sensation, providing a concrete excitability-braking mechanism in sensory neurons.

    Evidence Conditional Nav1.8-Slick KO mice, behavior, sensory neuron patch-clamp, ion substitution

    PMID:39744124

    Open questions at the time
    • Physical proximity of TRPM3 and Slick not shown
    • Whether coupling generalizes to other Na+-permeable channels unclear
  13. 2026 High

    Extended Slick function to cardiac fibroblasts, showing plasma-membrane Slick regulates SOCE and drives post-infarction fibrosis, a non-neuronal pathological role.

    Evidence Global and CMF-specific conditional KO, ischemia/reperfusion, Ca2+ imaging, histology

    PMID:41842949

    Open questions at the time
    • Molecular link between K+ efflux and SOCE machinery not defined
    • Translational relevance to human fibrosis untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the various ligand and signaling inputs (Na+/D757, Cl-, PIP2, volume, PKC) are mechanically integrated at the selectivity-filter gate, and how heteromeric Slick/Slack composition is set in vivo, remain unresolved.
  • No experimental high-resolution structure of Slick
  • PKC and p38 phosphorylation sites not identified
  • Native heteromer stoichiometry across tissues unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 3 GO:0140299 molecular sensor activity 2 GO:0008289 lipid binding 1
Localization
GO:0005886 plasma membrane 3 GO:0005739 mitochondrion 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-397014 Muscle contraction 2
Partners
DLG3DPP10KCNT1NALCNSNCBTMEM263TRPM3
Complex memberships
Slick/Slack (KCNT2/KCNT1) heteromeric KNa channel

