TNFRSF11B

Chr 8AR

TNF receptor superfamily member 11b

Also known as: OCIF, OPG, PDB5, TR1

The protein functions as a decoy receptor that inhibits bone resorption by binding to osteoprotegerin ligand and neutralizing osteoclast activation, serving as a key negative regulator of bone homeostasis. Mutations cause autosomal recessive juvenile-onset Paget disease of bone 5, characterized by early-onset abnormal bone remodeling. The gene is moderately constrained against loss-of-function variants (LOEUF 0.548), indicating some intolerance to complete protein loss.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Paget disease of bone 5, juvenile-onsetMIM #239000
AR
4
Active trials
37
Pubs (1 yr)
72
P/LP submissions
4%
P/LP missense
0.55
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryTNFRSF11B
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.26) despite low pLI — interpret in context.
📋
ClinVar Variants
72 unique Pathogenic / Likely Pathogenic· 146 VUS of 312 total submissions
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Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — TNFRSF11B
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.55LOEUF
pLI 0.162
Z-score 3.00
OE 0.26 (0.140.55)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
0.84Z-score
OE missense 0.84 (0.740.95)
184 obs / 219.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.26 (0.140.55)
00.351.4
Missense OE0.84 (0.740.95)
00.61.4
Synonymous OE0.92
01.21.6
LoF obs/exp: 5 / 19.2Missense obs/exp: 184 / 219.0Syn Z: 0.57
DN
0.6745th %ile
GOF
0.74top 25%
LOF
0.2485th %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

312 submitted variants in ClinVar

Classification Summary

Pathogenic69
Likely Pathogenic3
VUS146
Likely Benign54
Benign19
Conflicting6
69
Pathogenic
3
Likely Pathogenic
146
VUS
54
Likely Benign
19
Benign
6
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
3
2
64
0
69
Likely Pathogenic
1
1
1
0
3
VUS
2
118
25
1
146
Likely Benign
0
1
17
36
54
Benign
0
2
11
6
19
Conflicting
6
Total612411843297

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

View in ClinVar →

Protein Context — Lollipop Plot

TNFRSF11B · protein map & ClinVar variants

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

Clinical Literature
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