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Showing KCNU1 — SLO3 is a alias.

KCNU1

Potassium channel subfamily U member 1 · UniProt A8MYU2

Length
1149 aa
Mass
129.5 kDa
Annotated
2026-06-10
27 papers in source corpus 20 papers cited in narrative 22 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

KCNU1 (SLO3) encodes a sperm-specific, high-conductance potassium channel that constitutes the principal K+ conductance (KSper) governing membrane potential during sperm capacitation and is essential for male fertility (PMID:9452476, PMID:20138882, PMID:21427226). Cloned from spermatocytes as a Slo1/BK-related channel, SLO3 is gated jointly by intracellular alkalinization and membrane depolarization, with quantitatively distinct allosteric coupling and weaker intrinsic voltage dependence than Slo1 (PMID:9452476, PMID:16940555). Genetic deletion in mice abolishes all pH-dependent K+ current in sperm and converts capacitation-associated hyperpolarization into depolarization, producing infertility, hairpin morphology, motility defects, and failure of the acrosome reaction that is rescued by valinomycin-induced hyperpolarization, establishing hyperpolarization as the functionally critical output (PMID:20138882, PMID:21427226); double knockout with CatSper1 confirms SLO3 and CatSper as the dominant channels setting sperm membrane potential (PMID:23980198). Channel gating is tuned to physiological voltage and pH by the testis-specific leucine-rich-repeat auxiliary subunit LRRC52, whose own stability depends on SLO3, and whose loss severely impairs fertility in proportion to the reduction in available KSper conductance (PMID:22084117, PMID:25675513). SLO3 activity is further controlled by PIP2, which is required for current and whose hydrolysis (via EGF receptor or voltage-sensing phosphatase) inhibits the channel (PMID:20392696, PMID:32564653), by intracellular zinc, which directly and near-irreversibly inhibits the channel, and by PKA→cSrc signaling, which couples capacitation to SLO3-dependent hyperpolarization (PMID:26060254). The human channel diverges from mouse SLO3 in being activated preferentially by Ca2+ rather than alkaline pH, localizes to the sperm flagellum, and forms a Ca2+/voltage-dependent feedback loop with CatSper that limits progesterone-evoked Ca2+ influx and drives repolarization from a resting potential of ~−65 mV (PMID:24670955). Loss-of-function and bi-allelic missense/splice variants in human SLO3 cause acrosome reaction defects and male infertility, defining a Mendelian link to male factor infertility (PMID:34980136, PMID:35551387).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1998 High

    Established the existence of a distinct sperm/testis K+ channel gated by both pH and voltage, defining a new branch of the Slo channel family.

    Evidence Cloning from spermatocytes with RT-PCR, Northern, in situ hybridization, and heterologous electrophysiology

    PMID:9452476

    Open questions at the time
    • No native sperm conductance yet linked to the cloned channel
    • Physiological role undefined
  2. 2006 High

    Quantified how Slo3 gating differs mechanistically from the related BK channel, showing pH-dependent open probability and weaker voltage coupling.

    Evidence Two-electrode voltage-clamp in Xenopus oocytes with Horrigan-Aldrich allosteric modeling

    PMID:16940555

    Open questions at the time
    • Heterologous gating did not match native KSper voltage/pH range
    • No auxiliary subunits included
  3. 2009 Medium

    Identified accessory beta subunit co-assembly and mapped species-divergent gating to a rapidly evolving RCK1 loop, beginning to explain context- and species-specific channel behavior.

    Evidence Co-expression electrophysiology, surface biotinylation/YFP imaging, KCNMB4-KO mice, and bovine/mouse chimeric construct analysis

    PMID:19473978 PMID:19578543

    Open questions at the time
    • KCNMB4 not shown to be the physiological auxiliary subunit in sperm
    • Chimera analysis was structural inference without atomic-resolution data
  4. 2010 High

    Established Slo3 as the channel responsible for capacitation-induced hyperpolarization and proved hyperpolarization is required for the acrosome reaction and fertility.

