SCN11A

Chr 3AD

sodium voltage-gated channel alpha subunit 11

Also known as: FEPS3, HSAN7, NAV1.9, NaN, PN5, SCN12A, SNS-2

The protein forms voltage-gated sodium channels that mediate sodium ion permeability in excitable membranes and is highly expressed in nociceptive neurons where it transmits pain signals from the periphery to the central nervous system. Mutations cause familial episodic pain syndrome-3 and hereditary sensory and autonomic neuropathy type VII with autosomal dominant inheritance. The gene shows minimal constraint against loss-of-function variants (very low pLI score), suggesting the associated phenotypes may involve other mutational mechanisms.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismADLOEUF 0.832 OMIM phenotypes
Clinical SummarySCN11A
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Gene-Disease Validity (ClinGen)
obsolete autosomal dominant hereditary sensory and autonomic neuropathy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
4 unique Pathogenic / Likely Pathogenic· 330 VUS of 500 total submissions
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GeneReview available — SCN11A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.83LOEUF
pLI 0.000
Z-score 2.84
OE 0.66 (0.530.83)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.96Z-score
OE missense 0.91 (0.860.96)
881 obs / 965.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.66 (0.530.83)
00.351.4
Missense OE0.91 (0.860.96)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 53 / 80.5Missense obs/exp: 881 / 965.3Syn Z: -0.25
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveSCN11A-related episodic pain syndrome, familialGOFAD
definitiveSCN11A-related congenital inability to experience painGOFAD
DN
0.83top 10%
GOF
0.79top 25%
LOF
0.1796th %ile

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

GOFprediction above median · 1 literature citation
DNprediction above median

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 2013, discovery of a heterozygous gain-of-function mutation in SCN11A encoding voltage-gated sodium channel 1.9 (Nav1.9) established a distinctive CIP in three unrelated patients who suffered multiple painless fractures, self-inflicted mutilation, chronic diarrhea, and hyperhidrosis.PMID:26746779

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic3
Likely Pathogenic1
VUS330
Likely Benign144
Benign4
Conflicting12
3
Pathogenic
1
Likely Pathogenic
330
VUS
144
Likely Benign
4
Benign
12
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
3
0
3
Likely Pathogenic
0
1
0
0
1
VUS
34
271
17
8
330
Likely Benign
1
18
45
80
144
Benign
0
0
3
1
4
Conflicting
12
Total352906889494

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

View in ClinVar →

Protein Context — Lollipop Plot

SCN11A · 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 →
Key Publications
Landmark & review papers · by relevance
PubMed
The Evolving Landscape of Small Fiber Neuropathy.
Devigili G et al.·Semin Neurol
2025Review
Erythromelalgia.
Klein-Weigel PF et al.·Vasa
2018Review
Small fibre neuropathy.
Cazzato D et al.·Curr Opin Neurol
2017Review
Top 5 results · since 2015Search PubMed ↗