SCN3A

Chr 2AD

sodium voltage-gated channel alpha subunit 3

Also known as: DEE62, EIEE62, FFEVF4, NAC3, Nav1.3

Encodes a voltage-gated sodium channel alpha subunit that generates and propagates action potentials in neurons. Mutations cause developmental and epileptic encephalopathy 62 and familial focal epilepsy with variable foci through an autosomal dominant inheritance pattern. The gene is highly intolerant to loss-of-function variants, and mutations can cause disease predominantly through gain-of-function effects.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
GOF/LOFmechanismADLOEUF 0.172 OMIM phenotypes
VCEP Guidelines: Epilepsy Sodium ChannelReleased
View SpecificationsClinGen Panel
Clinical SummarySCN3A
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Gene-Disease Validity (ClinGen)
developmental and epileptic encephalopathy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
3 unique Pathogenic / Likely Pathogenic· 58 VUS of 100 total submissions
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GeneReview available — SCN3A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.17LOEUF
pLI 1.000
Z-score 7.63
OE 0.10 (0.060.17)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
4.62Z-score
OE missense 0.60 (0.560.64)
629 obs / 1050.1 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.10 (0.060.17)
00.351.4
Missense OE0.60 (0.560.64)
00.61.4
Synonymous OE1.08
01.21.6
LoF obs/exp: 8 / 83.1Missense obs/exp: 629 / 1050.1Syn Z: -1.24
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongSCN3A-related focal epilepsyOTHERAD
Mechanism Note (variant-dependent)
GOFLOF— mechanism depends on specific variant

Nav1.3 sodium channel. GOF variants with increased persistent current cause DEE. LOF variants associated with milder epilepsy phenotypes. Mechanism is variant-specific.

References:PMID:32989326
DN
0.5672th %ile
GOF
0.74top 25%
LOF
0.52top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF1 literature citation · LOEUF 0.17
GOFprediction above median · 1 literature citation

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

GOFIn conclusion, we report a cohort of four patients with infantile onset epileptic encephalopathy due to de novo heterozygous gain-of-function missense mutations in the gene SCN3A encoding the type 3 voltage gated sodium channel Nav1.3.PMID:29466837
LOFWe discuss the effects of haploinsufficiency of SCN2A and SCN3A on the genetic basis of neurodevelopmental and neurobehavioral disorders and we propose that this haploinsufficiency may be associated not only with epilepsy, but also with autistic features.PMID:24080482

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

100 submitted variants in ClinVar

Classification Summary

Pathogenic1
Likely Pathogenic2
VUS58
Likely Benign38
Benign1
1
Pathogenic
2
Likely Pathogenic
58
VUS
38
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
0
0
1
Likely Pathogenic
1
1
0
0
2
VUS
6
51
0
1
58
Likely Benign
0
1
15
22
38
Benign
0
0
1
0
1
Total8531623100

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

SCN3A · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →