NCF4

Chr 22AR

neutrophil cytosolic factor 4

Also known as: CGD3, NCF, P40PHOX, SH3PXD4

The protein is a cytosolic regulatory subunit of the phagocyte NADPH oxidase complex that mediates electron transfer from NADPH to oxygen to produce superoxide anions essential for antimicrobial host defense. Mutations cause chronic granulomatous disease, an autosomal recessive primary immunodeficiency characterized by recurrent severe bacterial and fungal infections due to defective neutrophil killing of pathogens. The gene shows low constraint against loss-of-function variants, consistent with the recessive inheritance pattern where both copies must be affected to cause disease.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 1.201 OMIM phenotype
Clinical SummaryNCF4
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
43 unique Pathogenic / Likely Pathogenic· 178 VUS of 465 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 — NCF4
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
1.20LOEUF
pLI 0.000
Z-score 0.95
OE 0.75 (0.491.20)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.23Z-score
OE missense 1.04 (0.931.17)
215 obs / 205.8 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.75 (0.491.20)
00.351.4
Missense OE1.04 (0.931.17)
00.61.4
Synonymous OE1.20
01.21.6
LoF obs/exp: 13 / 17.3Missense obs/exp: 215 / 205.8Syn Z: -1.41
DN
0.6259th %ile
GOF
0.6345th %ile
LOF
0.3162th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
DNprediction 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

465 submitted variants in ClinVar

Classification Summary

Pathogenic31
Likely Pathogenic12
VUS178
Likely Benign176
Benign48
Conflicting9
31
Pathogenic
12
Likely Pathogenic
178
VUS
176
Likely Benign
48
Benign
9
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
14
1
16
0
31
Likely Pathogenic
9
1
2
0
12
VUS
4
163
10
1
178
Likely Benign
0
8
72
96
176
Benign
0
1
39
8
48
Conflicting
9
Total27174139105454

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

View in ClinVar →

Protein Context — Lollipop Plot

NCF4 · 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 →