Hydroxysteroid Dehydrogenases: Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.3-Hydroxysteroid Dehydrogenases: Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.17-Hydroxysteroid Dehydrogenases: A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.20-Hydroxysteroid Dehydrogenases: A group of enzymes that catalyze the reversible reduction-oxidation reaction of 20-hydroxysteroids, such as from a 20-ketosteroid to a 20-alpha-hydroxysteroid (EC 1.1.1.149) or to a 20-beta-hydroxysteroid (EC 1.1.1.53).3-alpha-Hydroxysteroid Dehydrogenase (B-Specific): A 3-hydroxysteroid dehydrogenase which catalyzes the reversible reduction of the active androgen, DIHYDROTESTOSTERONE to 5 ALPHA-ANDROSTANE-3 ALPHA,17 BETA-DIOL. It also has activity towards other 3-alpha-hydroxysteroids and on 9-, 11- and 15- hydroxyprostaglandins. The enzyme is B-specific in reference to the orientation of reduced NAD or NADPH.11-beta-Hydroxysteroid Dehydrogenase Type 2: An high-affinity, NAD-dependent 11-beta-hydroxysteroid dehydrogenase that acts unidirectionally to catalyze the dehydrogenation of CORTISOL to CORTISONE. It is found predominantly in mineralocorticoid target tissues such as the KIDNEY; COLON; SWEAT GLANDS; and the PLACENTA. Absence of the enzyme leads to a fatal form of childhood hypertension termed, APPARENT MINERALOCORTICOID EXCESS SYNDROME.11-beta-Hydroxysteroid Dehydrogenase Type 1: A low-affinity 11 beta-hydroxysteroid dehydrogenase found in a variety of tissues, most notably in LIVER; LUNG; ADIPOSE TISSUE; vascular tissue; OVARY; and the CENTRAL NERVOUS SYSTEM. The enzyme acts reversibly and can use either NAD or NADP as cofactors.11-beta-Hydroxysteroid Dehydrogenases: Hydroxysteroid dehydrogenases that catalyzes the reversible conversion of CORTISOL to the inactive metabolite CORTISONE. Enzymes in this class can utilize either NAD or NADP as cofactors.Estradiol Dehydrogenases: Enzymes that catalyze the oxidation of estradiol at the 17-hydroxyl group in the presence of NAD+ or NADP+ to yield estrone and NADH or NADPH. The 17-hydroxyl group can be in the alpha- or beta-configuration. EC 1.1.1.62Sulfotransferases: Enzymes which transfer sulfate groups to various acceptor molecules. They are involved in posttranslational sulfation of proteins and sulfate conjugation of exogenous chemicals and bile acids. EC 2.8.2.Cortisone: A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)Steroid 17-alpha-Hydroxylase: A microsomal cytochrome P450 enzyme that catalyzes the 17-alpha-hydroxylation of progesterone or pregnenolone and subsequent cleavage of the residual two carbons at C17 in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP17 gene, generates precursors for glucocorticoid, androgen, and estrogen synthesis. Defects in CYP17 gene cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL) and abnormal sexual differentiation.Alcohol Oxidoreductases: A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).Steroids: A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)NAD: A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.L-Lactate Dehydrogenase: A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.Testosterone: A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.Kinetics: The rate dynamics in chemical or physical systems.Androsterone: A metabolite of TESTOSTERONE or ANDROSTENEDIONE with a 3-alpha-hydroxyl group and without the double bond. The 3-beta hydroxyl isomer is epiandrosterone.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Alcohol Dehydrogenase: A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.Glyceraldehyde-3-Phosphate Dehydrogenases: Enzymes that catalyze the dehydrogenation of GLYCERALDEHYDE 3-PHOSPHATE. Several types of glyceraldehyde-3-phosphate-dehydrogenase exist including phosphorylating and non-phosphorylating varieties and ones that transfer hydrogen to NADP and ones that transfer hydrogen to NAD.20-alpha-Hydroxysteroid Dehydrogenase: An enzymes that catalyzes the reversible reduction-oxidation reaction of 20-alpha-hydroxysteroids, such as from PROGESTERONE to 20-ALPHA-DIHYDROPROGESTERONE.Aldehyde Dehydrogenase: An enzyme that oxidizes an aldehyde in the presence of NAD+ and water to an acid and NADH. This enzyme was formerly classified as EC 1.1.1.70.Glutamate Dehydrogenase: An enzyme that catalyzes the conversion of L-glutamate and water to 2-oxoglutarate and NH3 in the presence of NAD+. (From Enzyme Nomenclature, 1992) EC 1.4.1.2.Glucosephosphate DehydrogenaseMalate Dehydrogenase: An enzyme that catalyzes the conversion of (S)-malate and NAD+ to oxaloacetate and NADH. EC 1.1.1.37.Isocitrate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the conversion of isocitrate and NAD+ to yield 2-ketoglutarate, carbon dioxide, and NADH. It occurs in cell mitochondria. The enzyme requires Mg2+, Mn2+; it is activated by ADP, citrate, and Ca2+, and inhibited by NADH, NADPH, and ATP. The reaction is the key rate-limiting step of the citric acid (tricarboxylic) cycle. (From Dorland, 27th ed) (The NADP+ enzyme is EC 1.1.1.42.) EC 1.1.1.41.Phosphoadenosine Phosphosulfate: 3'-Phosphoadenosine-5'-phosphosulfate. Key intermediate in the formation by living cells of sulfate esters of phenols, alcohols, steroids, sulfated polysaccharides, and simple esters, such as choline sulfate. It is formed from sulfate ion and ATP in a two-step process. This compound also is an important step in the process of sulfur fixation in plants and microorganisms.Arylsulfotransferase: A sulfotransferase that catalyzes the sulfation of a phenol in the presence of 3'-phosphoadenylylsulfate as sulfate donor to yield an aryl sulfate and adenosine 3',5'-bisphosphate. A number of aromatic compounds can act as acceptors; however, organic hydroxylamines are not substrates. Sulfate conjugation by this enzyme is a major pathway for the biotransformation of phenolic and catechol drugs as well as neurotransmitters. EC 2.8.2.1.Ketosteroids: Steroid derivatives formed by oxidation of a methyl group on the side chain or a methylene group in the ring skeleton to form a ketone.Dihydrolipoamide Dehydrogenase: A flavoprotein containing oxidoreductase that catalyzes the reduction of lipoamide by NADH to yield dihydrolipoamide and NAD+. The enzyme is a component of several MULTIENZYME COMPLEXES.NADP: Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5'-phosphate (NMN) coupled by pyrophosphate linkage to the 5'-phosphate adenosine 2',5'-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed)Carbohydrate Dehydrogenases: Reversibly catalyze the oxidation of a hydroxyl group of carbohydrates to form a keto sugar, aldehyde or lactone. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.; EC 1.1.2.; and 1.1.99.Succinate Dehydrogenase: A flavoprotein containing oxidoreductase that catalyzes the dehydrogenation of SUCCINATE to fumarate. In most eukaryotic organisms this enzyme is a component of mitochondrial electron transport complex II.L-Iditol 2-Dehydrogenase: An alcohol oxidoreductase which catalyzes the oxidation of L-iditol to L-sorbose in the presence of NAD. It also acts on D-glucitol to form D-fructose. It also acts on other closely related sugar alcohols to form the corresponding sugar. EC 1.1.1.14Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.Glycerolphosphate DehydrogenaseSubstrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.Glucose 1-Dehydrogenase: A glucose dehydrogenase that catalyzes the oxidation of beta-D-glucose to form D-glucono-1,5-lactone, using NAD as well as NADP as a coenzyme.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Ketoglutarate Dehydrogenase ComplexAldehyde Oxidoreductases: Oxidoreductases that are specific for ALDEHYDES.Glucose Dehydrogenases: D-Glucose:1-oxidoreductases. Catalyzes the oxidation of D-glucose to D-glucono-gamma-lactone and reduced acceptor. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.47; EC 1.1.1.118; EC 1.1.1.119 and EC 1.1.99.10.Phosphogluconate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the reaction 6-phospho-D-gluconate and NADP+ to yield D-ribulose 5-phosphate, carbon dioxide, and NADPH. The reaction is a step in the pentose phosphate pathway of glucose metabolism. (From Dorland, 27th ed) EC 1.1.1.43.Sugar Alcohol Dehydrogenases: Reversibly catalyzes the oxidation of a hydroxyl group of sugar alcohols to form a keto sugar, aldehyde or lactone. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.; EC 1.1.2. and EC 1.1.99.Stereoisomerism: The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)Acyl-CoA Dehydrogenases: Enzymes that catalyze the first step in the beta-oxidation of FATTY ACIDS.NADH Dehydrogenase: A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC 1.6.2.1.IMP Dehydrogenase: An enzyme that catalyzes the dehydrogenation of inosine 5'-phosphate to xanthosine 5'-phosphate in the presence of NAD. EC 1.1.1.205.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Lactate Dehydrogenases: Alcohol oxidoreductases with substrate specificity for LACTIC ACID.Gene Expression Regulation, Enzymologic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.Isoenzymes: Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.Formate Dehydrogenases: Flavoproteins that catalyze reversibly the reduction of carbon dioxide to formate. Many compounds can act as acceptors, but the only physiologically active acceptor is NAD. The enzymes are active in the fermentation of sugars and other compounds to carbon dioxide and are the key enzymes in obtaining energy when bacteria are grown on formate as the main carbon source. They have been purified from bovine blood. EC 1.2.1.2.Acyl-CoA Dehydrogenase: A flavoprotein oxidoreductase that has specificity for medium-chain fatty acids. It forms a complex with ELECTRON TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.Xanthine Dehydrogenase: An enzyme that catalyzes the oxidation of XANTHINE in the presence of NAD+ to form URIC ACID and NADH. It acts also on a variety of other purines and aldehydes.3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide): A ketone oxidoreductase that catalyzes the overall conversion of alpha-keto acids to ACYL-CoA and CO2. The enzyme requires THIAMINE DIPHOSPHATE as a cofactor. Defects in genes that code for subunits of the enzyme are a cause of MAPLE SYRUP URINE DISEASE. The enzyme was formerly classified as EC 1.2.4.3.Hydroxybutyrate DehydrogenaseBase Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Pyruvate Dehydrogenase (Lipoamide): The E1 component of the multienzyme PYRUVATE DEHYDROGENASE COMPLEX. It is composed of 2 alpha subunits (pyruvate dehydrogenase E1 alpha subunit) and 2 beta subunits (pyruvate dehydrogenase E1 beta subunit).3-Hydroxyacyl CoA Dehydrogenases: Enzymes that reversibly catalyze the oxidation of a 3-hydroxyacyl CoA to 3-ketoacyl CoA in the presence of NAD. They are key enzymes in the oxidation of fatty acids and in mitochondrial fatty acid synthesis.Ketone Oxidoreductases: Oxidoreductases that are specific for KETONES.Oxidoreductases: The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)Sulfates: Inorganic salts of sulfuric acid.Dihydrouracil Dehydrogenase (NADP): An oxidoreductase involved in pyrimidine base degradation. It catalyzes the catabolism of THYMINE; URACIL and the chemotherapeutic drug, 5-FLUOROURACIL.Uridine Diphosphate Glucose Dehydrogenase: An enzyme that catalyzes the oxidation of UDPglucose to UDPglucuronate in the presence of NAD+. EC 1.1.1.22.Catalysis: The facilitation of a chemical reaction by material (catalyst) that is not consumed by the reaction.Glucosephosphate Dehydrogenase Deficiency: A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of GLUCOSE-6-PHOSPHATE DEHYDROGENASE activity in erythrocytes, leading to hemolytic anemia.
(1/103) Characterization of homogeneous recombinant rat ovarian 20alpha-hydroxysteroid dehydrogenase: fluorescent properties and inhibition profile.

