F11

Chr 4

coagulation factor XI

Also known as: FXI, PTA

This gene encodes coagulation factor XI, a serine protease that triggers the middle phase of the intrinsic pathway of blood coagulation by activating factor IX. Mutations cause factor XI deficiency (Rosenthal syndrome), a bleeding disorder that can be inherited in either autosomal dominant or autosomal recessive patterns. The gene is not highly constrained against loss-of-function variants (pLI near zero), consistent with the viability of individuals with factor XI deficiency.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Factor XI deficiency, autosomal dominantMIM #612416
Factor XI deficiency, autosomal recessiveMIM #612416
0
Active trials
75
Pubs (1 yr)
130
P/LP submissions
16%
P/LP missense
1.45
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryF11
🧬
Gene-Disease Validity (ClinGen)
congenital factor XI deficiency · SDDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
114 unique Pathogenic / Likely Pathogenic· 167 VUS of 500 total submissions
📖
GeneReview available — F11
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
1.45LOEUF
pLI 0.000
Z-score -0.53
OE 1.10 (0.841.45)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.02Z-score
OE missense 1.00 (0.911.09)
342 obs / 343.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE1.10 (0.841.45)
00.351.4
Missense OE1.00 (0.911.09)
00.61.4
Synonymous OE1.05
01.21.6
LoF obs/exp: 37 / 33.7Missense obs/exp: 342 / 343.0Syn Z: -0.49
DN
0.6355th %ile
GOF
0.6639th %ile
LOF
0.3453th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports dominant-negative. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median · 1 literature citation
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.

Literature Evidence

DNThree dominant-negative mutations in factor XI-deficient patientsPMID:21457405

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic59
Likely Pathogenic55
VUS167
Likely Benign193
Benign7
Conflicting14
59
Pathogenic
55
Likely Pathogenic
167
VUS
193
Likely Benign
7
Benign
14
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
19
3
37
0
59
Likely Pathogenic
27
15
13
0
55
VUS
1
119
38
9
167
Likely Benign
1
5
88
99
193
Benign
0
0
7
0
7
Conflicting
14
Total48142183108495

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

View in ClinVar →

Protein Context — Lollipop Plot

F11 · 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 5 results · since 2015Search PubMed ↗