SERPINB11

Chr 18

serpin family B member 11

Also known as: EPIPIN, SERPIN11

The protein is predicted to have serine-type endopeptidase inhibitor activity in the cytoplasm and extracellular space, though UniProt notes it lacks actual serine protease inhibitory activity due to structural variants. This gene is not well-established as a cause of human genetic disease, as it shows very low intolerance to loss-of-function variants (pLI near 0, LOEUF >1). No clear Mendelian disease associations or inheritance patterns have been definitively established for SERPINB11 mutations.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
0
Pubs (1 yr)
98
P/LP submissions
0%
P/LP missense
1.16
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySERPINB11
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
95 unique Pathogenic / Likely Pathogenic· 78 VUS of 179 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.16LOEUF
pLI 0.000
Z-score 1.07
OE 0.72 (0.461.16)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-1.02Z-score
OE missense 1.21 (1.081.34)
235 obs / 194.9 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.72 (0.461.16)
00.351.4
Missense OE1.21 (1.081.34)
00.61.4
Synonymous OE1.14
01.21.6
LoF obs/exp: 12 / 16.7Missense obs/exp: 235 / 194.9Syn Z: -0.99
DN
0.78top 25%
GOF
0.6832th %ile
LOF
0.1994th %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

179 submitted variants in ClinVar

Classification Summary

Pathogenic88
Likely Pathogenic7
VUS78
Likely Benign4
88
Pathogenic
7
Likely Pathogenic
78
VUS
4
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
88
0
88
Likely Pathogenic
0
0
7
0
7
VUS
0
69
9
0
78
Likely Benign
0
4
0
0
4
Benign
0
0
0
0
0
Total0731040177

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

View in ClinVar →

Protein Context — Lollipop Plot

SERPINB11 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

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 3 results · since 2015Search PubMed ↗