    Evidence Slo3-knockout mice with membrane potential, motility, morphology, and acrosome reaction assays plus valinomycin pharmacological rescue

    PMID:20138882

    Open questions at the time
    • Did not resolve residual outward currents in null sperm
    • Mechanism coupling hyperpolarization to acrosome reaction not detailed
  5. 2010 High

    Defined PIP2 as a required activating lipid cofactor and a route for receptor-mediated channel inhibition, and characterized the channel's distinctive pharmacology.

    Evidence Inside-out macropatch electrophysiology with PIP2 depletion, EGF-receptor epistasis, mutagenesis of PIP2-binding residues, and systematic blocker profiling

    PMID:19934650 PMID:20392696

    Open questions at the time
    • PIP2 regulation in native sperm flagellum not directly demonstrated at this stage
    • Endogenous receptor driving PIP2 hydrolysis in sperm unidentified
  6. 2011 High

    Proved by genetics that Slo3 is the sole pH-dependent K+ conductance (KSper) and identified LRRC52 as the auxiliary subunit shifting gating into the physiological range.

    Evidence Slo3-KO sperm patch-clamp with pharmacology, and LRRC52 co-expression electrophysiology with Western blot in WT vs KO tissue

    PMID:21427226 PMID:22084117

    Open questions at the time
    • Source of residual outward current not yet genetically assigned
    • LRRC52 stoichiometry with channel undefined
  7. 2012 High

    Provided a structural view of the human SLO3 cytoplasmic gating ring and a candidate open-state conformation.

    Evidence X-ray crystallography of the human SLO3 gating ring with heterologous electrophysiology and LRRC52 co-expression

    PMID:23129643

    Open questions at the time
    • No full-length transmembrane structure
    • Open-state assignment is comparative inference
  8. 2013 High

    Resolved the channel identity of sperm K+ currents by showing Slo3 and CatSper together account for all voltage-activated outward K+ current.

    Evidence Slo3/CatSper1 double-knockout mouse breeding with sperm patch-clamp

    PMID:23980198

    Open questions at the time
    • Functional crosstalk between the two channels not yet defined
    • Result restricted to mouse
  9. 2014 High

    Showed the human channel is gated principally by Ca2+ rather than pH, redefining the species-specific physiology of human KSper and localizing the protein to the flagellum.

    Evidence Whole-cell patch-clamp of human sperm, heterologous expression of human vs mouse SLO3, pharmacology, and immunolocalization

    PMID:24670955

    Open questions at the time
    • Molecular basis of the human Ca2+ sensitivity not mapped
    • Lacked a SLO3-selective inhibitor to confirm channel identity
  10. 2015 Medium

    Established that LRRC52 is functionally essential for fertility and that fertility scales with physiologically available KSper conductance; added cSrc as the kinase linking PKA to SLO3-driven hyperpolarization.

    Evidence LRRC52-KO mouse with multi-genotype sperm electrophysiology and IVF, plus cSrc activation immunoblotting and pharmacological epistasis in capacitating sperm and heterologous SLO3

    PMID:25675513 PMID:26060254

    Open questions at the time
    • Direct phosphorylation of SLO3 or LRRC52 by cSrc not demonstrated
    • cSrc-channel linkage is pharmacological/indirect
  11. 2015 Medium

    Defined the pore-level pharmacology and located the activation gate between S6 residue F304 and the selectivity filter.

    Evidence Two-electrode voltage-clamp with quinine/quinidine/barium block, gain-of-function mutants, and in silico docking

    PMID:26045093

    Open questions at the time
    • Gate location inferred from mutagenesis/docking, not structure
    • Single lab
  12. 2019 Medium

    Showed that the full-length channel-forming protein is testis-exclusive while short cytoplasmic isoforms appear in somatic tissues, constraining where SLO3 can act as a channel.

