ArticleCell reports2016
Epilepsy-Related Slack Channel Mutants Lead to Channel Over-Activity by Two Different Mechanisms.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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Who cites it
47 citing papers in PubMed, 99 citations in OpenAlex.
- Discovery of non-opioid peptides that selectively relieve mechanical pain in rodents through inhibition of TRPV4 channels.Acta pharmacologica Sinica · 2026Article
- Unraveling the mechanisms of slack channel mutations in epileptic disorders.Acta epileptologica · 2026Review
- Information Entropy Metrics to Address the Complexity of Cooperative Gating of Ion Channels.Entropy (Basel, Switzerland) · 2026Article
- Efficient Regioselective Synthesis of Benzimidazoles and Azabenzimidazoles to Enable the Rapid Development of Structure-Activity Relationships for Activation of SLACK Potassium Channels.Synlett : accounts and rapid communications in synthetic organic chemistry · 2025Article
- Review
- KCNT1 gene variant-associated epilepsy: genetic insights, functional mechanisms, and emerging therapies.Journal of neurology · 2025Review
- Electrophysiological characterization of human KCNT1 channel modulators and the therapeutic potential of hydroquinine and tipepidine in KCNT1 mutation-associated epilepsy mouse model.Acta pharmacologica Sinica · 2025Article
- A synthetic peptide, derived from neurotoxin GsMTx4, acts as a non-opioid analgesic to alleviate mechanical and neuropathic pain through the TRPV4 channel.Acta pharmaceutica Sinica. B · 2025Article
- Structure-Activity Relationship Studies in a Series of 2-Aryloxy-Molecules (Basel, Switzerland) · 2024Article
- Molecular Profiling of Mouse Models of Loss or Gain of Function of the KCNT1 (Slack) Potassium Channel and Antisense Oligonucleotide Treatment.Biomolecules · 2024Article
- Heterozygous expression of aeLife · 2024Article
- Heterozygous expression of abioRxiv : the preprint server for biology · 2024Article
- Structure-Activity Relationship Studies in a Series of Xanthine Inhibitors of SLACK Potassium Channels.Molecules (Basel, Switzerland) · 2024Article
- Disease-causing Slack potassium channel mutations produce opposite effects on excitability of excitatory and inhibitory neurons.Cell reports · 2024Article
- Drosophila expressing mutant human KCNT1 transgenes make an effective tool for targeted drug screening in a whole animal model of KCNT1-epilepsy.Scientific reports · 2024Article
- Coupling of Slack and NaeLife · 2024Article
- Design, synthesis, and biological evaluation of a novel series of 1,2,4-oxadiazole inhibitors of SLACK potassium channels: Identification of in vitro tool VU0935685.Bioorganic & medicinal chemistry · 2023Article
- Slack KCommunications biology · 2023Article
- Identification of the Acid-Sensitive Site Critical for Chloral Hydrate (CH) Activation of the Proton-Activated Chloride Channel.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Antisense oligonucleotide therapy for KCNT1 encephalopathy.JCI insight · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Twelve sodium-activated potassium channel (KCNT1, Slack) genetic mutants have been identified from severe early-onset epilepsy patients. The changes in biophysical properties of these mutants and the underlying mechanisms causing disease remain elusive. Here, we report that seven of the 12 mutations increase, whereas one mutation decreases, the channel's sodium sensitivity. Two of the mutants exhibit channel over-activity only when the intracellular Na(+) ([Na(+)]i) concentration is ∼80 mM. In contrast, single-channel data reveal that all 12 mutants increase the maximal open probability (Po). We conclude that these mutant channels lead to channel over-activity predominantly by increasing the ability of sodium binding to activate the channel, which is indicated by its maximal Po. The sodium sensitivity of these epilepsy causing mutants probably determines the [Na(+)]i concentration at which these mutants exert their pathological effects.
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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.