KMO

Chr 1

kynurenine 3-monooxygenase

Also known as: dJ317G22.1

The KMO protein is a mitochondrial outer membrane enzyme that catalyzes the hydroxylation of L-kynurenine to form 3-hydroxy-L-kynurenine, which is required for synthesis of quinolinic acid, a neurotoxic compound that affects NMDA receptor signaling during brain development. Mutations cause autosomal recessive developmental delay and seizures, with the gene being loss-of-function intolerant (pLI near 0, LOEUF 0.698). The phenotype involves neurological manifestations affecting brain development, with potential effects on other organ systems including pancreatic, cardiac, and gastrointestinal function.

GeneReviewsOMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.70
Clinical SummaryKMO
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Gene-Disease Validity (ClinGen)
pellagra · ARNo Known Disease Relationship

No known disease relationship

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
64 unique Pathogenic / Likely Pathogenic· 69 VUS of 153 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — KMO
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.70LOEUF
pLI 0.000
Z-score 2.79
OE 0.43 (0.280.70)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.83Z-score
OE missense 0.68 (0.600.77)
180 obs / 263.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.43 (0.280.70)
00.351.4
Missense OE0.68 (0.600.77)
00.61.4
Synonymous OE1.19
01.21.6
LoF obs/exp: 12 / 27.9Missense obs/exp: 180 / 263.4Syn Z: -1.40
DN
0.81top 10%
GOF
0.6444th %ile
LOF
0.2288th %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

153 submitted variants in ClinVar

Classification Summary

Pathogenic61
Likely Pathogenic3
VUS69
Likely Benign7
Benign3
61
Pathogenic
3
Likely Pathogenic
69
VUS
7
Likely Benign
3
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
61
0
61
Likely Pathogenic
0
0
3
0
3
VUS
2
48
19
0
69
Likely Benign
0
6
1
0
7
Benign
0
1
1
1
3
Total255851143

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

View in ClinVar →

Protein Context — Lollipop Plot

KMO · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →