On the public citation graph
A novel KCNC1 gain‐of‐function variant causing developmental and epileptic encephalopathy: “Precision medicine” approach with fluoxetine
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
inferredcites →https://doi.org/10.1002/acn3.50799openalex-snapshot
KCNC1‐related disorders: new de novo variants expand the phenotypic spectrum
inferredcites →https://doi.org/10.1002/acn3.50822openalex-snapshot
Encephalopathies with KCNC1 variants: genotype‐phenotype‐functional correlations
inferredcites →https://doi.org/10.1002/acn3.51707openalex-snapshot
A KCNC1‐related neurological disorder due to gain of Kv3.1 function
inferredcites →https://doi.org/10.1002/ana.24929openalex-snapshot
Myoclonus epilepsy and ataxia due to KCNC 1 mutation: Analysis of 20 cases and K + channel properties
inferredcites →https://doi.org/10.1007/164_2021_502openalex-snapshot
Pharmacological Approaches to Studying Potassium Channels
inferredcites →https://doi.org/10.1016/s0028-3908(01)00088-0openalex-snapshot
Effects of norfluoxetine, the major metabolite of fluoxetine, on the cloned neuronal potassium channel Kv3.1
inferredcites →https://doi.org/10.1016/s0893-133x(00)00116-0openalex-snapshot
Brain Pharmacokinetics and Tissue Distribution In Vivo of Fluvoxamine and Fluoxetine by Fluorine Magnetic Resonance Spectroscopy
inferredcites →https://doi.org/10.1038/ejhg.2017.3openalex-snapshot
Loss of Function of KCNC1 is associated with intellectual disability without seizures
inferredcites →https://doi.org/10.1038/ng.3144openalex-snapshot
A recurrent de novo mutation in KCNC1 causes progressive myoclonus epilepsy
inferredcites →https://doi.org/10.1038/s41467-022-29594-wopenalex-snapshot
Cryo-EM structure of the human Kv3.1 channel reveals gating control by the cytoplasmic T1 domain
inferredcites →https://doi.org/10.1074/jbc.m310501200openalex-snapshot
MinK, MiRP1, and MiRP2 Diversify Kv3.1 and Kv3.2 Potassium Channel Gating
inferredcites →https://doi.org/10.1111/j.1749-6632.1999.tb11295.xopenalex-snapshot
Contributions of Kv3 Channels to Neuronal Excitability
inferredcites →https://doi.org/10.1152/jn.00257.2021openalex-snapshot
A KCNC1 mutation in epilepsy of infancy with focal migrating seizures produces functional channels that fail to be regulated by PKC phosphorylation
inferredcites →https://doi.org/10.1152/physrev.00002.2017openalex-snapshot
Kv3 Channels: Enablers of Rapid Firing, Neurotransmitter Release, and Neuronal Endurance
inferredcites →https://doi.org/10.1177/1073858418763752openalex-snapshot
Potassium Channel Gain of Function in Epilepsy: An Unresolved Paradox
inferredcites →https://doi.org/10.1254/jphs.fp0070759openalex-snapshot
Open Channel Block of Kv3.1 Currents by Fluoxetine
inferredcites →https://doi.org/10.1684/epd.2016.0859openalex-snapshot
Myoclonus epilepsy and ataxia due to potassium channel mutation (MEAK) is caused by heterozygous KCNC1 mutations
inferredcites →https://doi.org/10.21037/atm-21-1885openalex-snapshot
Kv3.1 channelopathy: a novel loss-of-function variant and the mechanistic basis of its clinical phenotypes
inferredcites →https://doi.org/10.7554/elife.01289openalex-snapshot
Hydrogen bonds as molecular timers for slow inactivation in voltage-gated potassium channels
What points at this work
Incoming claims: where this work appears in other papers’ reference lists and arguments.
