AKR1C3

Chr 10

aldo-keto reductase family 1 member C3

Also known as: DD3, DDX, HA1753, HAKRB, HAKRe, HSD17B5, PGFS, hluPGFS

This gene encodes a cytosolic aldo-keto reductase that catalyzes the NADPH-dependent reduction of ketosteroids to hydroxysteroids, playing key roles in androgen and estrogen metabolism by converting precursors to potent hormones like testosterone and 17beta-estradiol. The gene is not loss-of-function intolerant (high LOEUF score), and pathogenic variants have not been established to cause recognizable human disease. While the enzyme has important roles in steroid hormone biosynthesis and prostaglandin metabolism, clinical disorders specifically attributed to AKR1C3 mutations are not currently well-defined in pediatric populations.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
102
Pubs (1 yr)
27
P/LP submissions
0%
P/LP missense
1.86
LOEUF
DN
Mechanism· predicted
Clinical SummaryAKR1C3
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
27 unique Pathogenic / Likely Pathogenic· 69 VUS of 120 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.86LOEUF
pLI 0.000
Z-score -1.83
OE 1.43 (1.071.86)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-1.81Z-score
OE missense 1.39 (1.251.55)
237 obs / 170.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.43 (1.071.86)
00.351.4
Missense OE1.39 (1.251.55)
00.61.4
Synonymous OE1.29
01.21.6
LoF obs/exp: 30 / 21.0Missense obs/exp: 237 / 170.5Syn Z: -1.82
DN
0.75top 25%
GOF
0.6247th %ile
LOF
0.2873th %ile

The highest-scoring mechanism for this gene is dominant-negative.

DNprediction 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

120 submitted variants in ClinVar

Classification Summary

Pathogenic25
Likely Pathogenic2
VUS69
Likely Benign8
Benign5
25
Pathogenic
2
Likely Pathogenic
69
VUS
8
Likely Benign
5
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
25
0
25
Likely Pathogenic
0
0
2
0
2
VUS
0
58
11
0
69
Likely Benign
0
3
5
0
8
Benign
0
3
1
1
5
Total064441109

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

View in ClinVar →

Protein Context — Lollipop Plot

AKR1C3 · protein map & ClinVar variants

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

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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