In rat ovary, 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD), a member of the aldo-keto reductase (AKR) superfamily, converts progesterone into the inactive progestin 20alpha-hydroxyprogesterone and has been implicated in the termination of pregnancy. Here we report a convenient overexpression system that permits the purification of milligram quantities of homogeneous recombinant 20alpha-HSD with wild-type enzyme activity. The availability of this enzyme has permitted detailed kinetic, inhibition and fluorescence analyses. The enzyme exhibited narrow steroid specificity, catalysing reactions only at C-20; it reduced progesterone and 17alpha-hydroxyprogesterone and oxidized 20alpha-hydroxypregnanes. It also turned over common AKR substrates, such as 9, 10-phenanthrenequinone and 4-nitrobenzaldehyde. The intrinsic fluorescence spectrum of 20alpha-HSD was characterized and was quenched on the binding of NADP(H), yielding a KNADPd of 0.36 microM and a KNADPHd of 0.64 microM. NADP(H) binding generated an energy transfer band that could not be quenched by steroids. Inhibition studies conducted with non-steroidal and steroidal anti-inflammatory drugs and synthetic oestrogens indicated that even though rat ovarian 20alpha-HSD and rat liver 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) share more than 67% amino acid identity, their inhibition profiles are markedly different. Unlike 3alpha-HSD, most of these compounds did not inhibit 20alpha-HSD. Only meclofenamic acid and hexoestrol were potent competitive inhibitors for 20alpha-HSD, yielding K(i) values of 18.9 and 14.3 microM respectively. These studies suggest that selective non-steroidal AKR inhibitors could be developed for 20alpha-HSD that might be useful in maintaining pregnancy and that specific inhibitors might be developed from either N-phenylanthranilates or biphenols.  (+info)

(2/103) 26-cholesterol hydroxylase in rat corpora lutea: A negative regulator of progesterone secretion.

From a subtracted cDNA library of rat luteal tissue, where cDNA fragments in functional luteal tissue were subtracted from those in regressing luteal tissue, a cDNA clone corresponding to 26-cholesterol hydroxylase (P450(C26)) was obtained. It is known that P450(C26) catalyzes the conversion of cholesterol to 26-hydroxycholesterol, which blocks cholesterol utilization in the cell, and that 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) catalyzes the conversion of progesterone to an inactive steroid, 20alpha-dihydroprogesterone (20alpha-OHP). Thus, using pseudopregnant rats as a model, physiological cooperation of P450(C26) and 20alpha-HSD in the reduction of progesterone release toward the end of the luteal phase was evaluated. Levels of P450(C26) and 20alpha-HSD mRNA were examined in corpora lutea from pseudopregnant rats by Northern blot or reverse transcription-polymerase chain reaction or both. P450(C26) mRNA was ubiquitously expressed in corpora lutea, and its expression increased toward the end of pseudopregnancy, while 20alpha-HSD was expressed in all corpora lutea on Day 16 (Day 0 = the day of after cervical stimulation) but not detected before Day 10. An inhibitor of 20alpha-HSD, STZ26 (D-homo-16-oxa-4-androstene-3,16alpha-dione), was administered at various doses to rats from Day 12 to 20, effectively suppressing the elevation of 20alpha-OHP in a dose-dependent manner but not the depletion of progesterone completely. The expression of P450(C26) mRNA was increased as STZ26 dose increased, which negatively correlated with the progesterone levels. These results strongly suggest that P450(C26) cooperated with 20alpha-HSD in the reduction of progesterone release from the rat luteal tissue at the end of the functional luteal phase.  (+info)

(3/103) Conversion of mammalian 3alpha-hydroxysteroid dehydrogenase to 20alpha-hydroxysteroid dehydrogenase using loop chimeras: changing specificity from androgens to progestins.

Hydroxysteroid dehydrogenases (HSDs) regulate the occupancy and activation of steroid hormone receptors by converting potent steroid hormones into their cognate inactive metabolites. 3alpha-HSD catalyzes the inactivation of androgens in the prostate by converting 5alpha-dihydrotestosterone to 3alpha-androstanediol, where excess 5alpha-dihydrotestosterone is implicated in prostate disease. By contrast, 20alpha-HSD catalyzes the inactivation of progestins in the ovary and placenta by converting progesterone to 20alpha-hydroxyprogesterone, where progesterone is essential for maintaining pregnancy. Mammalian 3alpha-HSDs and 20alpha-HSDs belong to the aldo-keto reductase superfamily and share 67% amino acid sequence identity yet show positional and stereospecificity for the formation of secondary alcohols on opposite ends of steroid hormone substrates. The crystal structure of 3alpha-HSD indicates that the mature steroid binding pocket consists of 10 residues located on five loops, including loop A and the mobile loops B and C. 3alpha-HSD was converted to 20alpha-HSD by replacing these loops with those found in 20alpha-HSD. However, when pocket residues in 3alpha-HSD were mutated to those found in 20alpha-HSD altered specificity was not achieved. Replacement of loop A created a 17beta-HSD activity that was absent in either 3alpha- or 20alpha-HSD. Once loops A and C were replaced, the chimera had both 3alpha- and 20alpha-HSD activity. When loops A, B, and C were substituted, 3alpha-HSD was converted to a stereospecific 20alpha-HSD with a resultant shift in k(cat)/K(m) for the desired reaction of 2 x 10(11). This study represents an example where sex hormone specificity can be changed at the enzyme level.  (+info)

(4/103) Prostaglandin F2alpha-induced expression of 20alpha-hydroxysteroid dehydrogenase involves the transcription factor NUR77.

Prostaglandin F(2)alpha (PGF(2)alpha) binding to its receptor on the rat corpus luteum triggers various signal transduction pathways that lead to the activation of a steroidogenic enzyme, 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD), which in turn catabolizes progesterone. The molecular mechanism underlying PGF(2)alpha-induced 20alpha-HSD enzyme activity has not yet been explored. In this report we show, using mice lacking PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha is responsible for the rapid and massive expression of the 20alpha-HSD gene at the end of pregnancy leading to a decrease in progesterone secretion. We also present evidence that PGF(2)alpha enhances 20alpha-HSD promoter activity. We have determined a region upstream of the -1590 position in the 20alpha-HSD promoter that confers regulation by PGF(2)alpha in ovarian primary cells. This region encompasses a unique transcription factor-binding site with a sequence of a NUR77 response element. Deletion of this motif or overexpression of a NUR77 dominant negative protein caused a complete loss of 20alpha-HSD promoter activation by PGF(2)alpha. NUR77 also transactivated the 20alpha-HSD promoter in transient transfection experiments in corpus luteum-derived cells (GG-CL). This induction required the NUR77-transactivating domain. We also show that PGF(2)alpha induces a very rapid expression of NUR77 that binds to a distal response element located at -1599/-1606 but does not interact with another proximal putative NUR77 response element located downstream in the promoter. A rapid increase in NUR77 mRNA was observed in mice corpora lutea just before parturition at a time when 20alpha-HSD becomes expressed. This increase in the expression of both genes was not seen in PGF(2)alpha receptor knockout mice. By using cyclosporin A and PGF(2)alpha treatment, we established that inhibition of NUR77 DNA binding in vivo prevents PGF(2)alpha induction of the 20alpha-HSD gene in the corpus luteum. Taken together, our results demonstrate, for the first time, that PGF(2)alpha induces in the corpus luteum the expression of the nuclear orphan receptor and transcription factor, NUR77, which in turn leads to the transcriptional stimulation of 20alpha-HSD, triggering the decrease in serum progesterone essential for parturition.  (+info)

(5/103) Characterization of a human 20alpha-hydroxysteroid dehydrogenase.

It has been suggested that 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) is a T-cell differentiation marker in mice. In the human, this enzyme has generally been associated with types 1 and 2 17beta-HSDs, which belong to the short-chain alcohol dehydrogenase family, whereas the rat, rabbit, pig and bovine 20alpha-HSDs are members of the aldoketo reductase superfamily, which also includes the 3alpha-HSD family. In this study, we report the cloning, from a human skin cDNA library, of a cDNA that shows, after transfection into human embryonic kidney (HEK-293) cells, high 20alpha-HSD activity but negligible 3alpha- and 17beta-hydroxysteroid dehydrogenase activities. A comparison of the amino acid sequence of the human 20alpha-HSD with those of other related 20alpha- and 3alpha-HSDs indicates that the human 20alpha-HSD shares 79.9, 68.7 and 52.3% identity with rabbit, rat and bovine 20alpha-HSDs, whereas it shows 97, 84 and 65% identity with human type 3, type 1 and rat 3alpha-HSDs. In contrast, the enzyme shares only 15.2 and 15.0% identity with type 1 and type 2 human 17beta-HSDs. DNA analysis predicts a protein of 323 amino acids, with a calculated molecular weight of 36 767 Da. In intact transfected cells, the human 20alpha-HSD preferentially catalyzes the reduction of progesterone to 20alpha-hydroxyprogesterone with a K(m) value of 0.6 microM, the reverse reaction (oxidation) being negligible. In a cell cytosolic preparation, the enzyme could use both NADPH and NADH as cofactors, but NADPH, which gave 4-fold lower K(m) values, was preferred. We detected the expression of 20alpha-HSD mRNA in liver, prostate, testis, adrenal, brain, uterus and mammary-gland tissues and in human keratinocyte (HaCaT) cells. The present study clearly indicates that the genuine human 20alpha-HSD belongs to the aldoketo reductase family, like the 20alpha-HSDs from other species.  (+info)

(6/103) The reactive oxygen species--and Michael acceptor-inducible human aldo-keto reductase AKR1C1 reduces the alpha,beta-unsaturated aldehyde 4-hydroxy-2-nonenal to 1,4-dihydroxy-2-nonene.

The human aldo-keto reductase AKR1C1 (20alpha(3alpha)-hydroxysteroid dehydrogenase) is induced by electrophilic Michael acceptors and reactive oxygen species (ROS) via a presumptive antioxidant response element (Burczynski, M. E., Lin, H. K., and Penning, T. M. (1999) Cancer Res. 59, 607-614). Physiologically, AKR1C1 regulates progesterone action by converting the hormone into its inactive metabolite 20alpha-hydroxyprogesterone, and toxicologically this enzyme activates polycyclic aromatic hydrocarbon trans-dihydrodiols to redox-cycling o-quinones. However, the significance of its potent induction by Michael acceptors and oxidative stress is unknown. 4-Hydroxy-2-nonenal (HNE) and other alpha,beta-unsaturated aldehydes produced during lipid peroxidation were reduced by AKR1C1 with high catalytic efficiency. Kinetic studies revealed that AKR1C1 reduced HNE (K(m) = 34 microm, k(cat) = 8.8 min(-1)) with a k(cat)/K(m) similar to that for 20alpha-hydroxysteroids. Six other homogeneous recombinant AKRs were examined for their ability to reduce HNE. Of these, AKR1C1 possessed one of the highest specific activities and was the only isoform induced by oxidative stress and by agents that deplete glutathione (ethacrynic acid). Several hydroxysteroid dehydrogenases of the AKR1C subfamily catalyzed the reduction of HNE with higher activity than aldehyde reductase (AKR1A1). NMR spectroscopy identified the product of the NADPH-dependent reduction of HNE as 1,4-dihydroxy-2-nonene. The K(m) of recombinant AKR1C1 for nicotinamide cofactors (K(m) NADPH approximately 6 microm, K(m)(app) NADH >6 mm) suggested that it is primed for reductive metabolism of HNE. Isoform-specific reverse transcription-polymerase chain reaction showed that exposure of HepG2 cells to HNE resulted in elevated levels of AKR1C1 mRNA. Thus, HNE induces its own metabolism via AKR1C1, and this enzyme may play a hitherto unrecognized role in a response mounted to counter oxidative stress. AKRs represent alternative GSH-independent/NADPH-dependent routes for the reductive elimination of HNE. Of these, AKR1C1 provides an inducible cytosolic barrier to HNE following ROS exposure.  (+info)

(7/103) Characterization of the oxidative 3alpha-hydroxysteroid dehydrogenase activity of human recombinant 11-cis-retinol dehydrogenase.