inferred← citeshttps://doi.org/10.1002/ana.26826openalex-snapshot
De novo variants in KCNA3 cause developmental and epileptic encephalopathy
inferred← citeshttps://doi.org/10.1002/ana.27213openalex-snapshot
Fluoxetine Treatment in Epilepsy of Infancy with Migrating Focal Seizures Due to KCNT1 Variants: An Open Label Study
inferred← citeshttps://doi.org/10.1002/epi.70253openalex-snapshot
An n ‐of‐1 gene‐directed drug repurposing trial for an ultrarare genetic condition
inferred← citeshttps://doi.org/10.1002/epi4.13039openalex-snapshot
Next‐generation sequencing in pediatric‐onset epilepsies: Analysis with target panels and personalized therapeutic approach
inferred← citeshttps://doi.org/10.1002/epi4.70065openalex-snapshot
Precision therapies for genetic epilepsies in 2025: Promises and pitfalls
inferred← citeshttps://doi.org/10.1007/s40291-023-00676-9openalex-snapshot
Steps to Improve Precision Medicine in Epilepsy
inferred← citeshttps://doi.org/10.1016/s2352-4642(24)00196-2openalex-snapshot
The expanding field of genetic developmental and epileptic encephalopathies: current understanding and future perspectives
inferred← citeshttps://doi.org/10.1073/pnas.2424514123openalex-snapshot
A KCNC1 variant linked to Rett syndrome disrupts ER to Golgi trafficking of Kv3.1 channel
inferred← citeshttps://doi.org/10.1085/jgp.202513962openalex-snapshot
An epilepsy-associated KV3.1 potassium channel variant acts via dominant-positive effect
inferred← citeshttps://doi.org/10.1101/2024.05.16.594495openalex-snapshot
Neuronal phenotype defined by transcriptome-wide bursting kinetics in pyramidal and fast-spiking cells
inferred← citeshttps://doi.org/10.1152/ajpcell.00239.2026openalex-snapshot
Discovery of Kv3.1 channel inhibitors reveals VU0521426 as a state-dependent inactivator preferentially active against pathogenic gain-of-function mutants
inferred← citeshttps://doi.org/10.1186/s12883-026-04677-zopenalex-snapshot
A novel de Novo KCNC1 mutation (c.1147 C > T) presenting with epilepsy and ADHD: a case report and literature review
inferred← citeshttps://doi.org/10.18203/2349-3291.ijcp20263319openalex-snapshot
Pharmacogenetic based precision therapy in childhood epilepsy: a case series
inferred← citeshttps://doi.org/10.3389/fncel.2024.1367838openalex-snapshot
Case report: Marked electroclinical improvement by fluoxetine treatment in a patient with KCNT1-related drug-resistant focal epilepsy
inferred← citeshttps://doi.org/10.3389/fncel.2024.1449151openalex-snapshot
Voltage-gated potassium channels as a potential therapeutic target for the treatment of neurological and psychiatric disorders
inferred← citeshttps://doi.org/10.3389/fncel.2024.1512365openalex-snapshot
Pharmacological approaches in drug-resistant pediatric epilepsies caused by pathogenic variants in potassium channel genes
inferred← citeshttps://doi.org/10.3389/fncel.2025.1614320openalex-snapshot
Editorial: Pathogenic potassium channel variants in neurological disorders: from functional analysis to personalized pharmacological approaches
inferred← citeshttps://doi.org/10.3389/fphar.2024.1528541openalex-snapshot
Case Report: Targeted treatment by fluoxetine/norfluoxetine of a KCNC2 variant causing developmental and epileptic encephalopathy
inferred← citeshttps://doi.org/10.3389/fphar.2026.1821275openalex-snapshot
KV3.1 channel modulation: a systematic review of pharmacological intervention strategies
inferred← citeshttps://doi.org/10.3390/ijms26136069openalex-snapshot
Transcriptomic Profiling of Zebrafish Mutant for cdkl5 Reveals Dysregulated Gene Expression Associated with Neuronal, Muscle, Visual and Skeletal Development
inferred← citeshttps://doi.org/10.3988/jcn.2023.0435openalex-snapshot
Unusual Voltage-Gated Sodium and Potassium Channelopathies Related to Epilepsy
inferred← citeshttps://doi.org/10.4103/nrr.nrr-d-23-01766openalex-snapshot
Potassium and calcium channels in different nerve cells act as therapeutic targets in neurological disorders
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