SCNN1B

Chr 16ADAR

sodium channel epithelial 1 subunit beta

Also known as: BESC1, ENaCb, ENaCbeta, LIDLS1, PHA1B2, SCNEB, beta-ENaC, beta-NaCH

The SCNN1B gene encodes the beta subunit of the epithelial sodium channel (ENaC), which controls sodium and fluid transport across epithelial tissues in the kidneys, lungs, and other organs. Mutations cause pseudohypoaldosteronism type 1 (autosomal recessive) presenting with severe salt wasting and dehydration in infancy, or Liddle syndrome (autosomal dominant) characterized by early-onset hypertension and hypokalemia. The gene is not highly constrained against loss-of-function variants, consistent with recessive inheritance being possible for complete loss of function.

GeneReviewsOMIMResearchSummary from RefSeq, UniProt
MultiplemechanismAD/ARLOEUF 0.803 OMIM phenotypes
Clinical SummarySCNN1B
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
43 unique Pathogenic / Likely Pathogenic· 219 VUS of 400 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — SCNN1B
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 0.000
Z-score 2.45
OE 0.53 (0.360.80)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.21Z-score
OE missense 0.97 (0.891.06)
362 obs / 373.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.53 (0.360.80)
00.351.4
Missense OE0.97 (0.891.06)
00.61.4
Synonymous OE1.09
01.21.6
LoF obs/exp: 17 / 32.0Missense obs/exp: 362 / 373.5Syn Z: -0.87
DN
0.6744th %ile
GOF
0.72top 25%
LOF
0.1895th %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

GOFGain-of-function mutations in ENaC beta and gamma subunits cause pseudoaldosteronism (Liddle's syndrome), a severe form of salt-sensitive hypertension.PMID:11826291

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

ClinVar Variant Classifications

400 submitted variants in ClinVar

Classification Summary

Pathogenic20
Likely Pathogenic23
VUS219
Likely Benign74
Benign31
Conflicting25
20
Pathogenic
23
Likely Pathogenic
219
VUS
74
Likely Benign
31
Benign
25
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
10
1
9
0
20
Likely Pathogenic
16
6
1
0
23
VUS
3
194
18
4
219
Likely Benign
0
7
33
34
74
Benign
0
0
31
0
31
Conflicting
25
Total292089238392

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

View in ClinVar →

Protein Context — Lollipop Plot

SCNN1B · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