SCN3B

Chr 11AD

sodium voltage-gated channel beta subunit 3

Also known as: ATFB16, BRGDA7, HSA243396, SCNB3

The SCN3B gene encodes a beta subunit of voltage-gated sodium channels that regulates the inactivation kinetics of sodium channels responsible for action potential generation and propagation in neurons and muscle. Mutations cause autosomal dominant Brugada syndrome 7 and familial atrial fibrillation through a gain-of-function mechanism. The protein localizes to the cell membrane where it modulates sodium channel function.

Summary from RefSeq, OMIM, UniProt, Mechanism
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Primary Disease Associations & Inheritance

Atrial fibrillation, familial, 16MIM #613120
AD
Brugada syndrome 7MIM #613120
AD
0
Active trials
10
Pubs (1 yr)
54
P/LP submissions
4%
P/LP missense
0.80
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySCN3B
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Gene-Disease Validity (ClinGen)
Brugada syndrome · ADRefuted

Refuted — evidence has disproved this relationship

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.05) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
54 unique Pathogenic / Likely Pathogenic· 132 VUS of 327 total submissions
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GeneReview available — SCN3B
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
0.80LOEUF
pLI 0.051
Z-score 2.04
OE 0.35 (0.170.80)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.79Z-score
OE missense 0.80 (0.680.94)
100 obs / 125.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.35 (0.170.80)
00.351.4
Missense OE0.80 (0.680.94)
00.61.4
Synonymous OE0.99
01.21.6
LoF obs/exp: 4 / 11.4Missense obs/exp: 100 / 125.0Syn Z: 0.07
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedSCN3B-related Brugada syndromeOTHERAD
DN
0.7230th %ile
GOF
0.74top 25%
LOF
0.2484th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative 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 dominant-negative. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median · 1 literature citation
GOFprediction 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

DNFunctional dominant-negative mutation of sodium channel subunit gene SCN3B associated with atrial fibrillation in a Chinese GeneID population.PMID:20558140

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

ClinVar Variant Classifications

327 submitted variants in ClinVar

Classification Summary

Pathogenic52
Likely Pathogenic2
VUS132
Likely Benign94
Benign28
Conflicting12
52
Pathogenic
2
Likely Pathogenic
132
VUS
94
Likely Benign
28
Benign
12
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
2
50
0
52
Likely Pathogenic
0
0
2
0
2
VUS
10
101
20
1
132
Likely Benign
0
1
33
60
94
Benign
0
0
25
3
28
Conflicting
12
Total1010413064320

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

View in ClinVar →

Protein Context — Lollipop Plot

SCN3B · 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.

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Clinical Literature
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC