SCN1B

Chr 19ADAR

sodium voltage-gated channel beta subunit 1

Also known as: ATFB13, BRGDA5, DEE52, EIEE52, GEFSP1

The protein encodes the beta-1 subunit of voltage-gated sodium channels, which modulates the kinetics of channel inactivation during action potential generation and propagation in muscle and neuronal cells. Mutations cause generalized epilepsy with febrile seizures plus, developmental and epileptic encephalopathy, Brugada syndrome, and cardiac conduction defects through both autosomal dominant and autosomal recessive inheritance patterns. The pathogenic mechanism involves gain-of-function effects on sodium channel activity.

OMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismAD/ARLOEUF 1.265 OMIM phenotypes
VCEP Guidelines: Epilepsy Sodium ChannelReleased
View SpecificationsClinGen Panel
Clinical SummarySCN1B
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Gene-Disease Validity (ClinGen)
generalized epilepsy with febrile seizures plus · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

3 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.10) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
11 unique Pathogenic / Likely Pathogenic· 44 VUS of 124 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.26LOEUF
pLI 0.102
Z-score 1.22
OE 0.41 (0.171.26)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
1.22Z-score
OE missense 0.73 (0.630.85)
118 obs / 161.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.41 (0.171.26)
00.351.4
Missense OE0.73 (0.630.85)
00.61.4
Synonymous OE1.01
01.21.6
LoF obs/exp: 2 / 4.9Missense obs/exp: 118 / 161.8Syn Z: -0.06
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedSCN1B-related Brugada syndromeOTHERAD
definitiveSCN1B-related developmental and epileptic encephalopathyOTHERAR
DN
0.6938th %ile
GOF
0.76top 25%
LOF
0.2581th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. 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

GOFOur results suggest that R214Q variation in SCN1Bb is a functional polymorphism that may serve as a modifier of the substrate responsible for BrS or SIDS phenotypes via a combined loss of function of sodium channel current and gain of function of transient outward potassium current.PMID:22155597

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

ClinVar Variant Classifications

124 submitted variants in ClinVar

Classification Summary

Pathogenic9
Likely Pathogenic2
VUS44
Likely Benign40
Benign13
Conflicting16
9
Pathogenic
2
Likely Pathogenic
44
VUS
40
Likely Benign
13
Benign
16
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
3
1
5
0
9
Likely Pathogenic
0
2
0
0
2
VUS
4
36
3
1
44
Likely Benign
0
4
12
24
40
Benign
0
3
9
1
13
Conflicting
16
Total7462926124

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

View in ClinVar →

Protein Context — Lollipop Plot

SCN1B · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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