Disease relevance of Dhrs9

• Functional and immunological relationships between metyrapone reductase from mouse liver microsomes and 3 alpha-hydroxysteroid dehydrogenase from Pseudomonas testosteroni [1].

High impact information on Dhrs9

• ALLO and THDOC are synthesized in the brain from progesterone or deoxycorticosterone, respectively, by the sequential action of two enzymes: 5alpha-reductase (5alpha-R) type I and 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) [2].
• Using glutamic acid decarboxylase 67/65 antibodies to mark GABAergic neurons, we failed to detect 5alpha-R type I and 3alpha-HSD in cortical and hippocampal GABAergic interneurons [2].
• Neither 5alpha-R type I nor 3alpha-HSD mRNAs are expressed in S100beta- or glial fibrillary acidic protein-positive glial cells [2].
• We demonstrate that 5alpha-R type I and 3alpha-HSD colocalize in cortical, hippocampal, and olfactory bulb glutamatergic principal neurons and in some output neurons of the amygdala and thalamus [2].
• This study evaluates 5alpha-R type I and 3alpha-HSD mRNA expression level in mouse brain by using in situ hybridization combined with glutamic acid decarboxylase 67/65, vesicular glutamate transporter 2, glial fibrillary acidic protein, and S100beta immunohistochemistry [2].

Chemical compound and disease context of Dhrs9

• Carbonyl reduction was investigated in liver microsomes of 8 vertebrate species, as well as in insect larvae total homogenate and in purified 3 alpha-hydroxysteroid dehydrogenase preparations of the procaryont Pseudomonas testosteroni, using the ketone compound 2-methyl-1,2 di-(3-pyridyl)-1-propanone (metyrapone) as substrate [3].

Biological context of Dhrs9

• This hepatic dihydrodiol dehydrogenase demonstrates significant sequence homology with the cytosolic rat bile acid binder 3 alpha-hydroxysteroid dehydrogenase and other members of the monomeric oxidoreductase gene family [4].
• Enzymes that synthesize 3 alpha-Adiol, including 5 alpha-reductase type 1 and 3 alpha-hydroxysteroid dehydrogenase, are induced in wild type uterus during late gestation [5].
• The presence of specific binding sites for estrogen and androgens as well as the presence of the two major enzymatic pathways involved in modulation of androgen action (the 5 alpha-reductase/3 alpha-hydroxysteroid dehydrogenase and the aromatase) have been studied in the GT1-1 clone [6].
• 5 alpha-Reductive conversion (by 5 alpha-reductase) of testosterone and progesterone into dihydrotestosterone and dihydroprogesterone, and subsequent 3-alpha hydroxylation (by 3 alpha-hydroxysteroid dehydrogenase) to 3 alpha-diol and tetrahydroprogesterone were assayed in the cultures at 35, 38 and 45 days in vitro [7].

Anatomical context of Dhrs9

• Purification and characterization of NADP+-dependent 3 alpha-hydroxysteroid dehydrogenase from mouse liver cytosol [8].

Associations of Dhrs9 with chemical compounds

• In contrast, androgen-metabolizing enzyme mRNA species had either normal (3 alpha-hydroxysteroid dehydrogenase) or higher expression (5 alpha R-1) levels in IGF-I-null mice (P < 0.05) relative to wild-type controls [9].
• 3 alpha-Hydroxysteroid dehydrogenase activity converting dihydroprogesterone but not dihydrotestosterone was increased at 38 and 42 days in vitro [7].
• 5. Synthesis and inactivation of 5alpha-dihydrotestosterone occur through 5alpha-reductase and 3alpha-HSD activities, respectively [10].

References