FZD4

Chr 11AD

frizzled class receptor 4

Also known as: CD344, EVR1, FEVR, FZD4S, Fz-4, Fz4, FzE4, GPCR

FZD4 encodes a seven-transmembrane receptor for Wnt proteins and norrin that activates beta-catenin signaling and plays a critical role in retinal vascularization. Mutations cause exudative vitreoretinopathy and retinopathy of prematurity with autosomal dominant inheritance. The gene is highly constrained against loss-of-function variants, indicating strong selective pressure for normal protein function.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismADLOEUF 0.312 OMIM phenotypes
Clinical SummaryFZD4
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Gene-Disease Validity (ClinGen)
FZD4-related exudative vitreoretinopathy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.97). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
81 unique Pathogenic / Likely Pathogenic· 253 VUS of 475 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.31LOEUF
pLI 0.970
Z-score 3.38
OE 0.07 (0.020.31)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
0.73Z-score
OE missense 0.88 (0.790.97)
255 obs / 290.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.07 (0.020.31)
00.351.4
Missense OE0.88 (0.790.97)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 1 / 15.2Missense obs/exp: 255 / 290.1Syn Z: -0.57
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveFZD4-related exudative vitreoretinopathyLOFAD
DN
0.5180th %ile
GOF
0.7125th %ile
LOF
0.4430th %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.

LOF1 literature citation · 59% of P/LP variants are LoF · LOEUF 0.31
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

LOFKaryotype-phenotype insights from 11q14.1-q23.2 interstitial deletions: FZD4 haploinsufficiency and exudative vitreoretinopathy in a patient with a complex chromosome rearrangement.PMID:17103440

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

475 submitted variants in ClinVar

Classification Summary

Pathogenic65
Likely Pathogenic16
VUS253
Likely Benign97
Benign31
Conflicting9
65
Pathogenic
16
Likely Pathogenic
253
VUS
97
Likely Benign
31
Benign
9
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
42
9
14
0
65
Likely Pathogenic
6
9
1
0
16
VUS
3
218
32
0
253
Likely Benign
0
6
10
81
97
Benign
0
0
29
2
31
Conflicting
9
Total512428683471

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

View in ClinVar →

Protein Context — Lollipop Plot

FZD4 · 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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