    Evidence Computational isoform prediction with RT-PCR and Western blot across tissues

    PMID:31270758

    Open questions at the time
    • Function of somatic short isoforms unknown
    • No protein-interaction or activity data for isoforms
  13. 2020 Medium

    Showed the Slo3/LRRC52 complex retains PIP2-dependence under enzymatic phosphoinositide depletion, supporting lipid regulation of the native flagellar channel.

    Evidence Co-expression of Slo3 + Lrrc52 + voltage-sensing phosphatase in Xenopus oocytes with two-electrode voltage-clamp

    PMID:32564653

    Open questions at the time
    • Polarized PIP2 distribution in sperm not directly measured
    • Single heterologous method
  14. 2022 Medium

    Linked human SLO3 loss-of-function variants to acrosome reaction failure and male infertility, establishing a Mendelian disease connection.

    Evidence Whole-exome sequencing with Western blot, immunofluorescence, electron microscopy, and functional sperm assays; one cohort with a knock-in mouse model and ICSI rescue

    PMID:34980136 PMID:35551387

    Open questions at the time
    • Small numbers of patients
    • Variant effects on channel biophysics not directly recorded
  15. 2023 High

    Provided a selective human SLO3 inhibitor that definitively confirmed SLO3 as the sole hyperpolarizing K+ channel of human sperm.

    Evidence Pharmacological screen with heterologous and native human sperm electrophysiology, membrane potential, motility, and acrosome reaction assays

    PMID:36649421

    Open questions at the time
    • In vivo contraceptive potential untested
    • Off-target spectrum not fully defined
  16. 2024 Medium

    Identified intracellular zinc as a direct, slowly dissociating inhibitor of Slo3 with mapped coordinating residues, adding a metal-ion regulatory layer to channel control.

    Evidence Two-electrode voltage-clamp with intracellular zinc, MD simulations, mutagenesis, and sperm zinc imaging (preprint)

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Physiological consequence of zinc inhibition in capacitating sperm not established
  17. 2025 Medium

    Defined a dynamic CatSper-SLO3 feedback circuit in which SLO3-set membrane potential limits progesterone-evoked Ca2+ influx and drives repolarization.

    Evidence Simultaneous millisecond-resolution voltage and Ca2+ fluorimetry in human sperm (preprint)

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Molecular mediators of the feedback coupling not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the human-specific Ca2+ sensitivity is structurally encoded, and whether SLO3 inhibitors can serve as non-hormonal contraceptives in vivo, remains open.
  • No full-length structure resolving Ca2+/pH gating in human SLO3
  • No in vivo demonstration of pharmacological contraception

