WNT5A

Chr 3AD

Wnt family member 5A

WNT5A encodes a secreted signaling protein that serves as a ligand for frizzled receptors and can either activate or inhibit canonical Wnt signaling depending on receptor context, playing essential roles in embryonic axis extension, limb outgrowth, and chondrogenesis. Mutations cause autosomal dominant Robinow syndrome, which involves skeletal abnormalities and distinctive facial features. This gene is highly constrained against loss-of-function variation (pLI 0.99), indicating that such variants are likely to be pathogenic.

OMIMResearchSummary from RefSeq, OMIM, UniProt
ADLOEUF 0.271 OMIM phenotype
Clinical SummaryWNT5A
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Gene-Disease Validity (ClinGen)
autosomal dominant Robinow syndrome · ADModerate

Moderate evidence — consider for supplementary testing

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.99). One damaged copy is likely sufficient to cause disease.
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.27LOEUF
pLI 0.987
Z-score 3.67
OE 0.06 (0.020.27)
Highly constrained

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

Missense Constraint
1.98Z-score
OE missense 0.65 (0.570.74)
159 obs / 246.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.06 (0.020.27)
00.351.4
Missense OE0.65 (0.570.74)
00.61.4
Synonymous OE0.93
01.21.6
LoF obs/exp: 1 / 17.6Missense obs/exp: 159 / 246.5Syn Z: 0.59

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

WNT5A · 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.

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Clinical Literature
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