UGT1A6

Chr 2

UDP glucuronosyltransferase family 1 member A6

Also known as: GNT1, HLUGP, HLUGP1, UDPGT 1-6, UGT-1F, UGT1-06, UGT1.6, UGT1A6S

This gene encodes a UDP-glucuronosyltransferase, an enzyme of the glucuronidation pathway that transforms small lipophilic molecules, such as steroids, bilirubin, hormones, and drugs, into water-soluble, excretable metabolites. This gene is part of a complex locus that encodes several UDP-glucuronosyltransferases. The locus includes thirteen unique alternate first exons followed by four common exons. Four of the alternate first exons are considered pseudogenes. Each of the remaining nine 5' exons may be spliced to the four common exons, resulting in nine proteins with different N-termini and identical C-termini. Each first exon encodes the substrate binding site, and is regulated by its own promoter. The enzyme encoded by this gene is active on phenolic and planar compounds. Alternative splicing in the unique 5' end of this gene results in two transcript variants. [provided by RefSeq, Jul 2008]

1
Active trials
29
Pubs (1 yr)
116
P/LP submissions
18%
P/LP missense
1.06
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryUGT1A6
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
74 unique Pathogenic / Likely Pathogenic· 313 VUS of 495 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — UGT1A6
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.06LOEUF
pLI 0.000
Z-score 1.35
OE 0.67 (0.431.06)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.03Z-score
OE missense 1.00 (0.901.10)
294 obs / 295.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.67 (0.431.06)
00.351.4
Missense OE1.00 (0.901.10)
00.61.4
Synonymous OE1.05
01.21.6
LoF obs/exp: 13 / 19.4Missense obs/exp: 294 / 295.4Syn Z: -0.40
DN
0.79top 25%
GOF
0.73top 25%
LOF
0.1895th %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

495 submitted variants in ClinVar

Classification Summary

Pathogenic46
Likely Pathogenic28
VUS313
Likely Benign76
Benign6
Conflicting24
46
Pathogenic
28
Likely Pathogenic
313
VUS
76
Likely Benign
6
Benign
24
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
15
2
29
0
46
Likely Pathogenic
13
11
4
0
28
VUS
1
287
22
3
313
Likely Benign
1
18
15
42
76
Benign
0
3
1
2
6
Conflicting
24
Total303217147493

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

View in ClinVar →

Protein Context — Lollipop Plot

UGT1A6 · protein map & ClinVar variants

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

Clinical Literature
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