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0140299 molecular sensor activity 3 GO:0008289 lipid binding 2
Localization
GO:0005886 plasma membrane 3 GO:0005929 cilium 1
Pathway
R-HSA-1474165 Reproduction 4 R-HSA-162582 Signal Transduction 2
Partners
CATSPER1KCNMB4LRRC52
Complex memberships
SLO3/LRRC52 channel complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 Slo3 (KCNU1) encodes a novel potassium channel regulated by both intracellular pH and membrane voltage, cloned from mammalian spermatocytes with primary expression in testis; the protein shares sequence similarity with Slo1 (BK channel) and is activated by alkaline pH and depolarization in heterologous expression. Cloning, RT-PCR, Northern blot, in situ hybridization, heterologous expression with electrophysiology The Journal of biological chemistry High 9452476
2006 Detailed voltage and pH dependence of macroscopic Slo3 currents established: increases in cytosolic pH promote channel activation; Slo3 differs from Slo1 in that its limiting open probability is pH-dependent, its intrinsic voltage dependence (z_L) and coupling factor D are smaller, and both activation and deactivation kinetics are weakly voltage-dependent with two exponential components. Heterologous expression in Xenopus oocytes, two-electrode voltage-clamp, allosteric (Horrigan-Aldrich) modeling The Journal of general physiology High 16940555
2009 The beta4 subunit (KCNMB4) selectively co-assembles with Slo3 and produces 8–10-fold enhancement of Slo3 current expression and surface expression in Xenopus oocytes; beta1, beta2, and beta3 also co-assemble with Slo3 biochemically but do not mimic beta4's effect on surface expression. Beta4 promoter is active in spermatocytes and beta4 mRNA abundance is comparable to Slo3 in testes and sperm. Co-expression in Xenopus oocytes, electrophysiology, YFP-tagged and biotin-labeled surface expression assays, fluorescence microscopy in beta4-KO mice, quantitative RT-PCR PloS one High 19578543
2009 Functional divergence between bovine and mouse Slo3 channels (differences in voltage range of activation, kinetics, and pH sensitivity) maps to a rapidly evolving loop structure in the RCK1 domain linking the intermediate RCK1 subdomain to the C-terminal subdomain; small structural changes in this loop produce major changes in activation voltage range and kinetics. Heterologous expression electrophysiology of bovine and mouse Slo3; chimeric/mutant channel analysis The Journal of biological chemistry Medium 19473978
2010 Slo3 knockout male mice are infertile; wild-type sperm undergo membrane hyperpolarization during capacitation whereas Slo3-null sperm undergo depolarization, establishing Slo3 as the principal K+ channel responsible for capacitation-induced hyperpolarization. Slo3-null sperm exhibit impaired motility, bent 'hairpin' morphology, and failure to undergo the acrosome reaction; the acrosome reaction failure is rescued by valinomycin-induced hyperpolarization, showing that hyperpolarization is crucial for the acrosome reaction. Gene knockout mouse model, membrane potential measurements, motility assays, acrosome reaction assays, pharmacological rescue with valinomycin FEBS letters High 20138882
2010 Phosphatidylinositol 4,5-bisphosphate (PIP2) activates Slo3 currents; depletion of endogenous PIP2 in inside-out macropatches inhibits Slo3 currents. EGF receptor stimulation inhibits Slo3 currents in a PIP2-dependent manner (hydrolysis-dependent), and mutation of positively charged residues involved in channel-PIP2 interactions enhances EGF-induced inhibition, identifying a PIP2-binding site on Slo3. Inside-out macropatch electrophysiology in Xenopus oocytes, whole-cell recordings from sperm and co-expressed systems, EGF stimulation, site-directed mutagenesis The Journal of biological chemistry High 20392696
2010 Slo3 is resistant to block by iberiotoxin, charybdotoxin, and extracellular TEA (standard Slo1 blockers) and relatively insensitive to extracellular 4-AP; quinidine blocks Slo3 more potently than Slo1 with unusual voltage-dependence (block relieved by depolarization regardless of side of application), consistent with preferential binding to closed Slo3 channels. Cytosolic 4-AP blocks Slo3 via open-channel block ~10–15-fold more potently than Slo1. Heterologous expression in Xenopus oocytes, two-electrode voltage-clamp with pharmacological blockers, mutant channel constructs Channels (Austin, Tex.) High 19934650
