The protein is predicted to function in hematopoietic progenitor cell differentiation and as part of a transferase complex. The gene shows very low constraint against loss-of-function variants (pLI near 0, LOEUF 1.589), suggesting it tolerates protein-truncating mutations well. No established disease associations have been reported for WDR38 mutations.

ResearchSummary from RefSeq
DNmechanismLOEUF 1.59
Clinical SummaryWDR38
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.59LOEUF
pLI 0.000
Z-score -0.19
OE 1.05 (0.711.59)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.35Z-score
OE missense 0.93 (0.821.05)
172 obs / 185.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE1.05 (0.711.59)
00.351.4
Missense OE0.93 (0.821.05)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 16 / 15.2Missense obs/exp: 172 / 185.3Syn Z: -0.20
DN
0.6648th %ile
GOF
0.5366th %ile
LOF
0.4627th %ile

The highest-scoring mechanism for this gene is dominant-negative.

DNprediction 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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

WDR38 · 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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