11-cis-Retinol dehydrogenase catalyzes the oxidation of cis-retinols, a rate-limiting step in the biosynthesis of 9-cis-retinoic acid. It is also active toward 3alpha-hydroxysteroids, and thus might be involved in steroid metabolism. To better understand the role of this enzyme, we produced stable transfectants expressing 11-cis-retinol dehydrogenase in human embryonic kidney 293 cells. In vitro enzymatic assays have demonstrated that, with an appropriate exogenous cofactor, the enzyme catalyzes the interconversion of 5alpha-androstane-3alpha,17beta-diol and dihydrotestosterone and that of androsterone and androstanedione. However, using intact transfected cells, we found that the enzyme catalyzes reactions only in the oxidative direction. Thus, it is possible that 5alpha-androstane-3alpha,17beta-diol (an inactive androgen) can be converted into dihydrotestosterone, the most potent androgen, by the action of 11-cis-retinol dehydrogenase. This reaction could constitute a non-classical pathway of production of active androgens in the peripheral tissues. We also showed that all-trans-, 9-cis- and 13-cis-retinol inhibit the oxidative 3alpha-hydroxysteroid steroid activity of 11-cis-retinol dehydrogenase with similar K(i) values. Since all-trans-retinol is a precursor of cis-retinols, its inhibitory effect on the activity suggests that it could play an important role in modulating the formation of 9-cis-retinoic acid. In addition, we examined the effect of several known enzyme modulators, namely carbenoxolone, phenylarsine oxide and phosphatidylcholine, on 11-cis-retinol dehydrogenase activity. Taken together, our results suggest that, in humans, this enzyme might play a role in the biosynthesis of both 9-cis-retinoic acid and dihydrotestosterone.  (+info)

(8/103) Dietary indoles and isothiocyanates that are generated from cruciferous vegetables can both stimulate apoptosis and confer protection against DNA damage in human colon cell lines.

The natural indoles 3,3'-diindolylmethane (DIM), ascorbigen (ASG), indole-3-carbinol (I3C), and indolo[3,2-b]carbazole (ICZ), as well as the natural isothiocyanates sulforaphane (SUL), benzyl isothiocyanate (BITC) and phenethyl isothiocyanate (PEITC), all possess cancer chemopreventive properties. It is now shown that DIM, ICZ, SUL, and BITC can each stimulate apoptosis in human colon adenocarcinoma LS-174 and Caco-2 cells. Treatment of LS-174 cells with nontoxic doses of DIM, ASG, I3C, or ICZ affected an increase of up to 21-fold in cytochrome P450 1A1 (CYP1A1). None of these indoles caused an elevation in either aldo-keto reductase 1C1 (AKR1C1) or the gamma-glutamylcysteine synthetase heavy subunit (GCS(h)), but DIM, I3C, and ICZ produced a very modest increase in NAD(P)H:quinone oxidoreductase 1 (NQO1). By contrast, nontoxic doses of SUL, BITC, or PEITC failed to induce expression of CYP1A1 in LS-174 cells, but caused an increase of between 11- and 17-fold in the protein levels of AKR1C1, NQO1, and GCS(h). Treatment of the colon cell line with ICZ or SUL caused increases in the levels of mRNA for CYP1A1, AKR1C1, and NQO1 that were consistent with the enzyme data. Exposure of Caco-2 cells to media containing indoles or isothiocyanates gave similar results to those obtained using LS-174 cells. Evidence is presented that the ability of indoles and isothiocyanates to stimulate either xenobiotic response element- or antioxidant response element-driven gene expression accounts for the two groups of phytochemicals inducing different gene batteries. Pretreatment of LS-174 cells for 24 h with ICZ and SUL before exposure for 24 h to benzo(a)pyrene (BaP) reduced to <20% the number of single-strand DNA breaks produced by the carcinogen. Neither ICZ alone nor SUL alone were able to confer the same degree of protection against DNA damage produced by BaP as they achieved in combination. Similar results were obtained with H(2)O(2) as the genotoxic agent. Together, these phytochemicals may prevent colon tumorigenesis by both stimulating apoptosis and enhancing intracellular defenses against genotoxic agents.  (+info)

