ArticleScience signaling2014
KCNQ1, KCNE2, and Na+-coupled solute transporters form reciprocally regulating complexes that affect neuronal excitability.
Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 70 citations in OpenAlex.
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- The SIMDA framework maps PIP2-binding sites regulating the KCNQ1 channel.Nature communications · 2026Article
- KCNE gene family: From basic functions to diseases.Genes & diseases · 2026Review
- Discovery of Small-Molecule Inhibitors of the KCNQ1/Kv7.1 Potassium Channel with Virtual Screening and Functional Validation in Electrophysiological Assays and KCNQ1-Knockout Neural Stem Cells.ACS chemical neuroscience · 2026Article
- A patient with a rare metabolic disease and myo-inositol administration leading to a new treatment for epilepsy.Molecular genetics and metabolism · 2026Article
- Cell-specific isotope labeling identifiesbioRxiv : the preprint server for biology · 2026Article
- Mechanisms of KCNQ1 gating modulation by KCNE1/3 for cell-specific function.Cell research · 2025Article
- The Use of Synaptic Extracellular Myo-Inositol to Treat Developmental and Epileptic Encephalopathy.Annals of the Child Neurology Society · 2025Article
- Ion channel traffic jams: the significance of trafficking deficiency in long QT syndrome.Cell discovery · 2025Review
- The kynurenine pathway as a potential link between ethanol-induced behavioral alterations and neuroinflammation.Frontiers in pharmacology · 2025Article
- Analysis of the finasteride treatment and its withdrawal in the rat hypothalamus and hippocampus at whole-transcriptome level.Journal of endocrinological investigation · 2024Article
- SGLT1 contributes to glucose-mediated exacerbation of ischemia-reperfusion injury in ex vivo rat heart.Basic research in cardiology · 2024Article
- Kv7 channel activation reduces brain endothelial cell permeability and prevents kainic acid-induced blood-brain barrier damage.American journal of physiology. Cell physiology · 2024Article
- Multi-target Phenylpropanoids Against Epilepsy.Current neuropharmacology · 2024Review
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity.Channels (Austin, Tex.) · 2021Article
- The Amyloid Precursor Protein C99 Fragment Modulates Voltage-Gated Potassium Channels.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Article
- Fluorescence Fluctuation Spectroscopy enables quantification of potassium channel subunit dynamics and stoichiometry.Scientific reports · 2021Article
- Control of Biophysical and Pharmacological Properties of Potassium Channels by Ancillary Subunits.Handbook of experimental pharmacology · 2021Article
- Targeted deubiquitination rescues distinct trafficking-deficient ion channelopathies.Nature methods · 2020Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
Na(+)-coupled solute transport is crucial for the uptake of nutrients and metabolic precursors, such as myo-inositol, an important osmolyte and precursor for various cell signaling molecules. We found that various solute transporters and potassium channel subunits formed complexes and reciprocally regulated each other in vitro and in vivo. Global metabolite profiling revealed that mice lacking KCNE2, a K(+) channel β subunit, showed a reduction in myo-inositol concentration in cerebrospinal fluid (CSF) but not in serum. Increased behavioral responsiveness to stress and seizure susceptibility in Kcne2(-/-) mice were alleviated by injections of myo-inositol. Suspecting a defect in myo-inositol transport, we found that KCNE2 and KCNQ1, a voltage-gated potassium channel α subunit, colocalized and coimmunoprecipitated with SMIT1, a Na(+)-coupled myo-inositol transporter, in the choroid plexus epithelium. Heterologous coexpression demonstrated that myo-inositol transport by SMIT1 was augmented by coexpression of KCNQ1 but was inhibited by coexpression of both KCNQ1 and KCNE2, which form a constitutively active, heteromeric K(+) channel. SMIT1 and the related transporter SMIT2 were also inhibited by a constitutively active mutant form of KCNQ1. The activities of KCNQ1 and KCNQ1-KCNE2 were augmented by SMIT1 and the glucose transporter SGLT1 but were suppressed by SMIT2. Channel-transporter signaling complexes may be a widespread mechanism to facilitate solute transport and electrochemical crosstalk.
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