ArticleHuman molecular genetics2010
Lgi1 null mutant mice exhibit myoclonic seizures and CA1 neuronal hyperexcitability.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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.
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Who cites it
56 citing papers in PubMed, 135 citations in OpenAlex.
- Patient-derived monoclonal LGI1 autoantibodies elicit seizures, behavioral changes and brain MRI abnormalities in rodent models.Brain, behavior, and immunity · 2025Article
- LGI1 Autoantibodies Enhance Synaptic Transmission by Presynaptic KNeurology(R) neuroimmunology & neuroinflammation · 2024Article
- Oligodendrocyte-derived LGI3 and its receptor ADAM23 organize juxtaparanodal Kv1 channel clustering for short-term synaptic plasticity.Cell reports · 2024Article
- A patient-derived mutation of epilepsy-linked LGI1 increases seizure susceptibility through regulating KCell & bioscience · 2023Article
- Altered Extracellular Matrix as an Alternative Risk Factor for Epileptogenicity in Brain Tumors.Biomedicines · 2022Review
- Biallelic ADAM22 pathogenic variants cause progressive encephalopathy and infantile-onset refractory epilepsy.Brain : a journal of neurology · 2022Article
- The LGI1 protein: molecular structure, physiological functions and disruption-related seizures.Cellular and molecular life sciences : CMLS · 2021Review
- First Report of a de novo 10q23.31q23.33 Microdeletion: Obesity, Intellectual Disability and Microcephaly.Molecular syndromology · 2021Article
- LGI1-ADAM22-MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Personalized Medicine Using Cutting Edge Technologies for Genetic Epilepsies.Current neuropharmacology · 2021Review
- Insights into the mechanisms of epilepsy from structural biology of LGI1-ADAM22.Cellular and molecular life sciences : CMLS · 2020Review
- Down-Regulation of Astrocytic Kir4.1 Channels during the Audiogenic Epileptogenesis inInternational journal of molecular sciences · 2019Article
- Review
- LGI1 antibodies alter Kv1.1 and AMPA receptors changing synaptic excitability, plasticity and memory.Brain : a journal of neurology · 2018Article
- Structural basis of epilepsy-related ligand-receptor complex LGI1-ADAM22.Nature communications · 2018Article
- Celecoxib Ameliorates Seizure Susceptibility in Autosomal Dominant Lateral Temporal Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling.Frontiers in molecular neuroscience · 2018Article
- LGI1 tunes intrinsic excitability by regulating the density of axonal Kv1 channels.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Autoantibodies to Synaptic Receptors and Neuronal Cell Surface Proteins in Autoimmune Diseases of the Central Nervous System.Physiological reviews · 2017Review
- mTORC1 Is a Local, Postsynaptic Voltage Sensor Regulated by Positive and Negative Feedback Pathways.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
LGI1 in humans is responsible for a predisposition to autosomal dominant partial epilepsy with auditory features (ADPEAF). However, mechanisms of how LGI1 mutations cause epilepsy remain unclear. We have used a mouse chromosome engineering strategy to create a null mutation for the gene ortholog encoding LGI1. The Lgi1 null mutant mice show no gross overall developmental abnormalities from routine histopathological analysis. After 12-18 days of age, the homozygous mutant mice all exhibit myoclonic seizures accompanied by rapid jumping and running and die shortly thereafter. The heterozygous mutant mice do not develop seizures. Electrophysiological analysis demonstrates an enhanced excitatory synaptic transmission by increasing the release of the excitatory neurotransmitter glutamate, suggesting a basis for the seizure phenotype. This mouse model, therefore, provides novel insights into the mechanism behind ADPEAF and offers a new opportunity to study the mechanism behind the role of LGI1 in susceptibility to myoclonic seizures.
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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.