EC Number   |
General Information |
Reference |
|---|
    1.1.1.270 | drug target |
inhibition of 3beta-hydroxysteroid dehydrogenase type 1 suppresses interleukin-6 in breast cancer. The therapeutic potential of targeting HSD3B1 is in part mediated by IL-6 suppression |
763404 |
| 1.1.1.270 | drug target |
selective inhibition of 3beta-HSD1 may prevent spontaneous premature birth. Inhibition of 3beta-HSD1 decreases placental estradiol production that promotes labor. The 3beta-HSD1 inhibitor may be administered with 17alpha-hydroxyprogesterone caproate |
763397 |
| 1.1.1.270 | evolution |
human 3beta-hydroxysteroid dehydrogenase is a member of the short-chain dehydrogenase/reductase (SDR) family of enzymes, all of which contain the Rossmann-fold domain with a beta-alpha-beta-alpha-beta-alpha-beta-alpha-beta folding pattern that binds cofactor and substrate |
725813 |
| 1.1.1.270 | evolution |
the rabbit aldose reductase-like protein that shars an 86% sequence identity to human aldo-keto reductase (AKR) 1B10 and is assigned as AKR1B19 in the AKR superfamily. It is bifunctional and also acts as a 3-ketoreductase reducing 3-keto-5alpha/beta-dihydro-C19/C21/C24-steroids into the corresponding 3betahydroxysteroids |
724124 |
| 1.1.1.270 | malfunction |
interleukin-6 treatment partially reduces the cytotoxicity augmented by the HSD3B1 knockdown |
763404 |
| 1.1.1.270 | malfunction |
single and double mutations, F303Q, M304S and F303Q/M304S, significantly impair the 3-ketoreductase activity, suggesting that the two residues play critical roles in recognition of the steroidal substrate |
724124 |
| 1.1.1.270 | malfunction |
two Botrytis cinerea fenhexamid-resistant phenotypes both result from mutations in the erg27 gene encoding 3-ketoreductase. Erg27 mutations causing amino acid substitutions in or near the transmembrane domain strongly decrease the affinity of fenhexamid for 3-ketoreductase |
726098 |
| 1.1.1.270 | metabolism |
expression of 3beta-hydroxysteroid dehydrogenase type 1 (HSD3B1) in breast cancer is associated with shorter recurrence-free survival, and genetic or pharmacologic inhibition of HSD3B1 reduced colony formation and xenograft growth |
763404 |
| 1.1.1.270 | metabolism |
the 3-ketoreductase is involved at C-4 demethylation steps during ergosterol biosynthesis. Steryl compound contents of Botrytis strains with different fenhexamid susceptibilities, overview |
726098 |
| 1.1.1.270 | metabolism |
the anti-apoptotic protein GRP78 is a key regulatory protein related to 17beta-HSD7 inhibition and effect |
763396 |
