GJB3

Chr 1ADARDigenic dominant

gap junction protein beta 3

The encoded protein forms connexons that create gap junction channels allowing diffusion of small molecules between adjacent cells. Mutations cause autosomal dominant or digenic hearing loss (sometimes with peripheral neuropathy) and erythrokeratodermia variabilis et progressiva, a progressive skin disorder with variable erythematous and hyperkeratotic patches. The gene shows low constraint to loss-of-function variants, and inheritance patterns include autosomal dominant, autosomal recessive, and digenic mechanisms.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismAD/AR/Digenic dominantLOEUF 1.323 OMIM phenotypes
Clinical SummaryGJB3
🧬
Gene-Disease Validity (ClinGen)
nonsyndromic genetic hearing loss · ADDisputed

Disputed — evidence questions this relationship

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
💊
Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
Some data sources returned errors (1)

ncbi: Error: NCBI fetch failed: 429 https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.32LOEUF
pLI 0.002
Z-score 0.96
OE 0.63 (0.331.32)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.53Z-score
OE missense 1.11 (0.991.26)
187 obs / 167.8 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.63 (0.331.32)
00.351.4
Missense OE1.11 (0.991.26)
00.61.4
Synonymous OE0.87
01.21.6
LoF obs/exp: 5 / 7.9Missense obs/exp: 187 / 167.8Syn Z: 0.89
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongGJB3-related erythrokeratodermia variabilis et progressivaOTHERAD
moderateGJB3-related deafness (biallelic)LOFAR
moderateGJB3-related deafness (monoallelic)LOFAD
DN
0.84top 10%
GOF
0.84top 5%
LOF
0.2091th %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

DNBased on these findings, we suggest that the CX31V174M mutant may have an effect on the formation and function of the gap junction, and CX31V174M has a trans-dominant negative effect on the function of wild types CX26.PMID:24913888

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

GJB3 · 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 →