17β-Hydroxysteroid dehydrogenase | |||||||||
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Identifiers | |||||||||
EC number | 1.1.1.51 | ||||||||
CAS number | 9015-81-0 | ||||||||
Databases | |||||||||
IntEnz | IntEnz view | ||||||||
BRENDA | BRENDA entry | ||||||||
ExPASy | NiceZyme view | ||||||||
KEGG | KEGG entry | ||||||||
MetaCyc | metabolic pathway | ||||||||
PRIAM | profile | ||||||||
PDB structures | RCSB PDB PDBe PDBsum | ||||||||
Gene Ontology | AmiGO / EGO | ||||||||
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Search | |
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PMC | articles |
PubMed | articles |
NCBI | proteins |
17β-Hydroxysteroid dehydrogenases (17β-HSD, HSD17B) (EC 1.1.1.51), also 17-ketosteroid reductases (17-KSR), are a group of alcohol oxidoreductases which catalyze the reduction of 17-ketosteroids and the dehydrogenation of 17β-hydroxysteroids in steroidogenesis and steroid metabolism. This includes interconversion of DHEA and androstenediol, androstenedione and testosterone, and estrone and estradiol.
It should be noted that the major reactions catalyzed by 17β-HSD (e.g., the conversion of androstenedione to testosterone) are in fact hydrogenation (reduction) rather than dehydrogenation (oxidation) reactions.
17β-HSDs have been known to catalyze the following redox reactions of sex steroids:
Genes coding for 17β-HSD include:
At least 7 of the 14 isoforms of 17β-HSD are involved in interconversion of 17-ketosteroids and 17β-hydroxysteroids.
Mutations in HSD17B3 are responsible for 17β-HSD type III deficiency.
Inhibitors of 17β-HSD type II are of interest for the potential treatment of osteoporosis.
Some inhibitors of 17β-HSD type I have been identified, for example esters of cinnamic acid and various flavones (e.g. fisetin).