UGT1A9

Chr 2

UDP glucuronosyltransferase family 1 member A9

Also known as: HLUGP4, LUGP4, UDPGT, UDPGT 1-9, UGT-1I, UGT1-09, UGT1-9, UGT1.9

This gene encodes UDP-glucuronosyltransferase 1A9, an enzyme that conjugates lipophilic substrates with glucuronic acid to facilitate their excretion, playing a critical role in drug metabolism and detoxification of endogenous compounds like estrogen hormones and eicosanoids. Mutations cause Crigler-Najjar syndrome and Gilbert syndrome, autosomal recessive disorders of bilirubin metabolism that can present in the neonatal period with severe hyperbilirubinemia or later with milder jaundice. The gene shows tolerance to loss-of-function variants (LOEUF 1.112), suggesting that complete loss may be compatible with survival but can still cause clinically significant bilirubin metabolism defects.

Summary from RefSeq, UniProt
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1
Active trials
36
Pubs (1 yr)
73
P/LP submissions
20%
P/LP missense
1.11
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryUGT1A9
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
51 unique Pathogenic / Likely Pathogenic· 324 VUS of 497 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.11LOEUF
pLI 0.000
Z-score 1.19
OE 0.71 (0.471.11)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.94Z-score
OE missense 1.15 (1.051.26)
346 obs / 300.3 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.71 (0.471.11)
00.351.4
Missense OE1.15 (1.051.26)
00.61.4
Synonymous OE1.28
01.21.6
LoF obs/exp: 14 / 19.7Missense obs/exp: 346 / 300.3Syn Z: -2.38
DN
0.80top 25%
GOF
0.74top 25%
LOF
0.1697th %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

497 submitted variants in ClinVar

Classification Summary

Pathogenic29
Likely Pathogenic22
VUS324
Likely Benign88
Benign23
Conflicting9
29
Pathogenic
22
Likely Pathogenic
324
VUS
88
Likely Benign
23
Benign
9
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
13
3
13
0
29
Likely Pathogenic
13
7
2
0
22
VUS
4
301
18
1
324
Likely Benign
0
30
11
47
88
Benign
0
5
14
4
23
Conflicting
9
Total303465852495

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

View in ClinVar →

Protein Context — Lollipop Plot

UGT1A9 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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