2011 Genetic deletion of Slo3 abolishes all pH-dependent K+ current (KSper) at physiological membrane potentials in mouse sperm, establishing KSper/Slo3 as the sole pH-dependent K+ conductance. A residual outward current (I_Kres) at >0 mV in Slo3-null sperm is attributable to CatSper (monovalent flux), not Slo3. Slo3-null sperm depolarize upon alkalization (vs. hyperpolarization in WT), and exhibit morphological abnormalities and motility deficits. Slo3 knockout mouse, patch-clamp electrophysiology, pharmacological dissection with clofilium, motility assays, morphological analysis Proceedings of the National Academy of Sciences of the United States of America High 21427226
2011 LRRC52, a testis-specific leucine-rich repeat protein homologous to the Slo1-modifying LRRC26, is a Slo3 auxiliary subunit that shifts Slo3 gating to voltages and pH values matching native KSper current. LRRC52 protein expression is critically dependent on the presence of Slo3 (absent from Slo3-null sperm). LRRC52 is more effective at modifying Slo3 function than LRRC26 or other LRRC paralogs. Co-expression electrophysiology in Xenopus oocytes, Western blot and immunodetection in WT and Slo3-KO testis/sperm, qRT-PCR developmental expression analysis Proceedings of the National Academy of Sciences of the United States of America High 22084117
2012 Crystal structure of the human SLO3 gating ring (cytoplasmic domain) was solved; comparison with Slo1 gating ring structures suggests the SLO3 gating ring structure may represent an open state. Human SLO3 opens upon intracellular pH increase in heterologous electrophysiology, and its gating properties are modulated by LRRC52. X-ray crystallography (crystal structure of human SLO3 gating ring), heterologous electrophysiology, co-expression with LRRC52 Proceedings of the National Academy of Sciences of the United States of America High 23129643
2013 Double knockout of Slo3 and CatSper1 abolishes all voltage-activated outward K+ current in mouse sperm, confirming that the residual outward current in Slo3-null sperm arises from CatSper. Together, KSper (Slo3) and CatSper appear to be the sole ion channels in mouse sperm regulating membrane potential and Ca2+ influx in response to alkalization. Double-knockout mouse breeding, patch-clamp electrophysiology of sperm from Slo3-/- , CatSper1-/-, and double-KO mice The Journal of general physiology High 23980198
2014 In human sperm, IKSper (the principal K+ current) is activated more strongly by Ca2+ than by alkaline pHi (unlike mouse Slo3 which is pH-activated). Heterologously expressed human SLO3, but not mouse SLO3, is activated by Ca2+ rather than alkaline pHi. Slo3 protein is identified in the flagellum of human sperm. Slo3 inhibitors suppress human IKSper, and current-voltage relations of human Slo3 and human IKSper are similar, establishing human Slo3 as the principal K+ channel in human sperm. Whole-cell patch-clamp of human sperm, heterologous expression of human and mouse SLO3 in Xenopus oocytes, pharmacological inhibition, immunolocalization of Slo3 protein in human sperm flagellum eLife High 24670955
2015 Genetic knockout of LRRC52 in mice causes severely impaired fertility; KSPER current in LRRC52-null sperm requires more positive voltages and higher pH for activation than WT KSPER, establishing that LRRC52 is an essential auxiliary subunit that shifts Slo3/KSPER gating to physiologically relevant voltages and pH. IVF competence across multiple genotypes correlates with net KSPER conductance available under physiological conditions. LRRC52 knockout mouse, patch-clamp electrophysiology of sperm from multiple genotypes, fertility assays, in vitro fertilization Proceedings of the National Academy of Sciences of the United States of America High 25675513
2015 cSrc kinase is activated downstream of PKA during sperm capacitation and its inhibition blocks capacitation-induced hyperpolarization (mediated by SLO3) without blocking tyrosine phosphorylation. cSrc inhibitors significantly decrease SLO3-mediated currents in heterologous expression, placing cSrc as a connecting player between PKA activation and SLO3-mediated hyperpolarization. Anti-pTyr416-cSrc immunoblotting to track cSrc activation kinetics, pharmacological inhibition of cSrc in capacitating sperm (membrane potential measurements), heterologous expression of SLO3 with cSrc inhibitor electrophysiology, pharmacological rescue of acrosome reaction by valinomycin The Journal of biological chemistry Medium 26060254