*  20alpha-hydroxysteroid dehydrogenase
Other names in common use include 20alpha-hydroxy steroid dehydrogenase, 20alpha-hydroxy steroid dehydrogenase, 20alpha-HSD, ... "Expression of 17beta-hydroxysteroid dehydrogenase type 1 and type 2, P450 aromatase, and 20alpha-hydroxysteroid dehydrogenase ... Hershkovitz L, Beuschlein F, Klammer S, Krup M, Weinstein Y (March 2007). "Adrenal 20alpha-hydroxysteroid dehydrogenase in the ... Weinstein Y (October 1977). "20alpha-hydroxysteroid dehydrogenase: a T lymphocyte-associated enzyme". J. Immunol. 119 (4): 1223 ...
*  3alpha(or 20beta)-hydroxysteroid dehydrogenase
20beta-hydroxysteroid dehydrogenase, 3alpha,20beta-hydroxysteroid:NAD+-oxidoreductase, NADH-20beta-hydroxysteroid dehydrogenase ... In enzymology, a 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53) is an enzyme that catalyzes the chemical reaction ... The systematic name of this enzyme class is 3alpha(or 20beta)-hydroxysteroid:NAD+ oxidoreductase. Other names in common use ... dehydrogenase, 20beta-hydroxy steroid, Delta4-3-ketosteroid hydrogenase, ...
*  Indanol dehydrogenase
... α-Hydroxysteroid Dehydrogenase Activity of Monkey Liver Indanol Dehydrogenase". J. Biochem. Tokyo. 106 (5): 900-3. PMID 2559080 ... In enzymology, an indanol dehydrogenase (EC 1.1.1.112) is an enzyme that catalyzes the chemical reaction indan-1-ol + NAD(P ... Hara A, Nakagawa M, Taniguchi H, Sawada H (November 1989). "3(20) ...
*  3beta(or 20alpha)-hydroxysteroid dehydrogenase
... hydroxysteroid dehydrogenase (EC 1.1.1.210) is an enzyme that catalyzes the chemical reaction 5α-androstan-3β,17β-diol + NADP+ ... H+ This enzyme possesses the combined activities of the 3-β-hydroxysteroid dehydrogenase/Δ-5-4 isomerase and 20-α- ... hydroxysteroid dehydrogenase enzymes. Sharaf MA, Sweet F (September 1982). "Dual activity at an enzyme active site: 3 beta,20 ... alpha-hydroxysteroid oxidoreductase from fetal blood". Biochemistry. 21 (19): 4615-20. doi:10.1021/bi00262a016. PMID 6958329. ...
*  AKR1C1
3α-hydroxysteroid dehydrogenase, and dihydrodiol dehydrogenase 1/2 is an enzyme that in humans is encoded by the AKR1C1 gene. ... Khanna M, Qin KN, Cheng KC (Jun 1995). "Distribution of 3 alpha-hydroxysteroid dehydrogenase in rat brain and molecular cloning ... Couture JF, Legrand P, Cantin L, Luu-The V, Labrie F, Breton R (Aug 2003). "Human 20alpha-hydroxysteroid dehydrogenase: ... Zhang Y, Dufort I, Rheault P, Luu-The V (Oct 2000). "Characterization of a human 20alpha-hydroxysteroid dehydrogenase". Journal ...
*  Neurosteroid
... while 3β-hydroxysteroid dehydrogenase and hydroxysteroid sulfotransferases are involved in excitatory neurosteroid production. ... 5α-reductase type I and 3α-hydroxysteroid dehydrogenase are involved in the biosynthesis of inhibitory neurosteroids, ... alpha-hydroxysteroid dehydrogenase for neurosteroids and its inhibition by benzodiazepines" (pdf). Biological & Pharmaceutical ... Usami N, Yamamoto T, Shintani S, Ishikura S, Higaki Y, Katagiri Y, Hara A (April 2002). "Substrate specificity of human 3(20) ...
*  Short-chain dehydrogenase
Glucose/ribitol dehydrogenase InterPro: IPR002347 Insect alcohol dehydrogenase family InterPro: IPR002424 2,3-dihydro-2,3- ... alcohol dehydrogenases. Most members of this family are proteins of about 250 to 300 amino acid residues. Most dehydrogenases ... The short-chain dehydrogenases/reductases family (SDR) is a very large family of enzymes, most of which are known to be NAD- or ... Harayama S, Bairoch A, Hartnett C, Rekik M, Ornston LN, Neidle E (1992). "cis-diol dehydrogenases encoded by the TOL pWW0 ...
*  Cloxazolam
... alpha-hydroxysteroid dehydrogenase for neurosteroids and its inhibition by benzodiazepines" (pdf). Biol Pharm Bull. 25 (4): 441 ... Usami N; Yamamoto T; Shintani S; Ishikura S; Higaki Y; Katagiri Y; Hara A. (Apr 2002). "Substrate specificity of human 3(20) ...
*  3β-Hydroxysteroid dehydrogenase
... reductase Δ5-3β-hydroxysteroid dehydrogenase 3β-hydroxy-5-ene steroid dehydrogenase 3β-hydroxy steroid dehydrogenase/isomerase ... steroid-Δ5-3β-ol dehydrogenase 3β-HSDH 5-ene-3β-hydroxysteroid dehydrogenase 3β-hydroxy-5-ene-steroid dehydrogenase 3β-HSD is ... 3β-Hydroxysteroid dehydrogenase/Δ5-4 isomerase (3β-HSD) (EC 1.1.1.145) is an enzyme that catalyzes the biosynthesis of ... Steroidogenic enzyme 3α-Hydroxysteroid dehydrogenase Cravioto MD, Ulloa-Aguirre A, Bermudez JA, Herrera J, Lisker R, Mendez JP ...
*  17β-Hydroxysteroid dehydrogenase
17β-Hydroxysteroid dehydrogenases (17β-HSD, HSD17B) (EC 1.1.1.51), also 17-ketosteroid reductases (17-KSR), are a group of ... Ning X, Yang Y, Deng H, Zhang Q, Huang Y, Su Z, Fu Y, Xiang Q, Zhang S (2017). "Development of 17β-hydroxysteroid dehydrogenase ... Soubhye J, Alard IC, van Antwerpen P, Dufrasne F (2015). "Type 2 17-β hydroxysteroid dehydrogenase as a novel target for the ... Yang SY, He XY, Isaacs C, Dobkin C, Miller D, Philipp M (2014). "Roles of 17β-hydroxysteroid dehydrogenase type 10 in ...
*  11β-Hydroxysteroid dehydrogenase type 1
... , also known as cortisone reductase, is an NADPH-dependent enzyme highly expressed in ... Tannin GM, Agarwal AK, Monder C, New MI, White PC (September 1991). "The human gene for 11 beta-hydroxysteroid dehydrogenase. ... Whorwood CB, Mason JI, Ricketts ML, Howie AJ, Stewart PM (April 1995). "Detection of human 11 beta-hydroxysteroid dehydrogenase ... Pácha J, Lisá V, Miksík I (February 2002). "Effect of cellular differentiation on 11beta-hydroxysteroid dehydrogenase activity ...
*  Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency
In an XX (genetically female) fetus, elevated amounts of DHEA can produce moderate virilization by conversion in the liver to ... Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency is an uncommon form of congenital adrenal ... 3β-hydroxysteroid dehydrogenase (3β-HSD) type II (HSD3B2). As a result, higher levels of 17OH-pregnenolone appear in the blood ... and ambiguous genitalia 3β-Hydroxysteroid dehydrogenase (I, II) Simard J, Moisan AM, Morel Y (August 2002). "Congenital adrenal ...
*  Interleukin 3
He found a T cell derived factor that induced the synthesis of 20alpha-hydroxysteroid dehydrogenase in hematopoietic cells and ... Ihle JN, Pepersack L, Rebar L (June 1981). "Regulation of T cell differentiation: in vitro induction of 20 alpha-hydroxysteroid ... dehydrogenase in splenic lymphocytes from athymic mice by a unique lymphokine". J. Immunol. 126 (6): 2184-9. PMID 6971890. Ihle ...
*  HSD17B2
17β-Hydroxysteroid dehydrogenase 2 (17β-HSD2) is an enzyme of the 17β-hydroxysteroid dehydrogenase (17β-HSD) family that in ... dehydrogenase 2". Moeller G, Adamski J (2006). "Multifunctionality of human 17beta-hydroxysteroid dehydrogenases". Mol. Cell. ... Soubhye J, Alard IC, van Antwerpen P, Dufrasne F (2015). "Type 2 17-β hydroxysteroid dehydrogenase as a novel target for the ... Zhang Y, Word RA, Fesmire S, Carr BR, Rainey WE (Oct 1996). "Human ovarian expression of 17 beta-hydroxysteroid dehydrogenase ...
*  20-Dihydroprogesterone
20α-Dihydroprogesterone (20α-DHP), also known as 20α-hydroxyprogesterone (20α-OHP), is a naturally occurring, endogenous ... It is a metabolite of progesterone, converted by the 20α-hydroxysteroid dehydrogenases AKR1C1 and AKR1C3, and although still ... "Progestins as inhibitors of the human 20-ketosteroid reductases, AKR1C1 and AKR1C3". Chem. Biol. Interact. 191 (1-3): 227-33. ...
*  Anaphrodisiac
Studies have demonstrated that some of these products inhibit 17β-hydroxysteroid dehydrogenase and 17,20-lyase, which catalyzes ...
*  List of OMIM disorder codes
CYP17A1 17-beta-hydroxysteroid dehydrogenase X deficiency; 300438; HSD17B10 2-methylbutyrylglycinuria; 610006; ACADSB 3- ... PC Pyruvate dehydrogenase deficiency; 312170; PDHA1 Pyruvate dehydrogenase E2 deficiency; 245348; DLAT Pyruvate dehydrogenase ... SCARB2 Acyl-CoA dehydrogenase, long chain, deficiency of; 201460; ACADL Acyl-CoA dehydrogenase, medium chain, deficiency of; ... TMPRSS6 Isobutyryl-CoA dehydrogenase deficiency; 611283; ACAD8 Isovaleric acidemia; 243500; IVD IVIC syndrome; 147750; SALL4 ...
*  Follicle-stimulating hormone insensitivity
20-lyase deficiency Combined 17α-hydroxylase/17,20-lyase deficiency 17β-Hydroxysteroid dehydrogenase III deficiency Aromatase ...
*  Abiraterone
... abiraterone inhibits 3β-hydroxysteroid dehydrogenase (3β-HSD), steroid 11β-hydroxylase (CYP11B1), 5α-reductase (via a ... Yin L, Hu Q (January 2014). "CYP17 inhibitors--abiraterone, C17,20-lyase inhibitors and multi-targeting agents". Nature Reviews ... In addition to acting as an irreversible inhibitor of CYP17A1 (17α-hydroxylase/17,20-lyase), ...
*  Amphenone B
... and 3β-hydroxysteroid dehydrogenase, as well as of cholesterol side-chain cleavage enzyme, thereby inhibiting the production of ... It acts as competitive inhibitor of 11β-hydroxylase, 17α-hydroxylase, 17,20-lyase, 21-hydroxylase, ...
*  Leydig cell hypoplasia
20 (3): 199-204. doi:10.1055/s-2002-35384. PMID 12428200. Mendonca BB, Costa EM, Belgorosky A, Rivarola MA, Domenice S (April ... 20-lyase deficiency Combined 17α-hydroxylase/17,20-lyase deficiency 17β-Hydroxysteroid dehydrogenase III deficiency Androgen ...
*  Cyproterone acetate
Stalvey JR (July 2002). "Inhibition of 3beta-hydroxysteroid dehydrogenase-isomerase in mouse adrenal cells: a direct effect of ... Weak inhibitor of 3β-hydroxysteroid dehydrogenase, 17α-hydroxylase/17,20-lyase, and 21-hydroxylase CPA does not have ... and a suppressor of adrenal cortisol and corticosterone production by inhibiting the enzymes 3β-hydroxysteroid dehydrogenase ... It has been reported that as many as 20 to 30% of women treated with the drug for hirsutism (dosage range 25-100 mg) may show ...
*  Hypergonadotropic hypogonadism
17β-hydroxysteroid dehydrogenase III deficiency, and lipoid congenital adrenal hyperplasia. Gonadotropin resistance (e.g., due ... XX gonadal dysgenesis, and mosaicism. Defects in the enzymes involved in the gonadal biosynthesis of the sex hormones - 17α- ... Marschall Stevens Runge; Cam Patterson (20 June 2006). Principles of Molecular Medicine. Humana Press. p. 463. ISBN 978-1-58829 ...
*  Hypoestrogenism
3β-hydroxysteroid dehydrogenase deficiency, and cholesterol side-chain cleavage enzyme or steroidogenic acute regulatory ...
*  Gestrinone
Hydroxysteroid Dehydrogenase (3.BETA.-HSD), 17.ALPHA.-Hydroxylase and 17, 20 Lyase by Progestins and Danazol". Endocrinologia ... p. 5. Archived from the original (RTF) on 2006-06-20. Retrieved 2006-06-01. La Marca, A.; Giulini S.; Vito G.; Orvieto R.; ... 11-trien-20-yn-17β-ol-3-one, is a synthetic estrane steroid and a derivative of testosterone. It is more specifically a ...
*  List of diseases (C)
... adrenal hyperplasia due to 21-hydroxylase deficiency Congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase ... trisomy 2q37 Chromosome 20 - Chromosome 22 Chromosome 20 ring Chromosome 20, deletion 20p Chromosome 20, duplication 20p ... Chromosome 20, trisomy Chromosome 21 monosomy Chromosome 21 ring Chromosome 21, monosomy 21q22 Chromosome 21, tetrasomy 21q ...
Définitions de 21 hydroxysteroid dehydrogenase nad , synonymes, antonymes, dérivés de 21 hydroxysteroid dehydrogenase nad , dictionnaire analogique de 21 hydroxysteroid dehydrogenase nad (anglais)
The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is selectively expressed in aldosterone target tissues, conferring aldosterone selectivity for the mineralocorticoid receptor. A diminished activity causes salt-sensitive hypertension. The mechanism of the variable and distinct 11β-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) expression in the cortical collecting duct is poorly understood. Here, we analyzed for the first time whether the 11β-HSD2 expression is modulated by microRNAs (miRNAs). In silico analysis revealed 53 and 27 miRNAs with potential binding sites on human or rat HSD11B2 3′-untranslated region. A reporter assay demonstrated 3′-untranslated region-dependent regulation of human and rodent HSD11B2. miRNAs were profiled from cortical collecting ducts and proximal convoluted tubules. Bioinformatic analyses showed a distinct clustering for cortical collecting ducts and proximal convoluted tubules with 53 of 375 miRNAs, where 13 were predicted to bind to the ...
Looking for information on 3 beta hydroxysteroid dehydrogenase deficiency? Medigest has all you need to know about 3 beta hydroxysteroid dehydrogenase deficiency - Symptoms and Signs, Causes, Treatments and definition
In 2 unrelated patients, Ulick et al. (1979) described a disorder in the peripheral metabolism of cortisol, manifested by hypertension, hypokalemia, low plasma renin activity, and responsiveness to spironolactone. Aldosterone levels were subnormal.
Achim Recktenwald, PhD (achim at ibex.ca) wrote: : Robert S. Strauss wrote: : , : , Maxy Mariasegaram ,mariaseg at HERCULES.CS.UREGINA.CA, wrote: : , : , ,Hello everyone, : , : , ,I have to write a paper on the above enzyme as part of the course : , ,requirements for a fourth year biochemistry class. : , : , ,I would appreciate any leads to literature that cover the structure, : , ,function, kinetics and recent development on 3-beta HSD, preferably some : , ,review articles. Failing which, what would be a good way to start this : , ,search? I tried looking up the Bio Abstracts, but that didnt help much. : , : , ,I look forward to hearing from people out there, and thank you very much : , ,for reading this message. : , : , ,cheers, : , ,Max Youll find a lot of information if you search medline with the words : short-chain dehydrogenases. In 1995 Jornvall et al. published a review in Biochemistry, it is pretty informative, although incomplete. Lluis ...
