ArticleGenes, brain, and behavior2011
Etiology of a genetically complex seizure disorder in Celf4 mutant mice.
Article in Genes, brain, and behavior, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Pathological disruption of CELF2 shuttling causes neuronal hyperactivity, learning deficits, and seizures.The Journal of clinical investigation · 2026Article
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- Celf4 Regulates Excitability of Bushy Cells in the Cochlear Nucleus of the Mouse Brainstem.Cellular and molecular neurobiology · 2026Article
- The RNA-binding protein CELF4: from molecular regulatory networks to clinical translation in cross-system diseases.Frontiers in molecular biosciences · 2026Review
- Heterozygous CELF4 variants in the N-term region crucial for the RNA-binding activity lead to neurodevelopmental disorder and obesity.European journal of human genetics : EJHG · 2025Article
- Neonatal Encephalopathy: Novel Phenotypes and Genotypes Identified by Genome Sequencing.Neurology. Genetics · 2025Article
- Members of the CUGBP Elav-like family of RNA-binding proteins are expressed in distinct populations of primary sensory neurons.The Journal of comparative neurology · 2023Article
- Celf4 controls mRNA translation underlying synaptic development in the prenatal mammalian neocortex.Nature communications · 2023Article
- Clocking Epilepsies: A Chronomodulated Strategy-Based Therapy for Rhythmic Seizures.International journal of molecular sciences · 2023Review
- Initiation of migraine-related cortical spreading depolarization by hyperactivity of GABAergic neurons and NaV1.1 channels.The Journal of clinical investigation · 2021Article
- Absence of RNA-binding protein FXR2P prevents prolonged phase of kainate-induced seizures.EMBO reports · 2021Article
- Modelling and treating GRIN2A developmental and epileptic encephalopathy in mice.Brain : a journal of neurology · 2020Article
- Comprehensive transcriptome analysis of cochlear spiral ganglion neurons at multiple ages.eLife · 2020Article
- Haploinsufficiency of ARHGAP42 is associated with hypertension.European journal of human genetics : EJHG · 2019Article
- PRAS: Predicting functional targets of RNA binding proteins based on CLIP-seq peaks.PLoS computational biology · 2019Article
- Sequential Regulation of Maternal mRNAs through a Conserved cis-Acting Element in Their 3' UTRs.Cell reports · 2018Article
- meaRtools: An R package for the analysis of neuronal networks recorded on microelectrode arrays.PLoS computational biology · 2018Article
- Control of CNS functions by RNA-binding proteins in neurological diseases.Current pharmacology reports · 2018Article
- RNA-binding proteins, neural development and the addictions.Genes, brain, and behavior · 2016Review
- Regulation of membrane excitability: a convergence on voltage-gated sodium conductance.Molecular neurobiology · 2015Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mice deficient for the gene encoding the RNA-binding protein CELF4 (CUGBP, ELAV-like family member 4) have a complex seizure phenotype that includes both convulsive and non-convulsive seizures, depending upon gene dosage and strain background, modeling genetically complex epilepsy. Invertebrate CELF is associated with translational control in fruit fly ovary epithelium and with neurogenesis and neuronal function in the nematode. Mammalian CELF4 is expressed widely during early development, but is restricted to the central nervous system in adults. To better understand the etiology of the seizure disorder of Celf4 deficient mice, we studied seizure incidence with spatial and temporal conditional knockout Celf4 alleles. For convulsive seizure phenotypes, it is sufficient to delete Celf4 in adulthood at the age of 7 weeks. This timing is in contrast to absence-like non-convulsive seizures, which require deletion before the end of the first postnatal week. Interestingly, selective deletion of Celf4 from cerebral cortex and hippocampus excitatory neurons, but not from inhibitory neurons, is sufficient to lower seizure threshold and to promote spontaneous convulsions. Correspondingly, Celf4 deficient mice have altered excitatory, but not inhibitory, neurotransmission as measured by patch-clamp recordings of cortical layer V pyramidal neurons. Finally, immunostaining in conjunction with an inhibitory neuron-specific reporter shows that CELF4 is expressed predominantly in excitatory neurons. Our results suggest that CELF4 plays a specific role in regulating excitatory neurotransmission. We posit that altered excitatory neurotransmission resulting from Celf4 deficiency underlies the complex seizure disorder in Celf4 mutant mice.
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