ReviewThe Journal of physiology2008
Modification of K+ channel-drug interactions by ancillary subunits.
Review in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
16 citing papers in PubMed, 31 citations in OpenAlex.
- Pharmacological Approaches for the Modulation of the Potassium Channel KInternational journal of molecular sciences · 2021Review
- KCNE1 induces fenestration in the Kv7.1/KCNE1 channel complex that allows for highly specific pharmacological targeting.Nature communications · 2016Article
- Functional Expression Profile of Voltage-Gated K(+) Channel Subunits in Rat Small Mesenteric Arteries.Cell biochemistry and biophysics · 2016Article
- Sex differences in the mechanisms underlying long QT syndrome.American journal of physiology. Heart and circulatory physiology · 2014Review
- Effect of mosapride on Kv4.3 potassium channels expressed in CHO cells.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Insight into the modulation of Shaw2 Kv channels by general anesthetics: structural and functional studies of S4-S5 linker and S6 C-terminal peptides in micelles by NMR.Biochimica et biophysica acta · 2013Article
- Interaction of the S6 proline hinge with N-type and C-type inactivation in Kv1.4 channels.Biophysical journal · 2012Article
- Cytoplasmic domains and voltage-dependent potassium channel gating.Frontiers in pharmacology · 2012Article
- Sex specific association of potassium channel subunits.The Journal of physiology · 2011Article
- Inhibition of Kv4.3 by genistein via a tyrosine phosphorylation-independent mechanism.American journal of physiology. Cell physiology · 2011Article
- A model of the interaction between N-type and C-type inactivation in Kv1.4 channels.Biophysical journal · 2011Article
- Effects of lobeline, a nicotinic receptor ligand, on the cloned Kv1.5.Pflugers Archiv : European journal of physiology · 2010Article
- Effect of the I(to) activator NS5806 on cloned K(V)4 channels depends on the accessory protein KChIP2.British journal of pharmacology · 2010Article
- S3b amino acid substitutions and ancillary subunits alter the affinity of Heteropoda venatoria toxin 2 for Kv4.3.Molecular pharmacology · 2009Article
- Kv4 Channels Underlie the Subthreshold-Operating A-type K-current in Nociceptive Dorsal Root Ganglion Neurons.Frontiers in molecular neuroscience · 2009Article
- K(V)4.3 N-terminal deletion mutant Δ2-39: effects on inactivation and recovery characteristics in both the absence and presence of KChIP2b.Channels (Austin, Tex.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reconciling ion channel alpha-subunit expression with native ionic currents and their pharmacological sensitivity in target organs has proved difficult. In native tissue, many K(+) channel alpha-subunits co-assemble with ancillary subunits, which can profoundly affect physiological parameters including gating kinetics and pharmacological interactions. In this review, we examine the link between voltage-gated potassium ion channel pharmacology and the biophysics of ancillary subunits. We propose that ancillary subunits can modify the interaction between pore blockers and ion channels by three distinct mechanisms: changes in (1) binding site accessibility; (2) orientation of pore-lining residues; (3) the ability of the channel to undergo post-binding conformational changes. Each of these subunit-induced changes has implications for gating, drug affinity and use dependence of their respective channel complexes. A single subunit may modulate its associated alpha-subunit by more than one of these mechanisms. Voltage-gated potassium channels are the site of action of many therapeutic drugs. In addition, potassium channels interact with drugs whose primary target is another channel, e.g. the calcium channel blocker nifedipine, the sodium channel blocker quinidine, etc. Even when K(+) channel block is the intended mode of action, block of related channels in non-target organs, e.g. the heart, can result in major and potentially lethal side-effects. Understanding factors that determine specificity, use dependence and other properties of K(+) channel drug binding are therefore of vital clinical importance. Ancillary subunits play a key role in determining these properties in native tissue, and so understanding channel-subunit interactions is vital to understanding clinical pharmacology.
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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.