FAHD2B

Chr 2

fumarylacetoacetate hydrolase domain containing 2B

FAHD2B encodes a mitochondrial tautomerase that converts enol-oxaloacetate to keto-oxaloacetate, preventing inhibition of succinate dehydrogenase and maintaining efficient aerobic respiration. Mutations cause autosomal recessive mitochondrial complex II deficiency with early-onset developmental delays, seizures, and metabolic acidosis. The gene is highly constrained against loss-of-function variants, indicating intolerance to haploinsufficiency.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.36
Clinical SummaryFAHD2B
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
28 unique Pathogenic / Likely Pathogenic· 69 VUS of 111 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.36LOEUF
pLI 0.000
Z-score 0.56
OE 0.84 (0.541.36)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.41Z-score
OE missense 0.91 (0.801.04)
158 obs / 173.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.84 (0.541.36)
00.351.4
Missense OE0.91 (0.801.04)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 12 / 14.3Missense obs/exp: 158 / 173.1Syn Z: -0.20
DN
0.6842th %ile
GOF
0.6639th %ile
LOF
0.4136th %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

111 submitted variants in ClinVar

Classification Summary

Pathogenic19
Likely Pathogenic9
VUS69
Likely Benign5
Benign1
19
Pathogenic
9
Likely Pathogenic
69
VUS
5
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
19
0
19
Likely Pathogenic
0
0
9
0
9
VUS
0
47
22
0
69
Likely Benign
0
3
2
0
5
Benign
0
0
1
0
1
Total050530103

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

View in ClinVar →

Protein Context — Lollipop Plot

FAHD2B · 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
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 1 results · since 2015Search PubMed ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found