NDUFV1

Chr 11

NADH:ubiquinone oxidoreductase core subunit V1

Also known as: CI-51K, CI51KD, MC1DN4, UQOR1

The protein is a 51 kDa subunit of mitochondrial complex I that contains the NADH-binding site and flavin mononucleotide and iron-sulfur binding sites essential for electron transport in oxidative phosphorylation. Biallelic mutations cause mitochondrial complex I deficiency with autosomal recessive inheritance, presenting as myopathies, encephalomyopathies, and neurodegenerative disorders including Leigh syndrome. Disease results from loss of function leading to impaired mitochondrial energy production.

GeneReviewsResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismLOEUF 1.21
Clinical SummaryNDUFV1
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Gene-Disease Validity (ClinGen)
Leigh syndrome · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
84 unique Pathogenic / Likely Pathogenic· 176 VUS of 580 total submissions
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GeneReview available — NDUFV1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗
Some data sources returned errors (1)

omim: Error: OMIM fetch failed: 429

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.21LOEUF
pLI 0.000
Z-score 0.80
OE 0.82 (0.561.21)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.28Z-score
OE missense 0.95 (0.861.05)
281 obs / 294.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.82 (0.561.21)
00.351.4
Missense OE0.95 (0.861.05)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 18 / 22.0Missense obs/exp: 281 / 294.6Syn Z: 0.14
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveNDUFV1-related mitochondrial complex I deficiencyLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.6649th %ile
GOF
0.6053th %ile
LOF
0.4430th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

580 submitted variants in ClinVar

Classification Summary

Pathogenic38
Likely Pathogenic46
VUS176
Likely Benign239
Benign29
Conflicting40
38
Pathogenic
46
Likely Pathogenic
176
VUS
239
Likely Benign
29
Benign
40
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
22
4
12
0
38
Likely Pathogenic
22
19
5
0
46
VUS
0
157
17
2
176
Likely Benign
1
5
109
124
239
Benign
0
0
26
3
29
Conflicting
40
Total45185169129568

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

View in ClinVar →

Protein Context — Lollipop Plot

NDUFV1 · 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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Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