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Times Cited
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De novo mutations revealed by whole-exome sequencing are strongly associated with autism.
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Molecular correlates of age-dependent seizures in an inherited neonatal-infantile epilepsy.
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SCN2A encephalopathy: A major cause of epilepsy of infancy with migrating focal seizures.
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Nav1.2 haplodeficiency in excitatory neurons causes absence-like seizures in mice.
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De novo mutations in schizophrenia implicate synaptic networks.
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Further corroboration of distinct functional features in SCN2A variants causing intellectual disability or epileptic phenotypes.
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Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations.
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Most genetic risk for autism resides with common variation.
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Sodium channels SCN1A, SCN2A and SCN3A in familial autism.
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De novo genic mutations among a Chinese autism spectrum disorder cohort.
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Disruptive CHD8 mutations define a subtype of autism early in development.
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Benign familial neonatal-infantile seizures: characterization of a new sodium channelopathy.
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De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP.
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Strong association of de novo copy number mutations with autism.
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Effects in neocortical neurons of mutations of the Na(v)1.2 Na+ channel causing benign familial neonatal-infantile seizures.
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Relationship of electrophysiological dysfunction and clinical severity in SCN2A-related epilepsies.
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Nav1.2 is expressed in caudal ganglionic eminence-derived disinhibitory interneurons: Mutually exclusive distributions of Nav1.1 and Nav1.2.
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Molecular identity of axonal sodium channels in human cortical pyramidal cells.
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Multiple recurrent de novo CNVs, including duplications of the 7q11.23 Williams syndrome region, are strongly associated with autism.
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Impaired NaV1.2 function and reduced cell surface expression in benign familial neonatal-infantile seizures.
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Whole genome sequencing resource identifies 18 new candidate genes for autism spectrum disorder.
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Targeted sequencing identifies 91 neurodevelopmental-disorder risk genes with autism and developmental-disability biases.
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Integrative functional genomic analyses implicate specific molecular pathways and circuits in autism.
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Clinical and genetic spectrum of SCN2A-associated episodic ataxia.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.