2015 Quinine, quinidine, and barium block mouse Slo3 channels; barium inhibits from outside by interacting with the selectivity filter (block prevented by elevated extracellular K+); quinine and quinidine act from inside by binding a hydrophobic pocket formed by the S6 segment, with block not state-dependent. The F304Y pore mutation increases potency of quinine/quinidine ~10-fold but does not alter barium block, and the Slo3 activation gate is proposed to lie between F304 in S6 and the selectivity filter. Heterologous expression in Xenopus oocytes, two-electrode voltage-clamp, pharmacological analysis with gain-of-function Slo3 mutants (R196Q, F304Y), in silico docking of quinidine British journal of pharmacology Medium 26045093
2019 Two short cytoplasmic Slo3 isoforms (encoding the terminal 381 aa of the cytosolic domain) are expressed in somatic mouse tissues (brain, kidney, eye), identified by RT-PCR and confirmed by Western blot; the full-length ion channel-forming Slo3 is exclusively detected in testis at both transcript and protein level. Computational isoform prediction, RT-PCR, Western blot in multiple tissues Molecular biology reports Medium 31270758
2020 The Slo3/Lrrc52 complex retains sensitivity to phosphoinositide (PIP2) depletion by voltage-sensing phosphatase (VSP) in Xenopus oocytes, similarly to Slo3 alone, supporting that VSP-generated polarized PIP2 distribution in sperm flagellum regulates Slo3 activity in native sperm. Co-expression of Slo3 + Lrrc52 + VSP in Xenopus oocytes, two-electrode voltage-clamp measuring VSP-mediated current inhibition Channels (Austin, Tex.) Medium 32564653
2022 A homozygous missense variant (p.Ile413Phe) in human SLO3 causes reduced SLO3 mRNA and protein in sperm, leading to acrosome hypoplasia, disrupted mitochondrial sheath, coiled tails, motility defects, impaired acrosome reaction, and abnormal membrane potential during capacitation; LRRC52 levels are also reduced in affected sperm. Whole-exome sequencing, Sanger confirmation, RT-PCR, Western blot, immunofluorescence, electron microscopy, acrosome reaction and mitochondrial membrane potential assays on patient sperm Reproductive biology and endocrinology : RB&E Medium 34980136
2022 Bi-allelic KCNU1 variants in two infertile men (one homozygous missense p.His715Arg; one homozygous splice-site causing frameshift) cause impaired acrosome reactions and male infertility; the splice-site variant disrupts normal splicing causing loss of function, and the missense variant reduces KCNU1 protein in sperm of both patient and knock-in mouse model. ICSI rescues the deficiency. Whole-exome sequencing, Sanger sequencing, Western blot, acrosome reaction assay, immunofluorescence, knock-in mouse model, IVF/ICSI rescue Human reproduction (Oxford, England) Medium 35551387
2023 VU0546110, identified as the first selective inhibitor of human SLO3, completely blocks heterologous SLO3 currents and endogenous K+ currents in human sperm, prevents sperm hyperpolarization, and blocks hyperactivated motility and the acrosome reaction, establishing SLO3 as the sole K+ channel responsible for hyperpolarization in human sperm. Pharmacological screen, heterologous electrophysiology of human SLO3, whole-cell patch-clamp of human sperm, membrane potential assays, motility analysis, acrosome reaction assay Proceedings of the National Academy of Sciences of the United States of America High 36649421
2024 Intracellular zinc (Zn2+) directly inhibits mouse Slo3 currents in a dose-dependent manner at micromolar concentrations with exceptionally slow dissociation; sperm-enriched Zn2+ undergoes dynamic changes during capacitation; MD simulations combined with electrophysiology identified specific amino acid residues contributing to slow Zn2+ dissociation from Slo3. Xenopus oocyte expression with two-electrode voltage-clamp, intracellular zinc application, MD simulations, site-directed mutagenesis of zinc-coordinating residues, sperm zinc imaging bioRxivpreprint Medium
2025 In human sperm, progesterone evokes rapid pulse-like depolarization (via CatSper Ca2+ influx) followed by repolarization; Slo3 sets the resting membrane potential at −65 mV, and Ca2+/Vm-dependent feedback through Slo3 limits CatSper-mediated Ca2+ influx and promotes repolarization, establishing a dynamic interplay between CatSper and Slo3 in controlling membrane potential. Quantitative kinetic fluorimetry with voltage-sensitive fluorescent indicators, simultaneous millisecond-resolution Vm and Ca2+ recording (FAST_M technique) in human sperm bioRxivpreprint Medium

