Works in concert with the 5-alpha/5-beta-steroid reductases to convert steroid hormones into the 3-alpha/5-alpha and 3-alpha/5-beta-tetrahydrosteroids. Catalyzes the inactivation of the most potent androgen 5-alpha-dihydrotestosterone (5-alpha- DHT) to 5-alpha-androstane-3-alpha,17-beta-diol (3-alpha-diol). Has a high bile-binding ability. Defects in AKR1C2 are a cause of 46,XY sex reversal type 8 (SRXY8). A disorder of sex development. Affected individuals have a 46,XY karyotype but present as phenotypically normal females. Belongs to the aldo/keto reductase family. 2 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: EC 184.108.40.206; EC 1.-.-.-; EC 220.127.116.11; Xenobiotic Metabolism - metabolism by cytochrome P450; EC 1.1.1.-; Oxidoreductase
Cellular Component: cytoplasm
Molecular Function: oxidoreductase activity, acting on NADH or NADPH, quinone or similar compound as acceptor; ketosteroid monooxygenase activity; prostaglandin F receptor activity; carboxylic acid binding; bile acid binding; trans-1,2-dihydrobenzene-1,2-diol dehydrogenase activity; aldehyde reductase activity; phenanthrene 9,10-monooxygenase activity
Biological Process: steroid metabolic process; G-protein coupled receptor protein signaling pathway; positive regulation of protein kinase B signaling cascade; epithelial cell differentiation; digestion; positive regulation of cell proliferation; progesterone metabolic process; prostaglandin metabolic process
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.