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 KCNT2/Slick is a Na+-activated K+ channel that is activated by intracellular Na+ and Cl-, and inhibited by intracellular ATP. A consensus ATP binding site near the C terminus is required for ATP and its nonhydrolyzable analogs to reduce open probability. Heterologous expression, electrophysiology (patch-clamp), site-directed mutagenesis of ATP binding site The Journal of neuroscience High 14684870
2003 KCNT2/Slick channel activation is rapidly gating and the channel integrates intracellular Na+, Cl-, and ATP as indicators of metabolic state to regulate electrical excitability. Heterologous expression, whole-cell and single-channel electrophysiology in Xenopus oocytes and mammalian cells The Journal of neuroscience High 14684870
2005 Slick (KCNT2) protein is widely distributed in the rat CNS, including brainstem auditory neurons, olfactory bulb, hippocampal CA1-CA3 and dentate gyrus, cortical layers II/III/V, hypothalamus and thalamus, with a distribution overlapping but distinct from Slack. Computer simulations indicate Slick currents can cause adaptation during prolonged stimuli. In situ hybridization, immunohistochemistry, computational simulation The Journal of comparative neurology Medium 15717307
2006 KCNT2/Slo2.1 activity is strongly inhibited by Gαq-protein coupled receptor (GqPCR) stimulation (M1 muscarinic receptor and mGluR1), in contrast to Slo2.2 (Slack) which is activated. The inhibition involves PKC; PMA application inhibits Slo2.1 whole-cell currents. The distal carboxyl region of Slo2.1 controls sensitivity to PMA. Heterologous co-expression in Xenopus oocytes, pharmacological activation of GqPCRs, PMA application, chimera construction, immunocytochemistry The Journal of neuroscience High 16687497
2007 Slo2.1 (KCNT2) is expressed in striatal cholinergic interneurons and functions as a Cl--activated K+ channel that is inhibited by mGluR1/5 receptor activation. Under conditions of elevated intracellular NaCl, Slo2.1 provides a background K+ current that is inhibited by mGluR agonists and volatile anesthetics. Electrophysiological recordings in brain slices, HEK293 cell transfection reconstitution, immunohistochemistry, in situ hybridization, gramicidin perforated-patch recordings The Journal of neuroscience High 17699666
2008 Slack and Slick KNa channels are required for the depolarizing afterpotential (DAP) in medium diameter rat DRG neurons. Native KNa channels show 201 pS unitary conductance, are activated by cytoplasmic Na+ (EC50 ~35 mM) and by Cl-, and both Slack and Slick mRNA are expressed in DRG neurons. Inside-out and whole-cell patch-clamp, RT-PCR, pharmacology (TTX) Acta pharmacologica Sinica Medium 18664322
2009 Slick (KCNT2) and Slack subunits co-assemble to form heteromeric KNa channels with properties distinct from homomers: different unitary conductance, altered kinetics, different subcellular localization, and different response to PKC activation. Heteromer formation requires the N-terminal domain of Slack-B, which also facilitates trafficking of heteromeric channels to the plasma membrane. Co-immunoprecipitation, single-channel electrophysiology, immunocytochemistry, domain deletion/mutation analysis The Journal of neuroscience High 19403831
2010 Slo2.1 (KCNT2) channel gating can be activated by fenamates (niflumic acid, flufenamic acid) independent of intracellular Na+. Channel gating is modulated by extracellular K+ and Na+ concentrations. The weak voltage dependence of Slo2.1 is independent of charged residues in S1-S4 segments; mutation of R190 in the S4-S5 linker to Ala/Gln/Glu induces constitutive channel activity. Heterologous expression in Xenopus oocytes, voltage-clamp electrophysiology, site-directed mutagenesis The Journal of general physiology High 20176855
2012 Slick and Slack channels are regulated by the phosphoinositide PIP2. Exogenous PIP2 activates both channels. The activating effect of PIP2 on Slick involves direct interaction with lysine 306 in the proximal C-terminus. Xenopus oocyte expression, voltage-clamp electrophysiology, site-directed mutagenesis (K306 in Slick) Biochemical and biophysical research communications Medium 22728883
2012 Fenamates activate Slo2.1 (KCNT2) via two distinct sites: an extracellular accessible site mediating activation and a cytoplasmic accessible site in the pore (S6 segment) mediating inhibition. N-phenylanthranilic acid is the minimal pharmacophore for fenamate activation. Mutation A278R in the pore-lining S6 segment increases sensitivity to NFA activation and reduces inhibition. Xenopus oocyte expression, voltage-clamp electrophysiology, site-directed mutagenesis, structure-activity relationship analysis Molecular pharmacology Medium 22851714
2013 The activation gate of Slo2.1 (KCNT2) is located at the selectivity filter, not the S6 bundle crossing. Pro271 and Glu275 in S6 maintain the inner pore in an open configuration. Dynamic coupling between the pore helix residue Phe240 and S5/S6 segments mediates channel activation. Verapamil blocks Slo2.1 in an activation-independent manner confirming the S6 bundle crossing does not gate ion access. Heterologous expression in Xenopus oocytes, Ala scanning mutagenesis of S6 and S5, intragenic second-site rescue mutations, homology modeling, pharmacological analysis The Journal of general physiology High 24166878
