ACOX3

Chr 4

acyl-CoA oxidase 3, pristanoyl

The protein oxidizes CoA-esters of 2-methyl-branched fatty acids in peroxisomes as part of branched-chain fatty acid metabolism. Mutations cause autosomal recessive bile acid synthesis defect with epilepsy and intellectual disability, typically presenting in infancy or early childhood. The gene shows extremely low constraint to loss-of-function variants (pLI near zero), consistent with recessive inheritance where heterozygous carriers are unaffected.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
10
Pubs (1 yr)
75
P/LP submissions
0%
P/LP missense
1.06
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryACOX3
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
75 unique Pathogenic / Likely Pathogenic· 158 VUS of 286 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.06LOEUF
pLI 0.000
Z-score 1.25
OE 0.78 (0.571.06)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.44Z-score
OE missense 1.06 (0.981.14)
469 obs / 442.7 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.78 (0.571.06)
00.351.4
Missense OE1.06 (0.981.14)
00.61.4
Synonymous OE1.09
01.21.6
LoF obs/exp: 28 / 36.1Missense obs/exp: 469 / 442.7Syn Z: -0.94
DN
0.7035th %ile
GOF
0.6930th %ile
LOF
0.2385th %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

286 submitted variants in ClinVar

Classification Summary

Pathogenic72
Likely Pathogenic3
VUS158
Likely Benign22
Benign12
Conflicting1
72
Pathogenic
3
Likely Pathogenic
158
VUS
22
Likely Benign
12
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
72
0
72
Likely Pathogenic
0
0
3
0
3
VUS
0
146
12
0
158
Likely Benign
0
11
3
8
22
Benign
0
4
4
4
12
Conflicting
1
Total01619412268

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

View in ClinVar →

Protein Context — Lollipop Plot

ACOX3 · 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
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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found