AKR1C4

Chr 10AR

aldo-keto reductase family 1 member C4

Also known as: 3-alpha-HSD, C11, CDR, CHDR, DD-4, DD4, HAKRA

The AKR1C4 protein is 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 5α-dihydrotestosterone. Mutations cause autosomal recessive 46,XY sex reversal 8, where it acts as a modifier gene affecting male sexual development. The gene shows high tolerance to loss-of-function variants (LOEUF 1.719), suggesting that complete loss of function may be required for disease manifestation.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

{46XY sex reversal 8, modifier of}MIM #614279
AR
UniProt46,XY sex reversal 8
0
Active trials
13
Pubs (1 yr)
26
P/LP submissions
0%
P/LP missense
1.72
LOEUF
DN
Mechanism· predicted
Clinical SummaryAKR1C4
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
26 unique Pathogenic / Likely Pathogenic· 74 VUS of 150 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.72LOEUF
pLI 0.000
Z-score -0.92
OE 1.23 (0.881.72)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-1.04Z-score
OE missense 1.22 (1.091.37)
214 obs / 175.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.23 (0.881.72)
00.351.4
Missense OE1.22 (1.091.37)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 23 / 18.7Missense obs/exp: 214 / 175.2Syn Z: -0.95
DN
0.7230th %ile
GOF
0.5562th %ile
LOF
0.2971th %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

150 submitted variants in ClinVar

Classification Summary

Pathogenic24
Likely Pathogenic2
VUS74
Likely Benign38
Benign9
24
Pathogenic
2
Likely Pathogenic
74
VUS
38
Likely Benign
9
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
24
0
24
Likely Pathogenic
0
0
2
0
2
VUS
1
54
18
1
74
Likely Benign
0
7
17
14
38
Benign
0
5
3
1
9
Total1666416147

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

View in ClinVar →

Protein Context — Lollipop Plot

AKR1C4 · 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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