Bile acids (BAs) are important modulators of metabolic functions such as lipid, triglyceride and glucose homeostasis. Intrahepatic accumulation of BAs is known to cause liver injury in cholestatic conditions, where normal trans-hepatic BA flow is impaired due to pathological conditions or induced by toxic drugs. Therefore, it is important to understand the mechanisms of BA homeostasis regulation and to identify novel players and characterize their functions. The main goal of the present work was to investigate the impact of altered hepatic glucocorticoid activation by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) on BA homeostasis and to unravel the mechanisms of adaptations in a scenario of impaired 11β-HSD1 function. In order to achieve this goal, we developed and validated an ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) method for the quantification of a total of 24 BAs, including 11 unconjugated, 6 glycine-conjugated and 7 ...
Status of 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) immunoreactivity was significantly higher in invasive lobular carcinoma (ILC) than in invasive duc
11 beta-hydroxysteroid dehydrogenase (11 beta HSD) has both dehydrogenase (11 beta DH) and reductase (11 beta R) activities, which catalyse the interconversion of cortisol and cortisone, and prednisolone and prednisone. This enzyme confers specificity
HSD17B2; hydroxysteroid (17-beta) dehydrogenase 2; estradiol 17-beta-dehydrogenase 2; HSD17; SDR9C2; short chain dehydrogenase/reductase family 9C; member 2; 17 beta HSD 2; 20 alpha HSD; 20 alpha hydroxysteroid dehydrogenase; E2DH; Microsomal 17 beta hydroxysteroid dehydrogenase; Testosterone 17 beta dehydrogenase; 20-alpha-HSD; 17-beta-HSD 2; OTTHUMP00000174979; testosterone 17-beta-dehydrogenase; 20 alpha-hydroxysteroid dehydrogenase; 17-beta-hydroxysteroid dehydrogenase type 2; microsomal 17-beta-hydroxysteroid dehydrogenase; short chain dehydrogenase/reductase family 9C, member 2; EDH17B2 ...
Similar phenotypes in 46,XY DSD have different etiopathogenesis. Androgen (A) synthesis are rare respect to A action/metabolism defects. The most frequent cause in the former group is a mutation of HSD17B3, gene encoding for an enzyme (17BHSD3) converting delta4-androstenedione (D4) into testosterone (T). Homozygotes/compound heterozygotes have testes, male wolffian structures, completely female (F) or mildly virilized external genitalia (EG). Pts with not palpable testes may appear as F, but they virilize at puberty for the increase in serum T. Our patient (12-yrs-old. 46,XY) for FEG at birth was raised as girl until puberty, when clitoris enlargement (, 4 cm) and male pattern of body hair and timbre of voice appeared. The EG corresponded to Prader stage III. Pelvic echography: two hypoechogenic ovoid masses in inguinal regions, compatible with testes, no Müllerian structures, echogenic structure (20x5mm) like hypoplastic uterus, posteriorly to the bladder. T synthesis: reduced before (3.3 ...
The Report Corticosteroid 11 Beta Dehydrogenase Isozyme 1 (11 Beta Hydroxysteroid Dehydrogenase 1 or Short Chain Dehydrogenase/Reductase Family 26C Member 1 or HSD11B1 or EC 1.1.1.146) - Pipeline Review, H2 2017 provides information on pricing, market analysis, shares, forecast, and company profiles for key industry participants. - MarketResearchReports.biz". Corticosteroid 11 Beta Dehydrogenase Isozyme 1 (11 Beta Hydroxysteroid Dehydrogenase 1 or Short Chain Dehydrogenase/Reductase Family 26C Member 1 or HSD11B1 or EC 1.1.1.146) - 11beta-hydroxysteroid dehydrogenase type 1 is an NADPH-dependent enzyme highly expressed in key metabolic tissues including liver, adipose tissue, and the central nervous system. In these tissues HSD11B1 reduces cortisone to the active hormone cortisol that activates glucocorticoid receptors. This enzyme plays an important role in obesity and insulin resistance.. Corticosteroid 11 Beta Dehydrogenase Isozyme 1 (11 Beta Hydroxysteroid Dehydrogenase 1 or Short Chain ...
Bile-acid 7alpha-dehydroxylase (EC 1.17.99.5, cholate 7alpha-dehydroxylase, 7alpha-dehydroxylase, bile acid 7-dehydroxylase) is an enzyme with systematic name deoxycholate:NAD+ oxidoreductase. This enzyme catalyses the following chemical reaction (1) deoxycholate + NAD+ + H2O ⇌ {\displaystyle \rightleftharpoons } cholate + NADH + H+ (2) lithocholate + NAD+ + H2O ⇌ {\displaystyle \rightleftharpoons } chenodeoxycholate + NADH + H+ Bile-acid 7alpha-dehydroxylase is highly specific for bile acid substrates. White, B.A.; Cacciapuoti, A.F.; Fricke, R.J.; Whitehead, T.R.; Mosbach, E.H.; Hylemon, P.B. (1981). "Cofactor requirements for 7α-dehydroxylation of cholic and chenodeoxycholic acid in cell extracts of the intestinal anaerobic bacterium, Eubacterium species V.P.I. 12708". J. Lipid Res. 22 (6): 891-898. PMID 7276750. White, B.A.; Paone, D.A.; Cacciapuoti, A.F.; Fricke, R.J.; Mosbach, E.H.; Hylemon, P.B. (1983). "Regulation of bile acid 7-dehydroxylase activity by NAD+ and NADH in cell ...
KEE316Hu, HSD11b1L; SCDR10; HSD3; SDR26C2; 11-Beta Hydroxysteroid Dehydrogenase Type 1 Like Protein; Short chain dehydrogenase/reductase family 26C member 2 | Products for research use only!
China Supply Enoxolone 18alpha Glycyrrhetinic Acid 98% Glycyrrhetinic Acid, Find details about China Glycyrrhetinic Acid, Glycyrrhetinic Acid Price from Supply Enoxolone 18alpha Glycyrrhetinic Acid 98% Glycyrrhetinic Acid - Nanjing Zelang Medical Technology Co., Ltd.
Girls with idiopathic premature adrenarche, characterized by the early appearance of pubic hair and adrenal hyperandrogenism, may be at an increased risk for polycystic ovarian syndrome and its associated complications. Alterations of peripheral metabolism of adrenal steroids, specifically increased 5 alpha-reductase and 11 beta-hydroxysteroid dehydrogenase activities, have been documented in patients with polycystic ovarian syndrome and proposed as an underlying mechanism for the adrenal hyperandrogenism in this syndrome. We sought to investigate whether alterations in 5 alpha-reductase and 11 beta-hydroxysteroid dehydrogenase activities are present in girls with premature adrenarche, suggesting a possible role in the pathogenesis of the hyperandrogenism of this condition. We studied C19 and C21 urinary steroid metabolites, 5 alpha/5 beta and 11 oxo/11 hydroxy metabolite pairs as well as the ratios of the total 5 alpha/total 5 beta and total 11 oxo/total 11 hydroxy metabolites in 24-h urine samples
Several important studies have led to the hypothesis that changes in 11β-HSD activity are key to the anomalous regulation of Na+ retention by glucocorticoids. The studies of Ulick et al22 23 have clearly shown that children with apparent mineralocorticoid excess syndrome have a specific defect, with markedly diminished 11β-HSD activity leading to Na+ retention, hypokalemia, and low plasma aldosterone and renin levels. When treated with cortisol, these children developed Na+ retention and a marked increase in BP, indicating that cortisol was acting as a mineralocorticoid.24 The subsequent experiments of Stewart et al8 demonstrated that the hypertension caused by excessive licorice ingestion was also due to diminished 11β-HSD activity caused by glycyrrhetinic acid inhibition of this enzyme. The earlier work of Kornel et al10 11 also indicated that impaired 11β-HSD activity may play a role in essential hypertension by showing altered ratios of cortisol to cortisone in both the serum and urine ...
Accepted name: 17β-estradiol 17-dehydrogenase. Reaction: 17β-estradiol + NAD(P)+ = estrone + NAD(P)H + H+. Other name(s): 20α-hydroxysteroid dehydrogenase; 17β,20α-hydroxysteroid dehydrogenase; 17β-estradiol dehydrogenase; estradiol dehydrogenase; estrogen 17-oxidoreductase; 17β-HSD; HSD17B7. Systematic name: 17β-estradiol:NAD(P)+ 17-oxidoreductase. Comments: The enzyme oxidizes or reduces the hydroxy/keto group on C17 of estrogens and androgens in mammals and regulates the biological potency of these steroids. The mammalian enzyme is bifunctional and also catalyses EC 1.1.1.270, 3β-hydroxysteroid 3-dehydrogenase [3]. The enzyme also acts on (S)-20-hydroxypregn-4-en-3-one and related compounds, oxidizing the (S)-20-group, but unlike EC 1.1.1.149, 20α-hydroxysteroid dehydrogenase, it is Si-specific with respect to NAD(P)+.. Links to other databases: BRENDA, EXPASY, GTD, KEGG, Metacyc, PDB, CAS registry number: 9028-61-9. References:. 1. Kautsky, M.P. and Hagerman, D.D. 17β-Estradiol ...
Interestingly obesity may cause stress! Not because someone is stressed by his image looking into mirror. 11-Beta Hydroxysteroid Dehydrogenase Type 1 is an enzyme presents mainly in fat tissue which converts inactive cortisone into its active form known as cortisol. This means that fat tissue is able to produce via convertion its own stress hormone! Curcumin showed to be a powerful inhibitor of 11-HSD 1 having at the same time antioxidant capacity prevents fat from oxidazing itself. This amazing spice may add not only colour and flavour but also other value to Your diet ...
17 beta-hydroxysteroid dehydrogenases catalyze the oxidoreduction of hydroxy/oxo groups at position C17 of steroid hormones, thereby constituting a prereceptor control mechanism of hormone action. At present, 11 different mammalian 17 beta-hydroxysteroid dehydrogenases have been identified, catalyzing the cell- and steroid-specific activation and inactivation of estrogens and androgens. The human type 10 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD-10) is a multifunctional mitochondrial enzyme that efficiently catalyzes the oxidative inactivation at C17 of androgens and estrogens. However, it also mediates oxidation of 3 alpha-hydroxy groups of androgens, thereby reactivating androgen metabolites. Finally, it is involved in beta-oxidation of fatty acids by catalyzing the L-hydroxyacyl CoA dehydrogenase reaction of the beta-oxidation cycle. These features and expression profiles suggest a critical role of 17 beta-HSD-10 in neurodegenerative and steroid-dependent cancer forms. Since no three
Musto, N; Hafiez, A A.; and Bartke, A, "Prolactin increases 17beta-hydroxysteroid dehydrogenase activity in the testis." (1972). Subject Strain Bibliography 1972. 2710 ...
JS Scott.; J deSchoolmeester.; E Kilgour. Novel Acidic 11β-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) Inhibitor with Reduced Acyl Glucuronide Liability: The Discovery of 4-[4-(2-Adamantylcarbamoyl)-5-tert-butyl-pyrazol-1-yl]benzoic Acid (AZD8329). J. Med. Chem.201255 (22), 10136-10147.. SW Kwon.; SK Kang.; JH Lee.; JH Bok.; CH Kim. Synthesis and 11β hydroxysteroid dehydrogenase 1 inhibition of thiazolidine derivatives with an adamantyl group. Bioorganic & Medicinal Chemistry Letters. 201121 (1), 435-439.. ...
Mutations in HSD3B2, the gene for 3beta-hydroxysteroid dehydrogenase type II (3beta-HSD II) have been detected and activities analysed through the in vitro expression of mutant cDNAs. Two full sibs with male pseudohermaphroditism were found to be double heterozygotes: N100S/266DeltaA. This genotype leads to the most profound loss of 3beta-HSD II enzyme activity (1.3% of normal) described to date in cases without severe salt-loss. One sib (N100S/266DeltaA) is the first reported male case of type II deficiency affected with premature adrenarche. Three apparently independent kindreds had propositi affected with the HSD3B2 mutation A82T/A82T, which is associated with a non salt-losing phenotype with variable expressivity in females. These three families had the same extended HSD3B haplotype and are likely to have inherited the same ancestral mutation. The significance of this finding is discussed in the light of the presence of A82T mutation at a homologous position in pseudogene varphi5 that is ...
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We examined the immunohistochemical distribution of 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2), the enzyme responsible for the conversion of bioactive glucocorticoids to their receptor-inactive forms, in lung tissue obtained at autops
4FAL: Crystal structure of human 17beta-hydroxysteroid dehydrogenase type 5 in complex with 3-((3,4-dihydroisoquinolin-2(1H)-yl)sulfonyl)-N-methylbenzamide (80)
Alterations in glucocorticoid (GC) biosynthesis and metabolism are associated with a variety of pathophysiological disorders including cholestasis, diabetes and other metabolic disorders. Bile acids (BA) are also important modulators of metabolic functions and regulate cholesterol, triglyceride and glucose homeostasis as well as being critical for dietary fat digestion, enterohepatic function, and postprandial thermogenesis. In intact cells and in vivo, the 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme converts inactive GC precursors (cortisone in humans, and 11-dehydrocorticosterone in mice and rats) into their active forms (cortisol and corticosterone, respectively) thereby amplifying local intracellular GC levels. Interconversion by 11β-HSD1 of other sterols has also been described. These include conversions of 7keto-cholesterol to 7β-hydroxycholesterol, 7-oxodehydroepiandrosterone (7-oxo-DHEA) to 7α-hydroxy- and 7β-hydroxy DHEA, 7- oxo-lithocholic acid (LCA, a bile acid; ...
