FBXL2

Chr 3

F-box and leucine rich repeat protein 2

Also known as: FBL2, FBL3

The protein functions as a calcium-activated substrate recognition component of the SCF ubiquitin ligase complex, targeting specific proteins including cyclins and inflammatory regulators for degradation to control cell cycle progression, autophagy, and inflammation. Mutations cause autosomal recessive developmental and epileptic encephalopathy with onset in infancy, characterized by severe intellectual disability, refractory seizures, and progressive brain atrophy. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.52), consistent with its role in essential cellular processes.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.52
Clinical SummaryFBXL2
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.31) despite low pLI — interpret in context.
📋
ClinVar Variants
17 unique Pathogenic / Likely Pathogenic· 72 VUS of 119 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.52LOEUF
pLI 0.008
Z-score 3.67
OE 0.31 (0.190.52)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.46Z-score
OE missense 0.55 (0.480.64)
132 obs / 239.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.31 (0.190.52)
00.351.4
Missense OE0.55 (0.480.64)
00.61.4
Synonymous OE0.89
01.21.6
LoF obs/exp: 10 / 32.6Missense obs/exp: 132 / 239.0Syn Z: 0.82
DN
0.75top 25%
GOF
0.6834th %ile
LOF
0.3163th %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

119 submitted variants in ClinVar

Classification Summary

Pathogenic17
VUS72
Likely Benign5
17
Pathogenic
72
VUS
5
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
17
0
17
Likely Pathogenic
0
0
0
0
0
VUS
0
70
2
0
72
Likely Benign
0
4
0
1
5
Benign
0
0
0
0
0
Total07419194

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

View in ClinVar →

Protein Context — Lollipop Plot

FBXL2 · 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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