TNFRSF10B

Chr 8AR

TNF receptor superfamily member 10b

Also known as: CD262, DR5, KILLER, KILLER/DR5, TRAIL-R2, TRAILR2, TRICK2, TRICK2A

This protein is a tumor necrosis factor receptor superfamily member that contains an intracellular death domain and transduces apoptosis signals when activated by TRAIL ligand, recruiting FADD and caspase-8 to initiate programmed cell death cascades. Mutations cause squamous cell carcinoma of the head and neck with autosomal recessive inheritance. The gene shows tolerance to loss-of-function variants (low pLI score), suggesting that complete loss of function may be required for disease manifestation.

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

Squamous cell carcinoma, head and neckMIM #275355
AR
4
Active trials
26
Pubs (1 yr)
84
P/LP submissions
0%
P/LP missense
0.85
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryTNFRSF10B
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
84 unique Pathogenic / Likely Pathogenic· 60 VUS of 188 total submissions
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Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.85LOEUF
pLI 0.000
Z-score 2.05
OE 0.49 (0.290.85)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.67Z-score
OE missense 1.12 (1.011.24)
270 obs / 240.7 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.49 (0.290.85)
00.351.4
Missense OE1.12 (1.011.24)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 9 / 18.5Missense obs/exp: 270 / 240.7Syn Z: -0.22
DN
0.6551th %ile
GOF
0.79top 10%
LOF
0.1895th %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

188 submitted variants in ClinVar

Classification Summary

Pathogenic79
Likely Pathogenic5
VUS60
Likely Benign19
Benign4
79
Pathogenic
5
Likely Pathogenic
60
VUS
19
Likely Benign
4
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
78
0
79
Likely Pathogenic
1
0
4
0
5
VUS
0
54
6
0
60
Likely Benign
0
7
4
8
19
Benign
0
3
1
0
4
Total264938167

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

View in ClinVar →

Protein Context — Lollipop Plot

TNFRSF10B · 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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