SETMAR

Chr 3

SET and mariner transposase domain methyltransferase

Also known as: METNASE, Mar1

The protein is a fusion methyltransferase-transposase that methylates histones H3K4 and H3K36 and functions in DNA double-strand break repair through non-homologous end joining. This gene is extremely intolerant to loss-of-function variants (pLI = 1.0), suggesting that mutations would likely cause severe developmental phenotypes, though no specific human disease has been definitively associated with SETMAR mutations to date. The gene exists as a fusion only in anthropoid primates, making it evolutionarily unique among DNA repair genes.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
2
Pubs (1 yr)
83
P/LP submissions
0%
P/LP missense
1.13
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySETMAR
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
83 unique Pathogenic / Likely Pathogenic· 91 VUS of 187 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 1.24
OE 0.63 (0.371.13)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.26Z-score
OE missense 0.96 (0.881.05)
362 obs / 376.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.63 (0.371.13)
00.351.4
Missense OE0.96 (0.881.05)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 8 / 12.8Missense obs/exp: 362 / 376.4Syn Z: 0.21
DN
0.6358th %ile
GOF
0.6736th %ile
LOF
0.3068th %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

187 submitted variants in ClinVar

Classification Summary

Pathogenic78
Likely Pathogenic5
VUS91
Likely Benign7
78
Pathogenic
5
Likely Pathogenic
91
VUS
7
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
78
0
78
Likely Pathogenic
0
0
5
0
5
VUS
0
63
28
0
91
Likely Benign
0
3
1
3
7
Benign
0
0
0
0
0
Total0661123181

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

View in ClinVar →

Protein Context — Lollipop Plot

SETMAR · 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
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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC