ArticleThe Journal of biological chemistry2014
Conopeptide Vt3.1 preferentially inhibits BK potassium channels containing β4 subunits via electrostatic interactions.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Pooled it
- Pharmacological Relevance of β-, γ-, and LINGO Auxiliary Subunits in BK Channel Modulation.ChemMedChem · 2026Review
- Peptide Toxins from MarineToxins · 2024Review
- Snails In Silico: A Review of Computational Studies on the Conopeptides.Marine drugs · 2019Review
- Solution structure of extracellular loop of human β4 subunit of BK channel and its biological implication on ChTX sensitivity.Scientific reports · 2018Article
- Modulation of BK Channel Function by Auxiliary Beta and Gamma Subunits.International review of neurobiology · 2016Review
- BK Channels in the Central Nervous System.International review of neurobiology · 2016Review
- Bioinformatics-Aided Venomics.Toxins · 2015Review
- Conotoxin gene superfamilies.Marine drugs · 2014Review
- Big Potassium (BK) ion channels in biology, disease and possible targets for cancer immunotherapy.International immunopharmacology · 2014Review
- The OPEP protein model: from single molecules, amyloid formation, crowding and hydrodynamics to DNA/RNA systems.Chemical Society reviews · 2014Review
- Pharmacological consequences of the coexpression of BK channel α and auxiliary β subunits.Frontiers in physiology · 2014Review
- Current understanding of iberiotoxin-resistant BK channels in the nervous system.Frontiers in physiology · 2014Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
BK channel β subunits (β1-β4) modulate the function of channels formed by slo1 subunits to produce tissue-specific phenotypes. The molecular mechanism of how the homologous β subunits differentially alter BK channel functions and the role of different BK channel functions in various physiologic processes remain unclear. By studying channels expressed in Xenopus laevis oocytes, we show a novel disulfide-cross-linked dimer conopeptide, Vt3.1 that preferentially inhibits BK channels containing the β4 subunit, which is most abundantly expressed in brain and important for neuronal functions. Vt3.1 inhibits the currents by a maximum of 71%, shifts the G-V relation by 45 mV approximately half-saturation concentrations, and alters both open and closed time of single channel activities, indicating that the toxin alters voltage dependence of the channel. Vt3.1 contains basic residues and inhibits voltage-dependent activation by electrostatic interactions with acidic residues in the extracellular loops of the slo1 and β4 subunits. These results suggest a large interaction surface between the slo1 subunit of BK channels and the β4 subunit, providing structural insight into the molecular interactions between slo1 and β4 subunits. The results also suggest that Vt3.1 is an excellent tool for studying β subunit modulation of BK channels and for understanding the physiological roles of BK channels in neurophysiology.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.