ArticleMolecular neurobiology2014
Transcription of the human sodium channel SCN1A gene is repressed by a scaffolding protein RACK1.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Exploratory analysis of a Novel RACK1 mutation and its potential role in epileptic seizures via Microglia activation.Journal of neuroinflammation · 2025Article
- Preferential expression of SCN1A in GABAergic neurons improves survival and epileptic phenotype in a mouse model of Dravet syndrome.Journal of molecular medicine (Berlin, Germany) · 2023Article
- SCN1A: bioinformatically informed revised boundaries for promoter and enhancer regions.Human molecular genetics · 2023Article
- Whole-genome sequencing combined RNA-sequencing analysis of patients with mutations in SET binding protein 1.Frontiers in neuroscience · 2022Article
- Review
- Neddylation stabilizes Nav1.1 to maintain interneuron excitability and prevent seizures in murine epilepsy models.The Journal of clinical investigation · 2021Article
- Review
- Laser microdissection-based microproteomics of the hippocampus of a rat epilepsy model reveals regional differences in protein abundances.Scientific reports · 2020Article
- Influence of common SCN1A promoter variants on the severity of SCN1A-related phenotypes.Molecular genetics & genomic medicine · 2019Article
- FTO is a transcriptional repressor to auto-regulate its own gene and potentially associated with homeostasis of body weight.Journal of molecular cell biology · 2019Article
- Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies.Frontiers in cellular neuroscience · 2019Review
- Neogenin in Amygdala for Neuronal Activity and Information Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- The genetic variants in 3' untranslated region of voltage-gated sodium channel alpha 1 subunit gene affect the mRNA-microRNA interactions and associate with epilepsy.BMC genetics · 2016Article
- An update on transcriptional and post-translational regulation of brain voltage-gated sodium channels.Amino acids · 2016Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated sodium channel α subunit type I (Nav1.1, encoded by SCN1A gene) plays a critical role in the initiation of action potential in the central nervous system. Downregulated expression of SCN1A is believed to be associated with epilepsy. Here, we found that the SCN1A promoter (P1c), located at the 5' untranslated exon 1c, drove the reporter gene expression in human NT2 cells, and a region between nt +53 and +62 downstream of the P1c promoter repressed the promoter activity. Further analyses showed that a scaffolding protein RACK1 (receptor for activated C kinase 1) was involved in binding to this silencer. Knockdown of RACK1 expression in NT2 cells deprived the repressive role of the silencer on the P1c promoter and increased SCN1A transcription, suggesting the potential involvement of RACK1 in negatively regulating SCN1A transcription via interaction with the silencer. Furthermore, we demonstrated that the binding of the protein complex including RACK1 to the SCN1A promoter motif was decreased in neuron-like differentiation of the NT2 cells induced by retinoic acid and resulted in the upregulation of SCN1A transcription. Taken together, this study reports a novel role of RACK1 in regulating SCN1A expression that participates in retinoic acid-induced neuronal differentiation of NT2 cells.
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