Source papers

Stage 0 corpus · 27 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 The SLO3 sperm-specific potassium channel plays a vital role in male fertility. FEBS letters 202 20138882
1998 Slo3, a novel pH-sensitive K+ channel from mammalian spermatocytes. The Journal of biological chemistry 193 9452476
2011 Deletion of the Slo3 gene abolishes alkalization-activated K+ current in mouse spermatozoa. Proceedings of the National Academy of Sciences of the United States of America 156 21427226
2014 The Ca2+-activated K+ current of human sperm is mediated by Slo3. eLife 101 24670955
2011 LRRC52 (leucine-rich-repeat-containing protein 52), a testis-specific auxiliary subunit of the alkalization-activated Slo3 channel. Proceedings of the National Academy of Sciences of the United States of America 72 22084117
2010 Block of mouse Slo1 and Slo3 K+ channels by CTX, IbTX, TEA, 4-AP and quinidine. Channels (Austin, Tex.) 56 19934650
2012 Functional and structural analysis of the human SLO3 pH- and voltage-gated K+ channel. Proceedings of the National Academy of Sciences of the United States of America 54 23129643
2006 Slo3 K+ channels: voltage and pH dependence of macroscopic currents. The Journal of general physiology 50 16940555
2015 SLO3 auxiliary subunit LRRC52 controls gating of sperm KSPER currents and is critical for normal fertility. Proceedings of the National Academy of Sciences of the United States of America 48 25675513
2013 Simultaneous knockout of Slo3 and CatSper1 abolishes all alkalization- and voltage-activated current in mouse spermatozoa. The Journal of general physiology 48 23980198
2015 Src Kinase Is the Connecting Player between Protein Kinase A (PKA) Activation and Hyperpolarization through SLO3 Potassium Channel Regulation in Mouse Sperm. The Journal of biological chemistry 35 26060254
2023 A selective inhibitor of the sperm-specific potassium channel SLO3 impairs human sperm function. Proceedings of the National Academy of Sciences of the United States of America 33 36649421
2009 Interactions between beta subunits of the KCNMB family and Slo3: beta4 selectively modulates Slo3 expression and function. PloS one 30 19578543
2010 Phosphatidylinositol 4,5-bisphosphate activates Slo3 currents and its hydrolysis underlies the epidermal growth factor-induced current inhibition. The Journal of biological chemistry 28 20392696
2022 Homozygous mutation in SLO3 leads to severe asthenoteratozoospermia due to acrosome hypoplasia and mitochondrial sheath malformations. Reproductive biology and endocrinology : RB&E 23 34980136
2015 Mechanism of inhibition of mouse Slo3 (KCa 5.1) potassium channels by quinine, quinidine and barium. British journal of pharmacology 20 26045093
2009 Bovine and mouse SLO3 K+ channels: evolutionary divergence points to an RCK1 region of critical function. The Journal of biological chemistry 20 19473978
2022 Bi-allelic variants in KCNU1 cause impaired acrosome reactions and male infertility. Human reproduction (Oxford, England) 18 35551387
2023 SLO3: A Conserved Regulator of Sperm Membrane Potential. International journal of molecular sciences 15 37446382
2017 Premammalian origin of the sperm-specific Slo3 channel. FEBS open bio 9 28286733
2019 Onion peel extract and its constituent, quercetin inhibits human Slo3 in a pH and calcium dependent manner. The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 8 31496875
2018 Slo3 K+ channel blocker clofilium extends bull and mouse sperm-fertilizing competence. Reproduction (Cambridge, England) 7 30422808
2018 Analyzing the functional divergence of Slo1 and Slo3 channel subfamilies. Molecular phylogenetics and evolution 7 30586650
2019 A cytoplasmic Slo3 isoform is expressed in somatic tissues. Molecular biology reports 4 31270758
2020 The Slo3/Lrrc52 complex is sensitive to phosphoinositides. Channels (Austin, Tex.) 2 32564653
2023 Pharmacological Evidence Suggests That Slo3 Channel Is the Principal K+ Channel in Boar Spermatozoa. International journal of molecular sciences 1 37175513
2025 Differential molecular interactions between iberiotoxin and human SLO3 and SLO1 potassium channels. Journal of molecular modeling 0 40358624

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