EXT1

Chr 8ADSomatic

exostosin glycosyltransferase 1

Also known as: EXT, LGCR, LGS, TRPS2, TTV

This gene encodes an endoplasmic reticulum glycosyltransferase that catalyzes heparan sulfate chain elongation during biosynthesis. Loss-of-function mutations cause multiple exostoses type 1, an autosomal dominant disorder characterized by benign bone tumors that can undergo malignant transformation to chondrosarcoma. The pathogenic mechanism involves haploinsufficiency leading to disrupted heparan sulfate production and abnormal bone growth regulation.

Summary from RefSeq, OMIM, UniProt, Mechanism
Research Assistant →

Primary Disease Associations & Inheritance

Exostoses, multiple, type 1MIM #133700
AD
ChondrosarcomaMIM #215300
Somatic
Exostoses, multiple, type 1MIM #133700
AD
UniProtHereditary multiple exostoses 1
1
Active trials
51
Pubs (1 yr)
45
P/LP submissions
9%
P/LP missense
0.26
LOEUF· LoF intol.
LOF
Mechanism· G2P
Clinical SummaryEXT1
🧬
Gene-Disease Validity (ClinGen)
exostoses, multiple, type 1 · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
44 unique Pathogenic / Likely Pathogenic· 30 VUS of 100 total submissions
💊
Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
📖
GeneReview available — EXT1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.26LOEUF
pLI 0.997
Z-score 4.86
OE 0.11 (0.060.26)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
1.67Z-score
OE missense 0.77 (0.700.84)
317 obs / 412.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.11 (0.060.26)
00.351.4
Missense OE0.77 (0.700.84)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 4 / 35.0Missense obs/exp: 317 / 412.2Syn Z: -0.73
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveEXT1-related multiple exostosesLOFAD
definitiveEXT1-related trichorhinopharangeal syndrome (Langer-Giedon)LOFAD
DN
0.3793th %ile
GOF
0.3292th %ile
LOF
0.67top 25%

The highest-scoring mechanism for this gene is loss-of-function (haploinsufficiency).

LOFprediction above median · 1 literature citation · 64% of P/LP variants are LoF · LOEUF 0.26

Literature Evidence

LOFLanger-Giedion's syndrome (LGS) or trichorhinophalangeal syndrome type II (TRPS II; MIM:150230) is a contiguous gene deletion syndrome caused by the haploinsufficiency of the TRPS1 and EXT1 genes.PMID:31976145

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

100 submitted variants in ClinVar

Classification Summary

Pathogenic41
Likely Pathogenic3
VUS30
Likely Benign16
41
Pathogenic
3
Likely Pathogenic
30
VUS
16
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
25
4
12
0
41
Likely Pathogenic
3
0
0
0
3
VUS
1
25
3
1
30
Likely Benign
0
0
5
11
16
Benign
0
0
0
0
0
Total2929201290

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

View in ClinVar →

Protein Context — Lollipop Plot

EXT1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Membranous Nephropathy: Core Curriculum 2021.
Alsharhan L et al.·Am J Kidney Dis
2021Review
New 'Antigens' in Membranous Nephropathy.
Sethi S·J Am Soc Nephrol
2021Review
Mechanisms of Primary Membranous Nephropathy.
Gu Y et al.·Biomolecules
2021Review
Top 5 results · since 2015Search PubMed ↗