2014 Intracellular ATP does NOT inhibit Slo2.1 (KCNT2) channels. Direct application of 5 mM ATP to inside-out patches did not inhibit NFA-activated Slo2.1 currents; metabolic depletion of ATP did not increase Slo2.1 currents; mutation of the C-terminal ATP binding site did not enhance current magnitude. Excised inside-out macropatch recordings, whole-cell voltage clamp in HEK293 cells, site-directed mutagenesis of ATP binding site, metabolic inhibition with NaN3 Physiological reports High 25214519
2014 Slick (Slo2.1/KCNT2) channels, but not Slack (Slo2.2) channels, are regulated by cell volume changes: Slick is stimulated ~196% by cell swelling and inhibited ~57% by cell shrinkage. This volume sensitivity does not depend on an intact actin cytoskeleton, ATP release, or vesicle fusion. Co-expression with aquaporin 1 in Xenopus oocytes, two-electrode voltage clamp, hypo/hypertonic challenge, pharmacological dissection PloS one Medium 25347289
2015 The intracellular Na+ sensor of Slo2.1 (KCNT2) is identified as Asp757 in the C-terminus. D757R mutation abolishes Na+ sensitivity while preserving fenamate activation, demonstrating this single Asp residue accounts for intracellular Na+ sensitivity. Fenamates are ~14-fold more potent activators of Slo2.1 than intracellular Na+. Site-directed mutagenesis, heterologous expression in Xenopus oocytes and HEK293 cells, whole-cell voltage clamp, excised inside-out macropatch recordings The Journal of biological chemistry High 25903137
2015 KCNT2/Slick channel expression is transcriptionally regulated by NF-κB. Two NF-κB binding sites in the KCNT2/Kcnt2 promoter are required for transcriptional activation. NFκB binding was confirmed in vivo by ChIP in neurons. Under hypoxic conditions, NF-κB drives SLICK expression, and NF-κB inhibition reduces Slick transcript levels in primary neurons. ChIP assay, luciferase reporter assay, promoter mutagenesis, hypoxia exposure of PC-12 cells, primary neuron cultures with NF-κB inhibitor The Journal of biological chemistry High 26100633
2015 Hydrophobic interactions between residues on a single face of the S5 transmembrane segment and Phe240 in the pore helix stabilize Slo2.1 (KCNT2) channels in the closed state. Ala substitution of five S5 residues induces constitutive activity. Mutation of Leu209 (predicted to face Phe240) to Glu or Gln induces maximal activation. Ala-scanning mutagenesis of S5, additional point mutagenesis, heterologous expression in Xenopus oocytes, voltage-clamp electrophysiology Biochimica et biophysica acta Medium 26724206
2015 In mouse brain, Slick (KCNT2) channels show intense immunoreactivity in processes, varicosities, and neuronal cell bodies of olfactory bulb, hippocampus, amygdala, lateral septal nuclei, hypothalamic and midbrain nuclei, and brainstem; distinct from Slack's primarily diffuse pattern. Both channels overlap in some regions but diverge in others. In situ hybridization, immunohistochemistry in mouse brain sections The Journal of comparative neurology Medium 26587966
2015 Slick (KCNT2) and Slack (KCNT1) channels co-assemble into identical cellular complexes in mouse brain. Novel interaction partners of native Slick channel complexes identified by co-immunoprecipitation and mass spectrometry include: beta-synuclein, transmembrane protein 263 (TMEM263), inactive dipeptidyl-peptidase (DPP10), and synapse associated protein 102 (SAP102). Co-immunoprecipitation, Western blot, double immunofluorescence, mass spectrometric sequencing Biochemistry and biophysics reports Medium 29124216
2016 Slo2.1 (KCNT2/Slick) is required for volatile anesthetic (VA)-stimulated K+ transport in cardiac cells and for anesthetic preconditioning (APC)-induced cardioprotection. In Slo2.1 knockout hearts, APC protection against ischemia-reperfusion injury was absent, while Slo2.2 knockout hearts responded like wild-type. VA-stimulated K+ transport in cardiomyocytes and mitochondria from Slo2.1 KO mice was also absent. Perfused heart ischemia-reperfusion model, fluorescent K+ flux assay, Slo2.1 KO mice, Slo2.2 KO mice, double KO mice Anesthesiology High 26845140
2017 The de novo KCNT2 variant Phe240Leu causes altered ion selectivity: Cl- sensitivity is reversed, predominantly K+-selective WT channels are made to favor Na+ over K+, and inward conductance is increased. Expression of rSlick in primary neurons induced membrane hyperexcitability resembling a cellular seizure phenotype. Exome sequencing, Sanger sequencing, whole-cell patch-clamp electrophysiology in heterologous expression system, primary neuron recordings Cell reports High 29069600
