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Studies indicate that mutations in aldo-keto reductase family 1 (AKR1) enzymes AKR1C1 (show DDH ELISA Kits) and AKR1C4 are responsible for sexual development dysgenesis and mutations in AKR1D1 (show AKR1D1 ELISA Kits) are causative in bile-acid deficiency.
In women only, SNPs in AKR1C4 reduced the likelihood of having exhibited paranoid ideation by circa 60%.
Low progesterone levels and a cystine to serine change at position 145 in AKR1C4 gene are associated with manic/hypomanic irritability in males
role of AKR1C4 in the metabolism of testosterone and progesterone via the 5beta-reductase pathway.
Taken together, we conclude that the cell-type-specific expression of DD4 mRNA is regulated by vHNF-1 (show HNF1B ELISA Kits)-C.
the expression level of DD4 mRNA is cooperatively regulated by the amounts of HNF-1 alpha, HNF-4 alpha and HNF-4 gamma.
Impact of mirtazapine on the activity of a key neurosteroidogenic enzyme, the 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD (show DHRS9 ELISA Kits)), and on the levels of neuroactive steroids in relation to clinical response in depression.
Structure determination of human AKR1C4 and homology modelling of AKR1D1 (show AKR1D1 ELISA Kits) followed by docking experiments were used to explore active site geometries.
This gene encodes a member of the aldo\\/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and\\/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the bioreduction of chlordecone, a toxic organochlorine pesticide, to chlordecone alcohol in liver. This gene shares high sequence identity with three other gene members and is clustered with those three genes at chromosome 10p15-p14.
, aldo-keto reductase family 1 member C4
, chlordecone reductase; 3-alpha hydroxysteroid dehydrogenase, type I; dihydrodiol dehydrogenase 4
, dihydrodiol dehydrogenase isozyme DD4
, type I 3-alpha-hydroxysteroid dehydrogenase