ArticleThe Journal of biological chemistry2004
Novel isoforms of the sodium channels Nav1.8 and Nav1.5 are produced by a conserved mechanism in mouse and rat.
Article in The Journal of biological chemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Contribution of tetrodotoxin-resistant persistent NaThe journal of headache and pain · 2022Article
- Exome Sequencing Implicates Impaired GABA Signaling and Neuronal Ion Transport in Trigeminal Neuralgia.iScience · 2020Article
- Molecular expression of multiple Nav1.5 splice variants in the frontal lobe of the human brain.International journal of molecular medicine · 2018Article
- Multiple Nav1.5 isoforms are functionally expressed in the brain and present distinct expression patterns compared with cardiac Nav1.5.Molecular medicine reports · 2017Article
- Association of SCN10A Polymorphisms with the Recurrence of Atrial Fibrillation after Catheter Ablation in a Chinese Han Population.Scientific reports · 2017Article
- Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain.Molecular and cellular neurosciences · 2017Article
- Alternative RNA splicing: contribution to pain and potential therapeutic strategy.Drug discovery today · 2016Review
- The generation of knock-in mice expressing fluorescently tagged galanin receptors 1 and 2.Molecular and cellular neurosciences · 2015Article
- Specialized functions of Nav1.5 and Nav1.9 channels in electrogenesis of myenteric neurons in intact mouse ganglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Exon 11 skipping of SCN10A coding for voltage-gated sodium channels in dorsal root ganglia.Channels (Austin, Tex.) · 2014Article
- Early development of electrical excitability in the mouse enteric nervous system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Cloning and expression of the two new variants of Nav1.5/SCN5A in rat brain.Molecular and cellular biochemistry · 2012Article
- Recent developments regarding voltage-gated sodium channel blockers for the treatment of inherited and acquired neuropathic pain syndromes.Frontiers in pharmacology · 2011Article
- Characterisation of the nociceptive phenotype of suppressible galanin overexpressing transgenic mice.Molecular pain · 2010Article
- The expression of ELK transcription factors in adult DRG: Novel isoforms, antisense transcripts and upregulation by nerve damage.Molecular and cellular neurosciences · 2010Article
- A subtle alternative splicing event of the Na(V)1.8 voltage-gated sodium channel is conserved in human, rat, and mouse.Journal of molecular neuroscience : MN · 2010Article
- Genetic variation in SCN10A influences cardiac conduction.Nature genetics · 2010Article
- Pyramidal cells of rodent presubiculum express a tetrodotoxin-insensitive Na+ current.The Journal of physiology · 2009Article
- A novel Na+ channel splice form contributes to the regulation of an androgen-dependent social signal.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- 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
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3 authors.
Funding
Abstract
The voltage-gated sodium channel Na(v)1.8 is only expressed in subsets of neurons in dorsal root ganglia (DRG) and trigeminal and nodose ganglia. We have isolated mouse partial length Na(v)1.8 cDNA clones spanning the exon 17 sequence, which have 17 nucleotide substitutions and 12 predicted amino acid differences from the published sequence. The absence of a mutually exclusive alternative exon 17 was confirmed by sequencing 4.1 kilobases of genomic DNA spanning exons 16-18 of Scn10a. A novel cDNA isoform was identified, designated Na(v)1.8c, which results from alternative 3'-splice site selection at a CAG/CAG motif to exclude the codon for glutamine 1031 within the interdomain cytoplasmic loop IDII/III. The ratio of Na(v)1.8c (CAG-skipped) to Na(v)1.8 (CAG-inclusive) mRNA in mouse is approximately 2:1 in adult DRG, trigeminal ganglion, and neonatal DRG. A Na(v)1.8c isoform also occurs in rat DRG, but is less common. Of the two other tetrodotoxin-resistant channels, no analogous alternative splicing of mouse Na(v)1.9 was detected, whereas rare alternative splicing of Na(v)1.5 at a CAG/CAG motif resulted in the introduction of a CAG trinucleotide. This isoform, designated Na(v)1.5c, is conserved in rat and encodes an additional glutamine residue that disrupts a putative CK2 phosphorylation site. In summary, novel isoforms of Na(v)1.8 and Na(v)1.5 are each generated by alternative splicing at CAG/CAG motifs, which result in the absence or presence of predicted glutamine residues within the interdomain cytoplasmic loop IDII/III. Mutations of sodium channels within this cytoplasmic loop have previously been demonstrated to alter electrophysiological properties and cause cardiac arrhythmias and epilepsy.
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