USP Grape Seed Oil. If you prefer, you also could replace grape seed oil into ethyl oleate or MCT.. Drostanolone Enanthate Introduction and Usage:. Masteron is a modified form of Dihydrotestosterone, with a methyl group at the 2nd carbon (carbon alpha) atom. This modification is responsible for the anabolic strength increase. This methyl group makes it harder for the enzyme 3-hydroxysteroid dehydrogenase to metabolize Masteron. This enzyme is abundantly present in muscle tissue, and is responsible for degrading any DHT into two inactive metabolites: 3-Alpha Androstanediol and 3-Beta Androstanediol. Because of this enzyme DHT is not anabolic in muscle tissue at all. It is believed that if the enzyme 3-hydroxysteroid dehydrogenase was neutralized, DHT would actually be a very powerful anabolic steroid. Drostanolones methyl group addition makes it imune to this enzyme.. Drostanolone is injected into the body as an ester (bonded to either Propionate or Enanthate). Enzymes cleave off the ester from ...
Objective Increased glucocorticoid metabolite excretion and enhanced expression and activity of 11-hydroxysteroid dehydrogenase type 1 in adipose tissue are closely correlated with obesity and its detrimental consequences. Weight loss ameliorates the latter. The aim of this study was to explore whether increased glucocorticoid exposure in obesity is improved with substantial weight loss and thus is a consequence rather than a cause of obesity. Design and patients A prospective cohort study in 31 women. Measurements 11-HSD type 1 expression and activity, urinary glucocorticoid metabolite excretion, body composition including regional adipose tissue depots and insulin resistance by HOMA-IR before and 2years after gastric bypass surgery. Results After weight loss, excretion of cortisol and cortisone metabolites decreased. Both cortisol and cortisone metabolite excretion correlated with central obesity, where the intraabdominal fat depot showed the strongest association. Cortisol metabolites ...
A comparative approach was taken in this study to evaluate androgen (androstenedione and testosterone) metabolism in three invertebrate species: the gastropod Marisa cornuarietis, the amphipod Hyalella azteca, and the echinoderm Paracentrotus lividus. The existence of 17β/3β-hydroxysteroid dehydrogenase (HSD) and 5α-reductase catalyzed reactions was demonstrated in all three species. Androstenedione was primarily converted to 5α-androstanedione in M. cornuarietis, while it was primarily metabolized to testosterone in P. lividus and H. azteca. In addition, and consistent with vertebrate findings, tissue specific pathways and sexual dimorphism in androgen metabolism were observed. Namely, testosterone was metabolized to dihydrotestosterone in P. lividus gonads (via 5α-reductase), and metabolized to 4-androstene-3β,17β-diol in the digestive tube (via 3β-hydroxysteroid dehydrogenase). Furthermore, the synthesis of 17β-reduced metabolites of androstenedione (testosterone and ...
Fresh molar tissues obtained from seven patients were incubated in vitro with dehydroepiandrosterone and androstenedione. The testosterone concentration in molar tissue ranged from 5.4 ng/g wet weight to 43.8 ng/g wet weight. Both precursors were readily converted to testosterone indicating that 17-hydroxysteroid dehydrogenase and 3β-hydroxysteroid dehydrogenase are present in molar trophoblast. A 50 mg dose of dehydroepiandrosterone was infused into patients with hydatidiform mole before and after uterine evacuation. There was a testosterone peak preceding an oestrogen rise which disappeared after uterine evacuation. It is suggested that the elevated testosterone level in molar pregnancy is mainly due to the conversion of dehydroepiandrosterone in the molar trophoblast ...
Methods Fifty rats received cyclophosphamide injection over 5 consecutive days to induce PADAM, which was verified by comparing total testosterone (TT) and free testosterone (FT) levels with 10 non-PADAM healthy control rats (CON). Successful modelling was confirmed in 43 of 50 rats, 40 of which were randomly divided into untreated (PADAM), EA-treated (PADAM+EA), MM-treated (PADAM+MM), and androlin (AD)-treated (PADAM+AD) groups (n=10 each). EA and MM were administered at BL23 and CV4 acupuncture points for 8 weeks, and no treatment was given to rats in the PADAM and CON groups. Serum levels of luteinising hormone (LH) and follicle-stimulating hormone (FSH), mRNA expression of cytochrome P450c17 (P450c17) and 3β-hydroxysteroid dehydrogenase 1 (3β-HSD1), and protein levels of cytochrome P450 side chain cleavage (P450scc), 17β-hydroxysteroid dehydrogenase 3 (17β-HSD3) and steroidogenic factor 1 (SF-1) were evaluated after 8 weeks. ...
Androgens and estrogens increase the number of cell division and the opportunity for random genetic errors and are thus involved in carcinogenesis of hormone related cancers. [...]
3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the oxidative conversion of ketosteroids. The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids.
17Beta-hydroxysteroid dehydrogenases (17beta-HSDs) catalyze the NAD(P)(H) dependent oxidoreduction at C17 oxo/beta-hydroxyl groups of androgen and estrogen hormones. This reversible reaction constitutes an important pre-receptor control mechanism for nuclear receptor ligands, since the conversion switches between the 17beta-OH receptor ligands and their inactive 17-oxo metabolites. At present, 14 mammalian 17beta-HSDs are described, of which at least 11 exist within the human genome, encoded by different genes. The enzymes differ in their expression pattern, nucleotide cofactor preference, steroid substrate specificity and subcellular localization, and thus constitute a complex system ensuring cell-specific adaptation and regulation of sex steroid hormone levels. Broad and overlapping substrate specificities with enzymes involved in lipid metabolism suggest interactions of several 17beta-HSDs with other metabolic pathways. Several 17beta-HSDs enzymes constitute promising drug targets, of particular
To elucidate the role of endogenous glucocorticoid signaling in bone, we previously developed Col2.3-HSD2 and Col3.6-HSD2 transgenic mice in which a 2.3-kb or 3.6-kb Colla1 promoter fragment drives expression of 11β-hydroxysteroid dehydrogenase type 2 (HSD2) in mature and early osteoblasts, respectively. In the first study, we first characterized the bone phenotype of Col3.6-HSD2 mice. Col3.6-HSD2 mice had decreased trabecular bone in vertebra and decreased cortical bone in femur and tibia. Transgenic calvarial osteoblast and bone marrow stromal cultures had decreased alkaline phosphatase and mineral staining, and reduced Colla1, bone sialoprotein and osteocalcin mRNA expression. Cell growth and proliferation were decreased in transgenic cultures. Transgenic bone marrow cells showed more osteoclast formation in vitro. However, osteoclast resorptive activity was decreased in vitro and in vivo. Microarray analysis showed that multiple signaling pathways were affected in transgenic osteoblasts including
CONTEXT: Non alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD represents a spectrum of liver disease ranging from reversible hepatic steatosis, to non alcoholic steato-hepatitis (NASH) and cirrhosis. The potential role of glucocorticoids (GC) in the pathogenesis of NAFLD is highlighted in patients with GC excess, Cushings syndrome, who develop central adiposity, insulin resistance and in 20% of cases, NAFLD. Although in most cases of NAFLD, circulating cortisol levels are normal, hepatic cortisol availability is controlled by enzymes that regenerate cortisol (F) from inactive cortisone (E) (11β-hydroxysteroid dehydrogenase type 1, 11β-HSD1), or inactivate cortisol through A-ring metabolism (5α- and 5β-reductase, 5αR and 5βR). OBJECTIVE AND METHODS: In vitro studies defined 11β-HSD1 expression in normal and NASH liver samples. We then characterised hepatic cortisol metabolism in 16 patients with histologically proven NAFLD compared to 32 obese
Our immunohistochemistry results indicated that the MR was not primarily located in the nucleus in normal DRG, translocating there only early after DRG inflammation. For the classical nuclear actions of the MR receptor, such translocation is generally taken as evidence for activation. The observations in normal DRG may seem to contradict the general view that the MR in most tissues should be chronically activated by basal plasma levels of corticosterone (except in tissues such as kidney where corticosterone is enzymatically degraded)-the affinity of the MR for corticosterone is higher than its affinity for aldosterone, so the (much higher) basal plasma levels of corticosterone should chronically activate the MR. RNA for the enzyme that degrades corticosterone in classical aldosterone-sensitive tissues, 11-hydroxysteroid dehydrogenase type II, is present in DRG21 though it is not known if this is neuronal or perhaps associated with vascular cells. In addition, the MR can apparently have forms ...
Looking for the definition of 11-beta-hydroxysteroid dehydrogenases? Find out what is the full meaning of 11-beta-hydroxysteroid dehydrogenases on Abbreviations.com! Beta is one option -- get in to view more @ The Webs largest and most authoritative acronyms and abbreviations resource.
K00498 CYP11A; cholesterol monooxygenase (side-chain-cleaving) [EC:1.14.15.6] K00512 CYP17A; steroid 17alpha-monooxygenase / 17alpha-hydroxyprogesterone deacetylase [EC:1.14.14.19 1.14.14.32] K01131 STS; steryl-sulfatase [EC:3.1.6.2] K01015 SULT2B1; alcohol sulfotransferase [EC:2.8.2.2] K00513 CYP21A; steroid 21-monooxygenase [EC:1.14.14.16] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K00070 HSD3B; 3beta-hydroxy-Delta5-steroid dehydrogenase / steroid Delta-isomerase [EC:1.1.1.145 5.3.3.1] K12343 SRD5A1; ...
Glucocorticoids are important regulators of glucose, lipid and protein metabolism, acting mainly in the liver, adipose tissue and muscle. Chronic glucocorticoid excess is associated with clinical features, such as insulin resistance, visceral obesity, hypertension, and dyslipidemia, which also represent the classical hallmarks of the metabolic syndrome. Elevenbeta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1), a key intracellular enzyme which catalyses the conversion of inactive cortisone to active cortisol, has been implicated in the development of the metabolic syndrome. The shift of this reaction towards cortisol generation may lead to tissutal overexposure to glucocorticoids even with normal circulating cortisol levels. The most robust evidence in support of a pathogenetic role of this enzyme in the development of the metabolic syndrome has been reported in experimental animals, whereas results of human studies are less convincing with several case control and cross-sectional studies ...
We previously reported that a deficiency in the vasopressin V1a receptor (V1aR) results in type 4 renal tubular acidosis, which suggests that vasopressin exerts direct effects on the physiological actions of aldosterone. We investigated the role of vasopressin for nucleocytoplasmic transport of mineralocorticoid receptor in the intercalated cells. Vasopressin V1aR-deficient (V1aR-/-) mice showed largely decreased expression of MR and 11β-hydroxysteroid dehydrogenase type 2 in the medulla of the kidney, which was partially ameliorated by fludrocortisone treatment. The incubation of IN-IC cells, an intercalated cell line established from temperature-sensitive SV40 large T antigen-expressing rats, with aldosterone or vasopressin increased the nuclear-to-cytoplasmic ratio of the MR from 11.2 to 47.2% and from 18.7 to 61.2%, respectively, in 30 min without any changes in MR expression from the whole cell extract. The immunohistochemistry analysis of the IN-IC cells revealed the nuclear accumulation ...
Background 17β hydroxysteroid dehydrogenase type 2 (17β-HSD2) catalyzes in vivo the oxidation of the highly potent estrogens like estradiol (E2) and androgens like testosterone (T) into their less active forms estrone (E1) ...
A small amount of ursodeoxycholic acid, also known as UDCA or ursodiol, has been a component in Chinese traditional medicine treatment for liver disorders for centuries. In the Western world, UDCA is the only approved drug to treat primary biliary cirrhosis, an autoimmune disorder characterized by progressive damage to the bile ducts within the liver, causing a buildup of cholesterol in the liver and subsequent liver damage. Without treatment, most patients with this condition will need a liver transplant later in life, and a quarter of patients who have had the condition for more than 10 years will suffer liver failure. UDCA also has been shown to prevent the progression of colorectal cancer and the recurrence of colonic dysplasia, the development of precancerous, abnormal cells in the colon. But the mechanism by which UCDA counteracts these liver problems hasnt been completely elucidated.. In their paper entitled "Ursodeoxycholic acid binds ileal bile acid binding protein," to be published in ...
Glycyrrhiza glabra from Koehlers Medicinal-Plants. The compound glycyrrhizic acid, found in liquorice, is now routinely used throughout Japan for the treatment and control of chronic viral hepatitis, and there is a possible transaminase-lowering effect. Hepatoprotective mechanisms have been demonstrated in mice. Recent studies indicate that glycyrrhizic acid disrupts latent Kaposi sarcoma (as also demonstrated with other herpesvirus infections in the active stage), exhibiting a strong anti-viral effect.. Liquorice affects the bodys endocrine system as it contains isoflavones (phytoestrogens). It might lower the amount of serum testosterone slightly, but whether it affects the amount of free testosterone is unclear. Consuming liquorice can prevent hyperkalemia. Large doses of glycyrrhizinic acid and glycyrrhetinic acid in liquorice extract can lead to hypokalemia and serious increases in blood pressure, a syndrome known as apparent mineralocorticoid excess. These side effects stem from the ...
