Pathway candidateNCBI-verifiedprotein-coding

AKR1B1

aldo-keto reductase family 1 member B

NCBI Gene: 231 Ensembl GeneCards UniProt: P15121

Pathway candidate — not linked to PFS or PSSD by any record here

AKR1B1 is in the library because it belongs to the drug metabolism family. No study, report or commentary in the corpus names it, so a variant in AKR1B1 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 7 (drug metabolism (phase i)). Encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. This member catalyzes the reduction of a number of aldehydes, including the aldehyde form of glucose, and is thereby implicated in the development of diabetic complications by catalyzing the reduction of glucose to sorbitol.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Aldo-keto reductase family 1 member B1
Function (excerpt): Catalyzes the NADPH-dependent reduction of a wide variety of carbonyl-containing compounds to their corresponding alcohols. Displays enzymatic activity towards endogenous metabolites such as aromatic and aliphatic aldehydes, ketones, monosaccharides, bile acids and xenobiotics substrates. It catalyzes the reduction of glucose to sorbitol, the first step of the polyol pathway, an alternative route of glucose metabolism that converts glucose to fructose. This pathway becomes highly active under elevated glucose levels, such as during hyperglycemia. Reduces steroids and their derivatives and prostaglandins. Displays low enzymatic activity toward all-trans-retinal, 9-cis-retinal, and 13-cis-retinal. Catalyzes the reduction of diverse phospholipid aldehydes such as 1-palmitoyl-2-(5-oxovaleroyl)-sn -glycero-3-phosphoethanolamin (POVPC) and related phospholipid aldehydes that are generated from the oxydation of phosphotidylcholine and phosphatdyleethanolamides.
Subcellular location: Cytoplasm.
Tissue specificity: Highly expressed in embryonic epithelial cells (EUE) in response to osmotic stress.

Source: UniProtKB/Swiss-Prot P15121, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.

Why its pathway is in the library

Phase I enzymes determine exposure to finasteride, SSRIs, and other implicated drugs; variation here shapes the likelihood and persistence of adverse effects.

Written for the whole drug metabolism family, not for AKR1B1 specifically.

Mentioned in 0 corpus records

No corpus record names AKR1B1 directly yet. It is in the library because it sits in a pathway the corpus tracks (Drug metabolism).

Also in drug metabolism (phase i)

All 23 genes

Browse by family on the gene families page.

Gene summary

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Aldo-keto reductase family 1 member B1
Function (excerpt): Catalyzes the NADPH-dependent reduction of a wide variety of carbonyl-containing compounds to their corresponding alcohols. Displays enzymatic activity towards endogenous metabolites such as aromatic and aliphatic aldehydes, ketones, monosaccharides, bile acids and xenobiotics substrates. It catalyzes the reduction of glucose to sorbitol, the first step of the polyol pathway, an alternative route of glucose metabolism that converts glucose to fructose. This pathway becomes highly active under elevated glucose levels, such as during hyperglycemia. Reduces steroids and their derivatives and prostaglandins. Displays low enzymatic activity toward all-trans-retinal, 9-cis-retinal, and 13-cis-retinal. Catalyzes the reduction of diverse phospholipid aldehydes such as 1-palmitoyl-2-(5-oxovaleroyl)-sn -glycero-3-phosphoethanolamin (POVPC) and related phospholipid aldehydes that are generated from the oxydation of phosphotidylcholine and phosphatdyleethanolamides.
Subcellular location: Cytoplasm.
Tissue specificity: Highly expressed in embryonic epithelial cells (EUE) in response to osmotic stress.