NDUFB6

Chr 9

NADH:ubiquinone oxidoreductase subunit B6

Also known as: B17, CI

The NDUFB6 protein is an accessory subunit of mitochondrial respiratory complex I (NADH dehydrogenase), which transfers electrons from NADH to ubiquinone in the respiratory chain. Mutations cause autosomal recessive mitochondrial complex I deficiency, typically presenting in early childhood with neurological features including developmental delay, seizures, and progressive encephalopathy. This gene shows low constraint against loss-of-function variants, consistent with recessive inheritance patterns where heterozygous carriers are typically unaffected.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.67
Clinical SummaryNDUFB6
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
68 unique Pathogenic / Likely Pathogenic· 24 VUS of 95 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.67LOEUF
pLI 0.000
Z-score 0.27
OE 0.89 (0.481.67)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.29Z-score
OE missense 1.10 (0.911.35)
70 obs / 63.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.89 (0.481.67)
00.351.4
Missense OE1.10 (0.911.35)
00.61.4
Synonymous OE1.35
01.21.6
LoF obs/exp: 6 / 6.8Missense obs/exp: 70 / 63.5Syn Z: -1.33
DN
0.6648th %ile
GOF
0.6542th %ile
LOF
0.3161th %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

95 submitted variants in ClinVar

Classification Summary

Pathogenic60
Likely Pathogenic8
VUS24
60
Pathogenic
8
Likely Pathogenic
24
VUS

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
60
0
60
Likely Pathogenic
0
0
8
0
8
VUS
0
16
8
0
24
Likely Benign
0
0
0
0
0
Benign
0
0
0
0
0
Total01676092

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

View in ClinVar →

Protein Context — Lollipop Plot

NDUFB6 · 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.

Search ClinicalTrials.gov →
Clinical Literature
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