2017 Slick (KCNT2) channels are exclusively expressed in small- and medium-sized CGRP-containing DRG neurons. A pool of Slick channels localizes to large dense-core vesicles (LDCV) containing CGRP, and upon stimulation for CGRP release, Slick channels translocate from LDCVs to the neuronal membrane. Slick KO mice show increased basal heat detection and exacerbated thermal hyperalgesia; DRG neurons from Slick KO show reduced outward current and altered action potential properties. Immunohistochemistry, subcellular fractionation/colocalization, behavioral testing (Slick KO mice), whole-cell patch-clamp of DRG neurons Journal of experimental neuroscience Medium 28943756
2017 TNF-α inhibits the SLICK KNa current in rat dorsal horn neurons via the p38 MAPK pathway. The p38 inhibitor SB202190 blocks this effect. TNF-α modulation of SLICK does not affect channel gating directly but likely involves posttranslational modification. Cultured dorsal horn neurons, whole-cell patch-clamp, pharmacological inhibition of p38 MAPK Journal of pain research Medium 28579824
2017 Heteromeric Slick/Slack K+ channels show graded cell volume sensitivity dependent on the number of Slick α-subunits in the tetrameric channel. Channels with more Slick subunits show greater volume sensitivity, while channels with more Slack subunits show reduced sensitivity. Co-expression of varying ratios of Slick/Slack subunits with aquaporin 1 in Xenopus oocytes, two-electrode voltage clamp, osmotic challenge PloS one Medium 28222129
2018 SLO2.1 (KCNT2) is expressed and active at the resting membrane potential in myometrial smooth muscle cells (MSMCs). Oxytocin inhibits SLO2.1 via Gαq-protein coupled receptor activation of protein kinase C, leading to membrane depolarization, activation of voltage-dependent calcium channels, and calcium influx. Electrophysiological recordings in MSMCs, pharmacological dissection (oxytocin receptor, PKC inhibitors), calcium imaging The Journal of physiology High 30334255
2020 Two truncating KCNT2 mutations (frameshift p.L48Qfs43 in N-terminal domain; nonsense p.K564* in C-terminal region) significantly decrease global current density of heteromeric KNa1.1/KNa1.2 channels by ~55% and ~25% respectively, demonstrating loss-of-function effects on heteromeric channels in EOEE patients. Whole-cell patch-clamp in transfected CHO cells, homomeric and heteromeric channel reconstitution Frontiers in cellular neuroscience Medium 32038177
2021 SLO2.1 (KCNT2) and NALCN form a functionally coupled system in myometrial smooth muscle cells: Na+ entering through NALCN activates SLO2.1, and K+ efflux through SLO2.1 hyperpolarizes the membrane. NALCN and SLO2.1 are in close proximity in human MSMCs. Decreased SLO2.1/NALCN activity leads to membrane depolarization, Ca2+ entry via voltage-dependent channels, and contraction. Live-cell imaging, proximity assay (co-localization), electrophysiology, Ca2+ imaging, functional coupling assays in MSMCs iScience Medium 34746693
2022 Slick (KCNT2) in nociceptive Aδ-fibers modulates heat-induced pain, while Slick in spinal cord dorsal horn interneurons inhibits capsaicin-induced pain but facilitates somatostatin-induced itch. Slick co-localizes with SSTR2 in spinal dorsal horn. Conditional KO of Slick in Lbx1+ spinal neurons (Lbx1-Slick-/-) increased capsaicin-induced pain and reduced octreotide-induced scratching. Immunostaining, in situ hybridization, Western blot, qRT-PCR, global and conditional (Lbx1-Cre) Slick KO mice, behavioral testing, ERK phosphorylation assay Anesthesiology High 35303056
2023 Among 14 KCNT2 variants tested in HEK-293 and SH-SY5Y cells, 8 show gain-of-function and 6 show loss-of-function effects by whole-cell electrophysiology. Quinidine and fluoxetine block all GoF variants; loxapine and riluzole activate some LoF variants while blocking others, revealing variant-specific pharmacological profiles. Whole-cell electrophysiology in HEK-293 and SH-SY5Y cells, pharmacological profiling of 14 variants Annals of neurology High 37062836
2024 Slick (KCNT2) limits TRPM3-mediated noxious heat sensation in sensory neurons. Slick is highly co-expressed with TRPM3 (but not TRPV1, TRPA1, or TRPM2) in sensory neurons. Conditional KO of Slick in Nav1.8+ sensory neurons increases nocifensive behavior to heat and to the TRPM3 activator pregnenolone sulfate. TRPM3 activation increases Na+-dependent outward K+ current, which is absent when NaCl is replaced with choline chloride, indicating Na+ entry through TRPM3 activates Slick. Conditional KO mice (SNS-Slick-/-), behavioral testing, in situ hybridization, patch-clamp recordings in sensory neurons, ion substitution experiments Frontiers in pharmacology High 39744124
2026 Slick (Slo2.1/KCNT2) channels at the plasma membrane of cardiac fibroblasts and myofibroblasts regulate K+ efflux and modulate store-operated calcium entry (SOCE). Global and CMF-specific conditional Slick KO reduces fibrosis, preserves left ventricular function after ischemia/reperfusion injury, and is associated with diminished myofibroblast activation, reduced inflammation, and improved cardiomyocyte survival. Live-cell imaging, whole-cell patch-clamp, global and conditional (CMF-specific) KO mice, ischemia/reperfusion model, histological fibrosis assessment, functional cardiac measurements JCI insight High 41842949

