SCNN1G

Chr 16ADAR

sodium channel epithelial 1 subunit gamma

Also known as: BESC3, ENaCg, ENaCgamma, LDLS2, PHA1, PHA1B3, SCNEG

The protein forms the gamma subunit of the epithelial sodium channel (ENaC), which mediates sodium reabsorption in the kidneys and maintains airway surface liquid homeostasis for proper mucus clearance. Mutations cause Liddle syndrome, pseudohypoaldosteronism type IB3, and bronchiectasis with or without elevated sweat chloride, with both autosomal dominant and autosomal recessive inheritance patterns depending on the condition. The gene is moderately constrained against loss-of-function variants (LOEUF 0.408), reflecting its essential role in sodium and fluid homeostasis across multiple organ systems.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismAD/ARLOEUF 0.413 OMIM phenotypes
Clinical SummarySCNN1G
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Gene-Disease Validity (ClinGen)
Liddle syndrome · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.22) despite low pLI — interpret in context.
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ClinVar Variants
45 unique Pathogenic / Likely Pathogenic· 198 VUS of 391 total submissions
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GeneReview available — SCNN1G
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.41LOEUF
pLI 0.482
Z-score 4.12
OE 0.22 (0.120.41)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
0.56Z-score
OE missense 0.92 (0.841.00)
328 obs / 357.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.22 (0.120.41)
00.351.4
Missense OE0.92 (0.841.00)
00.61.4
Synonymous OE1.05
01.21.6
LoF obs/exp: 7 / 32.2Missense obs/exp: 328 / 357.9Syn Z: -0.49
DN
0.5576th %ile
GOF
0.5955th %ile
LOF
0.3356th %ile

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

LOF36% of P/LP variants are LoF · LOEUF 0.41
GOF1 literature citation

Literature Evidence

GOFLiddle syndrome is an autosomal dominant genetic condition that causes hypertension and hypokalemia due to a gain-of-function mutation in the SCNN1B or SCNN1G genes which code for the epithelial sodium channel in the kidney.PMID:28396810

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

391 submitted variants in ClinVar

Classification Summary

Pathogenic34
Likely Pathogenic11
VUS198
Likely Benign70
Benign50
Conflicting23
34
Pathogenic
11
Likely Pathogenic
198
VUS
70
Likely Benign
50
Benign
23
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
8
0
26
0
34
Likely Pathogenic
8
0
3
0
11
VUS
1
161
27
9
198
Likely Benign
0
4
32
34
70
Benign
0
1
44
5
50
Conflicting
23
Total1716613248386

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

View in ClinVar →

Protein Context — Lollipop Plot

SCNN1G · 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
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