The protein is a component of the exocyst complex that docks exocytic vesicles to the plasma membrane for secretion. Mutations cause a neurodevelopmental disorder with microcephaly, seizures, and brain atrophy, inherited in an autosomal recessive pattern. This gene is highly constrained against loss-of-function variants, indicating intolerance to protein disruption.

OMIMResearchSummary from RefSeq, OMIM, UniProt
ARLOEUF 0.191 OMIM phenotype
Clinical SummaryEXOC8
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.19LOEUF
pLI 0.999
Z-score 4.40
OE 0.04 (0.010.19)
Highly constrained

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

Missense Constraint
2.04Z-score
OE missense 0.72 (0.650.79)
294 obs / 410.4 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.04 (0.010.19)
00.351.4
Missense OE0.72 (0.650.79)
00.61.4
Synonymous OE1.01
01.21.6
LoF obs/exp: 1 / 24.5Missense obs/exp: 294 / 410.4Syn Z: -0.05

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

EXOC8 · 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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