CNTN3

Chr 3

contactin 3

Also known as: BIG-1, PANG, PCS

The protein mediates cell surface interactions during nervous system development and promotes neurite outgrowth as a cell adhesion molecule located in the extracellular region and plasma membrane. Mutations cause autosomal recessive developmental and epileptic encephalopathy with cortical blindness, intellectual disability, and seizures typically beginning in infancy. The gene shows low constraint against loss-of-function variants.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
1
Pubs (1 yr)
12
P/LP submissions
0%
P/LP missense
0.51
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryCNTN3
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.35) despite low pLI — interpret in context.
📋
ClinVar Variants
12 unique Pathogenic / Likely Pathogenic· 128 VUS of 191 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.51LOEUF
pLI 0.000
Z-score 4.37
OE 0.35 (0.240.51)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.32Z-score
OE missense 0.84 (0.780.91)
460 obs / 546.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.35 (0.240.51)
00.351.4
Missense OE0.84 (0.780.91)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 18 / 52.0Missense obs/exp: 460 / 546.8Syn Z: -0.41
DN
0.74top 25%
GOF
0.6541th %ile
LOF
0.3454th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
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.

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

ClinVar Variant Classifications

191 submitted variants in ClinVar

Classification Summary

Pathogenic10
Likely Pathogenic2
VUS128
Likely Benign20
Benign12
10
Pathogenic
2
Likely Pathogenic
128
VUS
20
Likely Benign
12
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
10
0
10
Likely Pathogenic
0
0
2
0
2
VUS
0
119
9
0
128
Likely Benign
0
10
3
7
20
Benign
0
6
3
3
12
Total01352710172

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

View in ClinVar →

Protein Context — Lollipop Plot

CNTN3 · 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.

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