ReviewMolecular neurobiology
Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolution.
Review in Molecular neurobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Alternative splicing in voltage-gated sodium channels: mechanisms, regulatory networks and therapeutic implications.Annals of medicine · 2026Review
- Article
- SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves.BMC neuroscience · 2021Article
- Article
- Gain-of-function mutations in SCN11A cause familial episodic pain.American journal of human genetics · 2013Article
- Cloning and expression of the two new variants of Nav1.5/SCN5A in rat brain.Molecular and cellular biochemistry · 2012Article
- Identification of the sensory neuron specific regulatory region for the mouse gene encoding the voltage-gated sodium channel NaV1.8.Journal of neurochemistry · 2008Article
- Interconversion of germline-limited and somatic DNA in a scrambled gene.Journal of molecular evolution · 2006Article
- Voltage-gated Na+ channels: multiplicity of expression, plasticity, functional implications and pathophysiological aspects.European biophysics journal : EBJ · 2004Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exon/intron boundaries in the regions encoding the trans-membrane segments of voltage-gated Na channel genes are conserved, supporting their proposed evolution from a single domain channel, while the exons encoding the cytoplasmic loops are less conserved with their evolutionary heritage being less defined. SCN11A encodes the tetrodotoxin-resistant (TTX-R) sodium channel Nav1.9a/NaN, which is preferentially expressed in nociceptive primary sensory neurons of dorsal root ganglia (DRG) and trigeminal ganglia. SCN11A is localized to human chromosome 3 (3p21-24) close to the other TTX-R sodium channel genes SCN5A and SCN10A. An alternative transcript, Nav1.9b, has been detected in rat DRG and trigeminal ganglion. Nav1.9b is predicted to produce a truncated protein due to a frame-shift, which is introduced by the new sequence of exon 23c (E23c). In human and mouse SCN11A, divergent splicing signals prevent utilization of E23c. Unlike exons 5A/N in genes encoding TTX-sensitive sodium channels, which appear to have resulted from exon duplication, E23c might have evolved from the conversion of an intronic sequence. Although a functional role for Nav1.9b has yet to be established, intron-to-exon conversion may represent a mechanism for ion channels to acquire novel features.
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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.