Citation: Bae, H., Kim, S., Reddy, V., Sicher Jr, R.C. 2003. Using functional genomics to identify plant genes that respond to carbon dioxide.[abstract]. ASA-CSSA-SSSA Proceedings. P. 308. Interpretive Summary: Technical Abstract: We are interested in determining plant genes affected by plant growth in elevated carbon dioxide. Arabidopsis thaliana plants were raised in growth chambers for six weeks at 36 and 100 Pa carbon dioxide. Total protein extracts were separated by two dimensional electrophoresis. Fourteen proteins were modified by carbon dioxide enrichment and we successfully identified six of these by MALDI TOF mass spectrometry. The six identified polypeptides were the following: 1) myrosinase precursor (63 kD), 2) luminal binding protein 2 (BIP2, 67.8 kD), 3) putative 3 beta hydroxysteroid dehydrogenase/isomerase protein (30.3 kD), 4) nucleoside dikinase II (20.0 kD), 5) major latex protein related (17.5 kD), and 6) photosystem II oxygen evolving complex 23 (OEC23, 23 kD). Carbon ...
3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the oxidative conversion of ketosteroids. The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. Efficiently catalyzes the transformation of pregnenolone to progesterone, 17-alpha-hydroxypregnenolone to 17-alpha-hydroxyprogesterone, DHEA to 4-androstenedione, dihydrotestosterone to 5-alpha-androstane-3 beta,17 beta-diol, dehydroepiandrosterone to androstenedione and 5-alpha-androstan-3 beta,17 beta-diol to 5-alpha-dihydrotestosterone ...
The enzyme 3beta/17beta-hydroxysteroid dehydrogenase (3beta/17beta-HSD) is a steroid-inducible component of the Gram-negative bacterium Conramonas testosteroni. It catalyzes the reversible reduction/ dehydrogenation of the oxo/beta-hydroxy groups at positions 3 and 17 of steroid compounds, including hormones and isobile acids. Crystallographic analysis at 1.2 Angstrom resolution reveals the enzyme to have nearly identical subunits that form a tetramer with 222 symmetry. This is one of the largest oligomeric structures refined at this resolution. The subunit consists of a monomer with a single-domain structure built around a seven-stranded beta-sheet flanked by six alpha-helices. The active site contains a Ser-Tyr-Lys triad, typical for short-chain dehydrogenases/reductases (SDR). Despite their highly diverse substrate specificities, SDR members show a close to identical folding pattern architectures and a common catalytic mechanism. In contrast to other SDR apostructures determined, the ...
Type 5 17β-hydroxysteroid dehydrogenase, aldo-keto reductase 1C3 (AKR1C3) converts Δ(4)-androstene-3,17-dione and 5α-androstane-3,17-dione to testosterone (T) and 5α-dihydrotestosterone, respectively, in castration resistant prostate cancer (CRPC). In CRPC, AKR1C3 is implicated in drug resistance, and enzalutamide drug resistance can be surmounted by indomethacin a potent inhibitor of AKR1C3. We examined a series of naproxen analogues and find that (R)-2-(6-methoxynaphthalen-2-yl)butanoic acid (in which the methyl group of R-naproxen was replaced by an ethyl group) acts as a potent AKR1C3 inhibitor that displays selectivity for AKR1C3 over other AKR1C enzymes. This compound was devoid of inhibitory activity on COX isozymes and blocked AKR1C3 mediated production of T and induction of PSA in LNCaP-AKR1C3 cells as a model of a CRPC cell line. R-Profens are substrate selective COX-2 inhibitors and block the oxygenation of endocannabinoids and in the context of advanced prostate cancer R-profens ...
Steroid sulfatases are responsible for the hydrolysis of 3beta-hydroxy steroid sulfates, such as cholesterol and pregnenolone sulfate, and have an important role in regulating the synthesis of estrogenic steroids, from estrone sulfate and dehydroepiandrosterone sulfate, in endocrine-dependent tumors. Although little is known about the mechanism by which the sulfate group is removed from a steroid nucleus, an active site-directed sulfatase inhibitor has been developed. This inhibitor, estrone-3-O-sulfamate (EMATE), was synthesized by treating the sodium salt of estrone with sulfamoyl chloride. This compound inhibited not only estrone sulfatase but also dehydroepiandrosterone sulfatase activity in placental microsomes and in intact MCF-7 breast cancer cells. Pretreatment of MCF-7 cells or placental microsomes with EMATE, followed by extensive washing or dialysis indicated irreversible inhibition. This was confirmed by showing that EMATE inhibited estrone sulfatase activity in placental microsomes in a
Inherited adrenal and gonadal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency is most likely caused by a mutation of the type II 3 beta-HSD gene. Cloning and sequencing of exons I-II, III, and IV and portions of the adjacent introns, amplified by polymerase chain reaction using primers specific for the type II gene, in one male pseudohermaphrodite with salt-wasting classic 3 beta-HSD deficiency congenital adrenal hyperplasia revealed the same mutation in all nine clones of exon IV consisting of a missense mutation at codon 248 [GTC(Val)--,AAC(Asn)] followed by a frameshift mutation at codon 249 [CGA (Arg)--,TA], resulting in a stop codon TAG, and normal sequences of exon I-II and III and the adjacent portions of introns ...
Primer reninismus: A kering sben jelenl v akt v renin f k nt a ves b l ered, a juxtaglomerularis appar tus (JGA) sejtjei termelik, proteolyticus aktiv l d st k vet en alakul ki preprorenin-, majd proreninb l. Primer reninismust okoz t pusosan a JGA-sejtek tumora, s az n. Zimmermann-pericyt kb l kifejl d haemangiopericytoma. A JGA sejtjein k v l a ves ben renint termelhetnek nephroblastoma-sejtek (Wilms-tumor), s egy b veser kok sejtjei is. Renintermel extrarenalis tumorok is ismertek, a t d , a m j, az urogenitalis traktus, az orbita s a pancreas bizonyos daganatai eset ben. L tsz lagos mineralokortikoid-t ls ly - apparent mineralocorticoid excess (AME): A gl kokortikoid hormonok mineralokortikoid aktivit s t a 11b-hidroxiszteroid-dehidrogen z (11b-HSD) enzimek szab lyozz k. Az enzimnek k t izoformja l tezik, 11b-HSD1 s 11b-HSD2. A 11b-HSD1 NADP-dependens, redukt z aktivit s enzim, melyet sz mos szerv nkben kimutattak, de AME-ben szenved betegek eset ben mut ci t nem igazoltak eddig az enzimet k ...
Human 17beta-hydroxysteroid dehydrogenase type 1 (17β-HSD1) is a steroid-converting enzyme that has long been known to play critical roles in estradiol synthesis and more recently in dihydrotestosterone (DHT) inactivation, showing a dual function that promotes breast cancer cell proliferation. Previously, we reported the first observation of the influence of the enzyme on endogenous estrogen-responsive gene expression. Here, we demonstrate the impact of 17β-HSD1 expression on the breast cancer cell proteome and investigate its role in cell migration. 17β-HSD1 was stably transfected in MCF7 cells and the proteome of the generated cells overexpressing 17β-HSD1 (MCF7-17βHSD1 cells) was compared to that of the wild type MCF7 cells. Proteomics study was performed using two-dimensional gel electrophoresis followed by mass spectrometry analysis of differentially expressed protein spots. Reverse transcription quantitative real-time PCR (RT-qPCR) was used to investigate the transcription of individual gene.
Estradiol 17-beta-dehydrogenase 11,1.1.1.62,17-beta-hydroxysteroid dehydrogenase 11,17-beta-HSD 11,17bHSD11,17betaHSD11,17-beta-hydroxysteroid dehydrogenase XI,17-beta-HSD XI,17betaHSDXI,Cutaneous T-cell lymphoma-associated antigen HD-CL-03,CTCL-associated antigen HD-CL-03,Dehydrogenase/reductase SDR family member 8,Retinal short-chain dehydrogenase/reductase 2,retSDR2,Short chain dehydrogenase/reductase family 16C member 2,HSD17B11,DHRS8,PAN1B,SDR16C2,PSEC0029,UNQ207/PRO233,. ...
17-beta-hydroxysteroid dehydrogenases, such as HSD17B14, are primarily involved in metabolism of steroids at the C17 position and also of other substrates, such as fatty acids, prostaglandins, and xenobiotics (Lukacik et al., 2007 [PubMed 17067289]).[supplied by OMIM, Jun 2009 ...
TY - JOUR. T1 - Bile acid efflux mediated by the rat liver canalicular bile acid transport/ecto-ATPase protein requires serine 503 phosphorylation and is regulated by tyrosine 488 phosphorylation. AU - Sippel, C. Jeffrey. AU - Fallon, Robert. AU - Perlmutter, David H.. PY - 1994/7/29. Y1 - 1994/7/29. N2 - Transfection of cDNA for a hepatocyte canalicular phosphoprotein, the rat liver canalicular bile acid transporter/ecto-ATPase/cell CAM 105, confers bile acid efflux and ecto-ATPase activities on heterologous cells (Sippel, C. J., Suchy, F. J., Ananthanarayanan, M., and Perlmutter D. H. (1993) J. Biol. Chem. 268, 2083-2091). Our previous studies have also indicated that there is a positive correlation between the degree of phosphorylation of this transporter and its bile acid efflux activity. In this study, we introduced site-specific mutations of amino acid residues within a protein kinase C- dependent (T502A, S503A) and a tyrosine kinase-dependent (Y488F) phosphorylation consensus sequence in ...
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AKR1C3 - AKR1C3 (untagged)-Human aldo-keto reductase family 1, member C3 (3-alpha hydroxysteroid dehydrogenase, type II) (AKR1C3) available for purchase from OriGene - Your Gene Company.
Sturve J., Berglund Å., Balk L., Broeg K., Böhmert Björn, Massey S., Savva D., Parkkonen J., Stephensen E., Koehler A. and Förlin L. 2005. Effects of dredging in Göteborg harbour, Sweden assessed by biomarkers in eelpout (Zoarces viviparus). Environmental Toxicology and Chemistry 24, 1951-1961.. Gercken J., Förlin L. and Andersson J. 2006 Developmental disorders in larvae of eelpout (Zoarces viviparus) from German and Swedish Baltic coastal waters. Marine Pollution Bullentin 53, 497-507.. Samuelsson L.M., Förlin L., Karlsson G., Adolfsson-Erici M. and Larsson D.G.J. 2006 Using NMR metabolomics to identify response of an environmental estrogen in blood plasma of fish. Aquatic Toxicology 78, 341-349.. Albertsson E., Kling P., Gunnarsson L., Larsson D.G.J. and Förlin L. 2007. Proteomic analyses indicate induction of hepatic carbonyl reductase/20β-hydroxysteroid dehydrogenase B in rainbow trout exposed to sewage effluent. Ecotoxicology and Environmental Safety, in press.. ...
In spawning Clarias gariepinus from the Hula Nature Reserve in Northern Israel, the mean value for the seminal vesicle somatic index (SVSI) had decreased as compared with that in prespawning fish, due to loss of seminal vesicle fluid. Mean gonadosomatic index (GSI), however, had increased, probably as a result of ... read more hydration, 3α-Hydroxysteroid dehydrogenase (3αHSD), 3βHSD and uridine diphosphoglucose dehydrogenase (UDPGD) reactions were demonstrated in interstitial cells of both testis and seminal vesicle. UDPGD reactions were also found in the epithelium of the seminal vesicle tubules. Quantitative determination of the enzyme reactions with a computerized image analysis system revealed that total activity of all three enzymes in interstitial cells of the seminal vesicle was distinctly stronger in spawning fish. Prespawning and spawning fish did not differ in total UDPGD activity in the epithelium lining the seminal vesicle tubules. In the testes of spawning fish, total 3βHSD ...
glycyrrhetinic acid: A pentacyclic triterpenoid derivative of the beta-amyrin type obtained from the hydrolysis of glycyrrhizic acid, used in flavouring to mask bitter tastes and in the treatment of peptic ulcer.
Hydroxysteroid sulfotransferase 2B1b (SULT2B1b) sulfates cholesterol and oxysterols. Hepatic oval cells (HOCs), thought to be progenitor cells, can be triggered in chemically injured livers. The...
Carbonyl reduction constitutes a phase I reaction for many xenobiotics and is carried out in mammals mainly by members of two protein families, namely aldo-keto reductases and short-chain dehydrogenases/reductases. In addition to their capacity to reduce xenobiotics, several of the enzymes act on endogenous compounds such as steroids or eicosanoids. One of the major carbonyl reducing enzymes found in humans is carbonyl reductase 1 (CBR1) with a very broad substrate spectrum. A paralog, carbonyl reductase 3 (CBR3) has about 70% sequence identity and has not been sufficiently characterized to date. Screening of a focused xenobiotic compound library revealed that CBR3 has narrower substrate specificity and acts on several orthoquinones, as well as isatin or the anticancer drug oracin. To further investigate structure-activity relationships between these enzymes we crystallized CBR3, performed substrate docking, site-directed mutagenesis and compared its kinetic features to CBR1. Despite high sequence
China 17beta-Hydroxy-2alpha-Methyl-5alpha-Androstan-3-One Propionate, Find details about China 17beta-Hydroxy-2alpha-Methyl-5alpha-Androstan-3-, Hormone from 17beta-Hydroxy-2alpha-Methyl-5alpha-Androstan-3-One Propionate - Shenzhen Simeiquan Biotechnology Co., Ltd.
