AKR1C2

Chr 10AR

aldo-keto reductase family 1 member C2

Also known as: AKR1C-pseudo, BABP, DD, DD-2, DD/BABP, DD2, DDH2, HAKRD

AKR1C2 encodes a cytosolic aldo-keto reductase that catalyzes NADPH-dependent reduction of ketosteroids to hydroxysteroids and is required for male sex determination as a component of the 'backdoor' androgen biosynthesis pathway that generates dihydrotestosterone. Mutations cause 46XY sex reversal 8 with autosomal recessive inheritance. The gene is not highly constrained (LOEUF 1.46), consistent with recessive disease requiring biallelic variants to cause phenotype.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 1.461 OMIM phenotype
Clinical SummaryAKR1C2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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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
1.46LOEUF
pLI 0.000
Z-score 0.14
OE 0.96 (0.651.46)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.87Z-score
OE missense 1.20 (1.061.36)
176 obs / 146.3 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.96 (0.651.46)
00.351.4
Missense OE1.20 (1.061.36)
00.61.4
Synonymous OE1.31
01.21.6
LoF obs/exp: 16 / 16.6Missense obs/exp: 176 / 146.3Syn Z: -1.87
DN
0.76top 25%
GOF
0.6443th %ile
LOF
0.2581th %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

AKR1C2 · 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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