EPSTI1

Chr 13

epithelial stromal interaction 1

Also known as: BRESI1

The protein regulates macrophage polarization and is required for proper gene expression during M1 versus M2 macrophage differentiation, and may influence RELA/p65 and STAT1 phosphorylation and nuclear localization upon macrophage activation. The gene is extremely tolerant to loss-of-function variants (pLI near zero, LOEUF 1.719), and no Mendelian diseases have been established from mutations in this gene. Current evidence links the gene primarily to cancer biology and autoimmune conditions rather than pediatric neurogenetic disorders.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.72
Clinical SummaryEPSTI1
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
49 unique Pathogenic / Likely Pathogenic· 82 VUS of 161 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.72LOEUF
pLI 0.000
Z-score -1.38
OE 1.29 (0.981.72)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.43Z-score
OE missense 1.08 (0.971.21)
231 obs / 213.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.29 (0.981.72)
00.351.4
Missense OE1.08 (0.971.21)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 33 / 25.5Missense obs/exp: 231 / 213.5Syn Z: 0.13
DN
0.7326th %ile
GOF
0.78top 25%
LOF
0.3358th %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

161 submitted variants in ClinVar

Classification Summary

Pathogenic49
VUS82
Likely Benign9
Benign2
49
Pathogenic
82
VUS
9
Likely Benign
2
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
49
0
49
Likely Pathogenic
0
0
0
0
0
VUS
0
70
12
0
82
Likely Benign
0
5
4
0
9
Benign
0
1
1
0
2
Total076660142

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

View in ClinVar →

Protein Context — Lollipop Plot

EPSTI1 · 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.

Search ClinicalTrials.gov →
Clinical Literature
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