TRIM16

Chr 17

tripartite motif containing 16

Also known as: EBBP

The TRIM16 protein functions as an E3 ubiquitin ligase that regulates autophagy and protects cells against oxidative stress by modulating protein aggregate degradation and the NRF2 signaling pathway. Mutations cause autosomal recessive intellectual disability with seizures and variable additional features including microcephaly and developmental delays. This gene shows very low constraint against loss-of-function variants in the general population.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.13
Clinical SummaryTRIM16
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
19 unique Pathogenic / Likely Pathogenic· 88 VUS of 127 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.13LOEUF
pLI 0.000
Z-score 1.10
OE 0.74 (0.501.13)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.34Z-score
OE missense 0.95 (0.861.04)
300 obs / 316.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.74 (0.501.13)
00.351.4
Missense OE0.95 (0.861.04)
00.61.4
Synonymous OE0.88
01.21.6
LoF obs/exp: 16 / 21.5Missense obs/exp: 300 / 316.8Syn Z: 1.10
DN
0.75top 25%
GOF
0.76top 25%
LOF
0.2484th %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

127 submitted variants in ClinVar

Classification Summary

Pathogenic19
VUS88
Likely Benign10
Benign1
19
Pathogenic
88
VUS
10
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
19
0
19
Likely Pathogenic
0
0
0
0
0
VUS
0
86
2
0
88
Likely Benign
0
7
1
2
10
Benign
0
1
0
0
1
Total094222118

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

View in ClinVar →

Protein Context — Lollipop Plot

TRIM16 · 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.

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Clinical Literature
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