ArticleCell reports2014
Human slack potassium channel mutations increase positive cooperativity between individual channels.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed.
- RNA targeting therapy for a prenatally enriched potassium channel associated with severe childhood epilepsy and premature death.Nature communications · 2026Article
- Antisense oligonucleotide-mediated knockdown therapy in two infants with severe KCNT1 epileptic encephalopathy.Nature medicine · 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
- Expanding the phenotypic and genotypic spectrum ofBrain communications · 2026Article
- Neuronal potassium channel activity triggers initiation of mRNA translation through binding of translation regulators.Science advances · 2025Article
- Genomic Exploration of Essential Hypertension in African-Brazilian Quilombo Populations: A Comprehensive Approach With Pedigree Analysis and Family-Based Association Studies.Journal of the American Heart Association · 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
- KCNT1 Channel Blockers: A Medicinal Chemistry Perspective.Molecules (Basel, Switzerland) · 2024Review
- Article
- Structure-Activity Relationship Studies in a Series of Xanthine Inhibitors of SLACK Potassium Channels.Molecules (Basel, Switzerland) · 2024Article
- Interaction Between HCN and Slack Channels Regulates mPFC Pyramidal Cell Excitability in Working Memory Circuits.Molecular neurobiology · 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
- Increased Expression of KNeurochemical research · 2024Article
- Pathogenic genes implicated in sleep-related hypermotor epilepsy: a research progress update.Frontiers in neurology · 2024Review
- 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
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Disease-causing mutations in ion channels generally alter intrinsic gating properties such as activation, inactivation, and voltage dependence. We examined nine different mutations of the KCNT1 (Slack) Na(+)-activated K(+) channel that give rise to three distinct forms of epilepsy. All produced many-fold increases in current amplitude compared to the wild-type channel. This could not be accounted for by increases in the intrinsic open probability of individual channels. Rather, greatly increased opening was a consequence of cooperative interactions between multiple channels in a patch. The degree of cooperative gating was much greater for all of the mutant channels than for the wild-type channel, and could explain increases in current even in a mutant with reduced unitary conductance. We also found that the same mutation gave rise to different forms of epilepsy in different individuals. Our findings indicate that a major consequence of these mutations is to alter channel-channel interactions.
Indexed as
Identifiers
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.