SCN11A

Chr 3AD

sodium voltage-gated channel alpha subunit 11

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

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family, and is highly expressed in nociceptive neurons of dorsal root ganglia and trigeminal ganglia. It mediates brain-derived neurotrophic factor-evoked membrane depolarization and is a major effector of peripheral inflammatory pain hypersensitivity. Mutations in this gene have been associated with hereditary sensory and autonomic neuropathy type VII and familial episodic pain syndrome-3. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2017]

Primary Disease Associations & Inheritance

Episodic pain syndrome, familial, 3MIM #615552
AD
Neuropathy, hereditary sensory and autonomic, type VIIMIM #615548
AD
0
Active trials
9
Pubs (1 yr)
4
P/LP submissions
67%
P/LP missense
0.83
LOEUF
GOF*
Mechanism· G2P
Clinical SummarySCN11A
🧬
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.
📋
ClinVar Variants
3 unique Pathogenic / Likely Pathogenic· 417 VUS of 600 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

600 submitted variants in ClinVar

Classification Summary

Pathogenic1
Likely Pathogenic2
VUS417
Likely Benign165
Benign4
Conflicting5
1
Pathogenic
2
Likely Pathogenic
417
VUS
165
Likely Benign
4
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
1
0
1
Likely Pathogenic
0
2
0
0
2
VUS
27
338
43
9
417
Likely Benign
1
6
67
91
165
Benign
0
0
3
1
4
Conflicting
5
Total28346114101594

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.

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
Top 5 results · since 2015Search PubMed ↗