UGT1A8

Chr 2

UDP glucuronosyltransferase family 1 member A8

Also known as: UDPGT, UDPGT 1-8, UGT-1H, UGT1-08, UGT1.8, UGT1A8S, UGT1H

UGT1A8 encodes a UDP-glucuronosyltransferase that conjugates lipophilic substrates with glucuronic acid to facilitate their excretion, playing an essential role in drug metabolism and detoxification of endogenous compounds including steroid hormones. The gene shows low constraint to loss-of-function variation (pLI near 0, LOEUF 1.08), and no Mendelian diseases have been definitively associated with UGT1A8 mutations in pediatric patients. This enzyme is part of a complex gene family where different isoforms have distinct substrate specificities for various drugs, xenobiotics, and endogenous molecules.

Summary from RefSeq, UniProt
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0
Active trials
10
Pubs (1 yr)
0
P/LP submissions
P/LP missense
1.08
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryUGT1A8
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.08LOEUF
pLI 0.000
Z-score 1.32
OE 0.65 (0.411.08)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.25Z-score
OE missense 1.04 (0.951.14)
309 obs / 297.0 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.65 (0.411.08)
00.351.4
Missense OE1.04 (0.951.14)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 11 / 16.9Missense obs/exp: 309 / 297.0Syn Z: -0.22
DN
0.74top 25%
GOF
0.6833th %ile
LOF
0.2288th %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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

UGT1A8 · 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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