ArticleG3 (Bethesda, Md.)2013
Drosophila as a model for intractable epilepsy: gilgamesh suppresses seizures in para(bss1) heterozygote flies.
Article in G3 (Bethesda, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- The First Report of a Bang-Sensitive Strain inInternational journal of molecular sciences · 2026Article
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- Investigating rare and ultrarare epilepsy syndromes withFaculty reviews · 2021Review
- Humanization ofBiomedicines · 2020Article
- Investigating Developmental and Epileptic Encephalopathy UsingInternational journal of molecular sciences · 2020Review
- Reduced Function of the Glutathione S-Transferase S1 Suppresses Behavioral Hyperexcitability inG3 (Bethesda, Md.) · 2020Article
- Vgsc-interacting proteins are genetically associated with pyrethroid resistance in Aedes aegypti.PloS one · 2019Article
- Recent Developments in UsingInternational journal of molecular sciences · 2018Review
- A Systematic Review on Non-mammalian Models in Epilepsy Research.Frontiers in pharmacology · 2018Article
- Identification of a novel synaptic protein, TMTC3, involved in periventricular nodular heterotopia with intellectual disability and epilepsy.Human molecular genetics · 2017Article
- Mutation of orthologous prickle genes causes a similar epilepsy syndrome in flies and humans.Annals of clinical and translational neurology · 2016Article
- Mutations of the Calcium Channel Gene cacophony Suppress Seizures in Drosophila.PLoS genetics · 2016Article
- Drosophila sodium channel mutations: Contributions to seizure-susceptibility.Experimental neurology · 2015Review
- Seizure suppression through manipulating splicing of a voltage-gated sodium channel.Brain : a journal of neurology · 2015Article
- Pathway-driven discovery of epilepsy genes.Nature neuroscience · 2015Review
- Clinical whole-genome sequencing in severe early-onset epilepsy reveals new genes and improves molecular diagnosis.Human molecular genetics · 2014Article
- The ATP-sensitive K channel is seizure protective and required for effective dietary therapy in a model of mitochondrial encephalomyopathy.Journal of neurogeneticsArticle
- Attenuation of Seizures, Cognitive Deficits, and Brain Histopathology by Phytochemicals ofJournal of evidence-based integrative medicineArticle
- Seizure-suppressor genes: can they help spearhead the discovery of novel therapeutic targets for epilepsy?Expert opinion on therapeutic targetsReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Intractable epilepsies, that is, seizure disorders that do not respond to currently available therapies, are difficult, often tragic, neurological disorders. Na(+) channelopathies have been implicated in some intractable epilepsies, including Dravet syndrome (Dravet 1978), but little progress has been forthcoming in therapeutics. Here we examine a Drosophila model for intractable epilepsy, the Na(+) channel gain-of-function mutant para(bss1) that resembles Dravet syndrome in some aspects (parker et al. 2011a). In particular, we identify second-site mutations that interact with para(bss1), seizure enhancers, and seizure suppressors. We describe one seizure-enhancer mutation named charlatan (chn). The chn gene normally encodes an Neuron-Restrictive Silencer Factor/RE1-Silencing Transcription factor transcriptional repressor of neuronal-specific genes. We identify a second-site seizure-suppressor mutation, gilgamesh (gish), that reduces the severity of several seizure-like phenotypes of para(bss1)/+ heterozygotes. The gish gene normally encodes the Drosophila ortholog of casein kinase CK1g3, a member of the CK1 family of serine-threonine kinases. We suggest that CK1g3 is an unexpected but promising new target for seizure therapeutics.
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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.