ITGAE

Chr 17

integrin subunit alpha E

Also known as: CD103, HUMINAE

The ITGAE protein is an integrin alpha subunit that pairs with integrin beta-7 to form a receptor for E-cadherin, mediating adhesion of intraepithelial T-lymphocytes to epithelial cells in the intestinal mucosa. Mutations in ITGAE cause autosomal recessive inflammatory bowel disease, typically presenting in infancy or early childhood with severe diarrhea and intestinal inflammation. The gene shows tolerance to loss-of-function variants in the general population, suggesting that biallelic mutations are required for disease manifestation.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.88
Clinical SummaryITGAE
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
32 unique Pathogenic / Likely Pathogenic· 328 VUS of 435 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.88LOEUF
pLI 0.000
Z-score 2.28
OE 0.68 (0.530.88)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.24Z-score
OE missense 0.97 (0.911.04)
676 obs / 693.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.68 (0.530.88)
00.351.4
Missense OE0.97 (0.911.04)
00.61.4
Synonymous OE0.94
01.21.6
LoF obs/exp: 40 / 58.9Missense obs/exp: 676 / 693.5Syn Z: 0.80
DN
0.6648th %ile
GOF
0.6541th %ile
LOF
0.2872th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction 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

435 submitted variants in ClinVar

Classification Summary

Pathogenic31
Likely Pathogenic1
VUS328
Likely Benign39
Benign2
Conflicting1
31
Pathogenic
1
Likely Pathogenic
328
VUS
39
Likely Benign
2
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
31
0
31
Likely Pathogenic
0
0
1
0
1
VUS
0
309
19
0
328
Likely Benign
0
31
3
5
39
Benign
0
1
1
0
2
Conflicting
1
Total0341555402

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

View in ClinVar →

Protein Context — Lollipop Plot

ITGAE · 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
Open Research Assistant →