Source papers

Stage 0 corpus · 57 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Slick (Slo2.1), a rapidly-gating sodium-activated potassium channel inhibited by ATP. The Journal of neuroscience : the official journal of the Society for Neuroscience 172 14684870
2008 Differences in thermoregulatory ability between slick-haired and wild-type lactating Holstein cows in response to acute heat stress. Journal of dairy science 116 18765598
2014 Functionally reciprocal mutations of the prolactin signalling pathway define hairy and slick cattle. Nature communications 113 25519203
2014 The SLICK hair locus derived from Senepol cattle confers thermotolerance to intensively managed lactating Holstein cows. Journal of dairy science 102 24996281
2005 Localization of the Na+-activated K+ channel Slick in the rat central nervous system. The Journal of comparative neurology 87 15717307
2006 Opposite regulation of Slick and Slack K+ channels by neuromodulators. The Journal of neuroscience : the official journal of the Society for Neuroscience 82 16687497
2009 The N-terminal domain of Slack determines the formation and trafficking of Slick/Slack heteromeric sodium-activated potassium channels. The Journal of neuroscience : the official journal of the Society for Neuroscience 68 19403831
2007 TrpC3/C7 and Slo2.1 are molecular targets for metabotropic glutamate receptor signaling in rat striatal cholinergic interneurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 65 17699666
2018 Convergent Evolution of Slick Coat in Cattle through Truncation Mutations in the Prolactin Receptor. Frontiers in genetics 55 29527221
2016 Virion Glycoprotein-Mediated Immune Evasion by Human Cytomegalovirus: a Sticky Virus Makes a Slick Getaway. Microbiology and molecular biology reviews : MMBR 54 27307580
2015 Differential distribution of the sodium-activated potassium channels slick and slack in mouse brain. The Journal of comparative neurology 53 26587966
2008 BALLDock/SLICK: a new method for protein-carbohydrate docking. Journal of chemical information and modeling 46 18646839
2014 Genome-wide association study and ancestral origins of the slick-hair coat in tropically adapted cattle. Frontiers in genetics 45 24808908
2014 Not just an oil slick: how the energetics of protein-membrane interactions impacts the function and organization of transmembrane proteins. Biophysical journal 44 24896109
2012 A quasi-exclusive European ancestry in the Senepol tropical cattle breed highlights the importance of the slick locus in tropical adaptation. PloS one 43 22675421
2011 Efficient inducible Pan-neuronal cre-mediated recombination in SLICK-H transgenic mice. Genesis (New York, N.Y. : 2000) 40 21671347
2017 A De Novo Mutation in the Sodium-Activated Potassium Channel KCNT2 Alters Ion Selectivity and Causes Epileptic Encephalopathy. Cell reports 37 29069600
2007 The slick hair coat locus maps to chromosome 20 in Senepol-derived cattle. Animal genetics 35 17257189
2006 SLICK--scoring and energy functions for protein-carbohydrate interactions. Journal of chemical information and modeling 32 16859295
2018 Oxytocin can regulate myometrial smooth muscle excitability by inhibiting the Na+ -activated K+ channel, Slo2.1. The Journal of physiology 31 30334255
2020 The Epilepsy of Infancy With Migrating Focal Seizures: Identification of de novo Mutations of the KCNT2 Gene That Exert Inhibitory Effects on the Corresponding Heteromeric KNa1.1/KNa1.2 Potassium Channel. Frontiers in cellular neuroscience 29 32038177
2008 Slack and Slick KNa channels are required for the depolarizing afterpotential of acutely isolated, medium diameter rat dorsal root ganglion neurons. Acta pharmacologica Sinica 28 18664322
2017 BREEDING AND GENETICS SYMPOSIUM:Breeding heat tolerant dairy cattle: the case for introgression of the "slick" prolactin receptor variant into dairy breeds. Journal of animal science 24 28464106
2010 Activation of Slo2.1 channels by niflumic acid. The Journal of general physiology 23 20176855
2017 Slick (Kcnt2) Sodium-Activated Potassium Channels Limit Peptidergic Nociceptor Excitability and Hyperalgesia. Journal of experimental neuroscience 20 28943756
2012 Structure-activity relationship of fenamates as Slo2.1 channel activators. Molecular pharmacology 19 22851714
2023 KCNT2-Related Disorders: Phenotypes, Functional, and Pharmacological Properties. Annals of neurology 18 37062836
2013 Structural basis of ion permeation gating in Slo2.1 K+ channels. The Journal of general physiology 18 24166878
