ArticleGenomics2007
Characterization of 5' untranslated regions of the voltage-gated sodium channels SCN1A, SCN2A, and SCN3A and identification of cis-conserved noncoding sequences.
Article in Genomics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Epilepsy, hippocampal sclerosis and febrile seizures linked by common genetic variation around SCN1A.Brain : a journal of neurology · 2013Pooled it
- Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.Neural regeneration research · 2026Article
- Gene therapy as an emerging treatment forFundamental research · 2024Review
- SCN1A: bioinformatically informed revised boundaries for promoter and enhancer regions.Human molecular genetics · 2023Article
- Non-coding regulatory elements: Potential roles in disease and the case of epilepsy.Neuropathology and applied neurobiology · 2022Review
- mTORC1 induces plasma membrane depolarization and promotes preosteoblast senescence by regulating the sodium channel Scn1a.Bone research · 2022Article
- Deletion of a non-canonical regulatory sequence causes loss of Scn1a expression and epileptic phenotypes in mice.Genome medicine · 2021Article
- Influence of common SCN1A promoter variants on the severity of SCN1A-related phenotypes.Molecular genetics & genomic medicine · 2019Article
- Aberrant Inclusion of a Poison Exon Causes Dravet Syndrome and Related SCN1A-Associated Genetic Epilepsies.American journal of human genetics · 2018Article
- A Point Mutation in SCN1A 5' Genomic Region Decreases the Promoter Activity and Is Associated with Mild Epilepsy and Seizure Aggravation Induced by Antiepileptic Drug.Molecular neurobiology · 2017Article
- An update on transcriptional and post-translational regulation of brain voltage-gated sodium channels.Amino acids · 2016Review
- Transcription of the human sodium channel SCN1A gene is repressed by a scaffolding protein RACK1.Molecular neurobiology · 2014Article
- A human Dravet syndrome model from patient induced pluripotent stem cells.Molecular brain · 2013Article
- Promoter analysis of mouse Scn3a gene and regulation of the promoter activity by GC box and CpG methylation.Journal of molecular neuroscience : MN · 2011Article
- A role of SCN9A in human epilepsies, as a cause of febrile seizures and as a potential modifier of Dravet syndrome.PLoS genetics · 2009Article
- A BAC transgenic mouse model reveals neuron subtype-specific effects of a Generalized Epilepsy with Febrile Seizures Plus (GEFS+) mutation.Neurobiology of disease · 2009Article
- Novel mRNA isoforms of the sodium channels Na(v)1.2, Na(v)1.3 and Na(v)1.7 encode predicted two-domain, truncated proteins.Neuroscience · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human voltage-gated sodium channel gene cluster on chromosome 2q24 contains three paralogs, SCN1A, SCN2A, and SCN3A, which are expressed in the central nervous system. Mutations in SCN1A and SCN2A cause several subtypes of idiopathic epilepsy. Furthermore, many SCN1A mutations are predicted to reduce protein levels, emphasizing the importance of precise sodium channel gene regulation. To investigate the genetic factors that regulate the expression of SCN1A, SCN2A, and SCN3A, we characterized the 5' untranslated region of each gene. We identified multiple noncoding exons and observed brain region differences in the expression levels of noncoding exons. Comparative sequence analysis revealed 33 conserved noncoding sequences (CNSs) between the orthologous mammalian genes and 6 CNSs between the three human paralogs. Seven CNSs corresponded to noncoding exons. Twelve CNSs were evaluated for their ability to alter the transcription of a luciferase reporter gene, and 3 resulted in a modest, but statistically significant change.
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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.