2016 Cardiac Slo2.1 Is Required for Volatile Anesthetic Stimulation of K+ Transport and Anesthetic Preconditioning. Anesthesiology 17 26845140
2015 Identification of the Intracellular Na+ Sensor in Slo2.1 Potassium Channels. The Journal of biological chemistry 17 25903137
2014 Cell volume changes regulate slick (Slo2.1), but not slack (Slo2.2) K+ channels. PloS one 17 25347289
2018 Chemogenetic Enhancement of Axon Regeneration Following Peripheral Nerve Injury in the SLICK-A Mouse. Brain sciences 16 29786639
2012 PIP₂ modulation of Slick and Slack K⁺ channels. Biochemical and biophysical research communications 15 22728883
2017 Tumor necrosis factor α modulates sodium-activated potassium channel SLICK in rat dorsal horn neurons via p38 MAPK activation pathway. Journal of pain research 14 28579824
2019 Impact of slick hair trait on physiological and reproductive performance in beef heifers consuming ergot alkaloids from endophyte-infected tall fescue1. Journal of animal science 13 30772895
2015 Transcriptional Regulation of the Sodium-activated Potassium Channel SLICK (KCNT2) Promoter by Nuclear Factor-κB. The Journal of biological chemistry 13 26100633
2021 Case Report: Causative De novo Variants of KCNT2 for Developmental and Epileptic Encephalopathy. Frontiers in genetics 12 34276763
2022 Slick Potassium Channels Control Pain and Itch in Distinct Populations of Sensory and Spinal Neurons in Mice. Anesthesiology 11 35303056
2020 Additional observation of a de novo pathogenic variant in KCNT2 leading to epileptic encephalopathy with clinical features of frontal lobe epilepsy. Brain & development 10 32773162
2021 SLO2.1/NALCN a sodium signaling complex that regulates uterine activity. iScience 9 34746693
2020 Long Non-Coding RNA HAND2-AS1 Inhibits Growth and Migration of Gastric Cancer Cells Through Regulating the miR-590-3p/KCNT2 Axis. OncoTargets and therapy 9 32368078
2024 Thermotolerance capabilities, blood metabolomics, and mammary gland hemodynamics and transcriptomic profiles of slick-haired Holstein cattle during mid lactation in Puerto Rico. Journal of dairy science 8 38246540
2015 Hydrophobic interactions between the S5 segment and the pore helix stabilizes the closed state of Slo2.1 potassium channels. Biochimica et biophysica acta 8 26724206
2015 Identification of potential novel interaction partners of the sodium-activated potassium channels Slick and Slack in mouse brain. Biochemistry and biophysics reports 8 29124216
2014 Intracellular ATP does not inhibit Slo2.1 K+ channels. Physiological reports 8 25214519
2020 New mutations in KCNT2 gene causing early infantile epileptic encephalopathy type 57: Case study and literature review. Acta biochimica Polonica 7 32931186
2017 Heteromeric Slick/Slack K+ channels show graded sensitivity to cell volume changes. PloS one 6 28222129
2021 Exposure and Recovery of the Gulf Toadfish (Opsanus beta) to Weathered Deepwater Horizon Slick Oil: Impacts on Liver and Blood Endpoints. Environmental toxicology and chemistry 5 33326153
2024 Circular RNA-GRIN2B Suppresses Neuropathic Pain by Targeting the NF-κB/SLICK Pathway. Neuromolecular medicine 3 38600344
2024 Slick potassium channels limit TRPM3-mediated activation of sensory neurons. Frontiers in pharmacology 2 39744124
2023 Lhermitte-Duclos disease with concomitant KCNT2 gene mutation: report of an extremely rare combination. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery 2 37368068
2024 Identification of a novel KCNT2 variant in a family with developmental and epileptic encephalopathies: a case report and literature review. Frontiers in genetics 1 38510274
2026 Slick K+ channels contribute to cardiac remodeling, fibrosis and dysfunction in post-infarction hearts. JCI insight 0 41842949
2025 SLICK: A Sandwich-LIke Culturing Kit for in situ Cryo-ET Sample Preparation. bioRxiv : the preprint server for biology 0 39990359
2025 Quantitative analysis of yearling traits in Senepol cattle carrying the slick hair gene. Tropical animal health and production 0 40624397
2025 KCNT1 (Slack/Slo2.2) and KCNT2 (Slick/Slo2.1) Dysregulation in Intellectual Disability and Behavioral Phenotypes: A Systematic Review. Cureus 0 41189825
2021 Long Non-Coding RNA HAND2-AS1 Inhibits Growth and Migration of Gastric Cancer Cells Through Regulating the miR-590-3p/KCNT2 Axis [Retraction]. OncoTargets and therapy 0 34675541

Missed literature

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