Morgan, S. A. and Sherlock, M. and Gathercole, L.L and Lavery, Gareth G. and Lenaghan, C. and Bujalska, I.J and Laber, D. and Yu, A. and Convey, G. and Mayers, R. and Hegyi, K. and Sethi, J. K. and Stewart, P M and Smith, D. M. and Tomlinson, J W (2009) 11 beta-hydroxysteroid dehydrogenase type 1 regulates glucocorticoid-induced insulin resistance in skeletal muscle. Diabetes, 58 (11). pp. 2506-2515. ISSN 0012-1797. Bujalska, I.J and Gathercole, L.L and Tomlinson, J W and Darimont, C and Ermolieff, J and Fanjul, A.N and Rejto, P.A and Stewart, P M (2008) A novel selective 11b-hydroxysteroid dehydrogenase type 1 inhibitor prevents human adipogenesis. Journal of Endocrinology, 197. pp. 297-307. ISSN 0022-0795. Krone, Nils and Hughes, Beverly and Lavery, Gareth G. and Stewart, P M and Shackleton, Cedric H.L. and Arlt, Wiebke (2010) Gas chromatography/mass spectrometry (GC/MS) remains a pre-eminent discovery tool in clinical steroid investigations even in the era of fast liquid chromatography tandem ...
0034]150 to 210 g of plate-like(the diameter is 50 times of the thickness) silver powder having an average particle size of 2 μm, 0 to 30 g of N-methylpyrrolidone and 6 to 150 g of the polyamic acid binder prepared above are thoroughly mixed together according to the proportions as shown in Table 1 to prepare silver pastes. On polyimide film (1), patterns are printed as shown in FIG. 1 and FIG. 2 by a screen printer using the silver pastes as ink. The printing including the film is baked for about 10 minutes at 200° C. to get rid of volatile organic compounds. Surface resistance, adhesion, hardness and stability under heat of the pattern formed were measured and indicated Table 2. The surface resistances according to Examples were indicated as a graph in FIG. 4. Surface resistance is measured by 4-probe method, adhesion force by tape method (ASTM-D3359B) and hardness by pencil-hardness-test (ASTM-D3369). Stability under heat for pastes is rated by observing melting and deformation under ...
Bile acid is the main component of bile, divided into primary bile acid (cholic acid, |a href=http://www.nwsbio.com/chenodeoxycholic-acid.htm
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
Compare aldo-keto reductase family 1, member D1 (delta 4-3-ketosteroid-5-beta-reductase) ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
We have investigated the effects of fetal growth restriction, induced by restriction of placental growth and function (PR), on 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD-1) and 11betaHSD-2 messenger RNA (mRNA) expression in fetal tissues in the sheep, using Northern blot analysis. Fetal liver, kidney, and adrenals were collected from normally grown fetuses at 90 days (n = 6), 125 days (n = 6), and 141-145 days (n = 7) and from PR fetuses at 141-145 days (n = 6). Expression of 11betaHSD-1 mRNA in the fetal liver increased significantly between 125 days (7.4+/-0.8) and 141-145 days gestation (27+/-5.3). There was also an approximately 2-fold increase in the ratio of 11betaHSD-1 mRNA/18S rRNA expression in the PR group (53.8+/-7.9) compared with that in control animals at 141-145 days gestation. There was a significant decrease in 11betaHSD-2 mRNA in fetal adrenals between 125 days (41.6+/-2.4) and 141-145 days (26.7+/-1.1) gestation, but there was no effect of PR on the expression of ...
Tooze, Alana (2010) The neurocognitive consequences of non-functioning pituitary adenoma and its treatment. Ph.D. thesis, University of Birmingham.. Sherlock, Mark (2011) The regulation of 11 beta-hydroxysteroid dehydrogenase type 1 by ageing and glucocorticoids in key tissues. Ph.D. thesis, University of Birmingham.. ...
Aldo-keto Reductase 1B10/AKR1B10 Proteins available through Novus Biologicals. Browse our Aldo-keto Reductase 1B10/AKR1B10 Protein catalog backed by our Guarantee+.
Glycyrrhizin is a bioactive component found in liquorice root. It is rapidly metabolized by gut bacteria into 18β- glycyrrhetinic acid. These compounds have been shown to have antiviral and anti-inflammatory activity, amongst other benefits in vitro or in vivo. In a study by Hendricks et al, the ability of glycyrrhetinic acid to modulate immune responses…
The role of the fecal microflora in the induction of colon cancer was investigated in individuals believed to be genetically predisposed to colon cancer. Subjects were members of families with increased occurrence of colon and endometrial carcinomas characteristic of the cancer family syndrome. Group 1 consisted of 5 cancer family syndrome individuals previously diagnosed with colon cancer. Group 2 consisted of 6 cancer family syndrome individuals previously diagnosed with endometrial cancer but free of colon cancer. An environmental control group (Group 3) consisted of 8 spouses of subjects in Groups 1 and 2. Quantitative bacterial cultures and assays of β-glucuronidase and 7α-dehydroxylase activity were performed on fecal samples. No differences in bacterial quantities or levels of β-glucuronidase or 7α-dehydroxylase activity were found among Groups 1, 2, and 3 or between spouse pairs. The results fail to associate quantities or enzymatic activity of the intestinal flora to colon cancer in ...
16alpha-bromo-3beta-hydroxy-5alpha-androstan-17-one: a synthetic adrenal hormone that reduced the incidence of tuberculosis and other opportunistic infections in AIDS patients
From: Susan Borkowsky ,email @ redacted, Subject: results.) [IP] Cortisone (was: frozen shoulder test Jonathan has this horrible rash (infussion allergy we think) on his stomache. The cortisone we were prescribed to heal it also caused a rise in bs. We noticed it right from the start. Interestingly enough, they thought that Jon had a cortisone issue (imbalance) pre-pump but it turned out to be a "mother not in control" issue instead ; ) Susan Jan Clinthorne wrote: , I believe that your doctor is incorrect about the cortisone injection not , effecting your blood sugar as much. My blood sugar jumped 75 points within , an hour after having an injection in my foot. Be prepared for your numbers , to rise. , ---------------------------------------------------------- I had a rather nasty allergic reaction to one of the anti depressants I was taking and rather stupidly took 5 mg of prednisone which put me in DKA. It did stop the itching I was happy about that but never believed only 5 mg was enough to ...
20α-Hydroxysteroid dehydrogenase (20α-HSD), which metabolizes progesterone to an inactive steroid in the corpus luteum of mice and rats but not of humans, is thought to play a crucial role in shortening the oestrous cycles in these rodent species. We determined the nucleotide sequence of the 5′-flanking region of the mouse 20α-HSD gene, and examined its promoter activity using a rat luteinized granulosa cell culture. A reporter assay, using reporter constructs of various lengths of the 5′-flanking region, revealed that the region between −83 and 60 bp upstream of the transcription start site was essential for transcriptional activity. Furthermore, mutational analysis demonstrated that a putative Sp1 site in this region was critical to the expression of the reporter gene. Electrophoretic mobility-shift assays showed that the interaction of proteins in a nuclear extract from rat luteinized granulosa cells with this region was inhibited by a competitor having the wild-type Sp1 sequence in ...
The primary source of oestrogen in premenopausal women is the ovary but, after menopause, oestrogen biosynthesis in peripheral tissue is the exclusive site of formation. An enzyme group that affects the availability of active oestrogens is the 17β-hydroxysteroid dehydrogenase (17HSD) family. In breast cancer, 17HSD type 1 and type 2 have been mostly investigated and seem to be the principal 17HSD enzymes involved thus far. The question whether 17HSD type 1 or type 2 is of greatest importance in breast tumour development is still not clear. The aim of this study was to investigate how the loss of 17HSD type 2 expression, using siRNA in the non-tumour breast epithelial cells HMEC (human mammal epithelial cells) and MCF10A, and gain of 17HSD type 2 expression, using transient transfection in the breast cancer derived cell lines MCF7 and T47D, affect oestradiol conversion and proliferation rate measured as S-phase fraction. We further investigated how this was related to the endogenous expression ...
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La 7alfa-idrossisteroide deidrogenasi è un enzima appartenente alla classe delle ossidoreduttasi, che catalizza la seguente reazione: 3α,7α,12α-triidrossi-5β-ciolanato + NAD+ ⇄ 3β,12α-diidrossi-7-osso-5β-ciolanato + NADH + H+ Lenzima catalizza lossidazione del gruppo 7α-idrossile degli acidi biliari e degli alcoli sia nella forma libera che legata. Gli enzimi di Bacteroides fragilis e Clostridium possono utilizzare anche il NADP+. Macdonald, I.A., Williams, C.N. and Mahony, D.E., 7α-Hydroxysteroid dehydrogenase from Escherichia coli B: preliminary studies, in Biochim. Biophys. Acta, vol. 309, 1973, pp. 243-253, Entrez PubMed 4581498. Macdonald, I.A. and Roach, P.D., Bile induction of 7α- and 7β-hydroxysteroid dehydrogenases in Clostridium absonum, in Biochim. Biophys. Acta, vol. 665, 1981, pp. 262-269, Entrez PubMed 6945134. Haslewood, E.S. and Haslewood, G.A.D., The specificity of a 7α-hydroxy steroid dehydrogenase from Escherichia coli, in Biochem. J., vol. 157, 1976, pp. ...
Human fetal adrenal glands are highly active and, with the placenta, regulate circulating progesterone, estrogen and corticosteroids in the fetus. At birth the adrenals are essential for neonate salt retention through secretion of aldosterone, while adequate glucocorticoids are required to prevent adrenal insufficiency. The objective of this study was to carry out the first comprehensive analysis of adrenal steroid levels and steroidogenic enzyme expression in normal second trimester human fetuses. This was an observational study of steroids, messenger RNA transcripts and proteins in adrenals from up to 109 second trimester fetuses (11 weeks to 21 weeks) at the Universities of Aberdeen and Glasgow. The study design was balanced to show effects of maternal smoking. Concentrations of 19 intra-adrenal steroids were quantified using liquid chromatography and mass spectrometry. Pregnenolone was the most abundant steroid while levels of 17α-hydroxyprogesterone, dehydroepiandrosterone sulphate (DHEAS) and
The metabolism of progesterone is rapid and extensive and occurs mainly in the liver,[84][85][86] though enzymes that metabolize progesterone are also expressed widely in the brain, skin, and various other extrahepatic tissues.[58][87] Progesterone has a terminal half-life of only approximately 5 minutes in circulation.[84] The metabolism of progesterone is complex, and it may form as many as 35 different unconjugated metabolites when it is ingested orally.[86][88] Progesterone is highly susceptible to enzymatic reduction via reductases and hydroxysteroid dehydrogenases due to its double bond (between the C4 and C5 positions) and its two ketones (at the C3 and C20 positions).[86]. The major metabolic pathway of progesterone is reduction by 5α-reductase[58] and 5β-reductase into the dihydrogenated 5α-dihydroprogesterone and 5β-dihydroprogesterone, respectively.[85][86][89][90] This is followed by the further reduction of these metabolites via 3α-hydroxysteroid dehydrogenase and ...
Real-time PCR indicated that ovarian KiSS-1 mRNA levels increased significantly, showing a peak at the luteal period in gonadotropin-primed immature rats. Immunostaining analysis showed that following gonadotropin treatment, kisspeptin was strongly localized in theca cells, the interstitial compartment and the corpus luteum, and GPR54 protein was clearly detected in the corpus luteum of rat ovaries. In cultured luteal cells, kisspeptin treatment augmented basal and hCG-induced progesterone levels, but not estradiol production, with concomitant increases detected in the transcript levels of key steroidogenic enzymes (StAR, CYP11A, and 3β-HSD). Furthermore, treatment with kisspeptin increased the phosphorylation of Erk1/2 mitogen-activated protein kinase in cultured luteal cells.. Conclusion(s): ...
Trilostane. Currently the most common method for treating pituitary-dependent hyperadrenocorticism (PDH) in Europe is oral administration of trilostane on a daily basis. Trilostane is a synthetic, orally active steroid analogue that competitively inhibits 3β hydroxysteroid dehydrogenase and hence synthesis of several steroids, including cortisol and aldosterone. This competitive inhibition is reversible and seems to be dose-related. There is also increasing evidence to suggest that trilostane may modify peripheral conversion of cortisol to cortisone and cause some degree of adrenocortical destruction in dogs with PDH.. In dogs peak trilostane concentrations are seen within 1.5 hours of dosing and decrease to baseline values in about 18 hours. Trilostane is variably absorbed after oral administration, at least partly due to its poor water solubility. Absorption may be enhanced by administering the drug with food although this phenomenon has not been investigated in dogs with ...
BioMed Research International is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies covering a wide range of subjects in life sciences and medicine. The journal is divided into 55 subject-specific sections.
Mouse polyclonal antibody raised against a partial recombinant NSDHL. NSDHL (NP_057006, 1 a.a. ~ 110 a.a) partial recombinant protein with GST tag. (H00050814-A01) - Products - Abnova
Meiosis-activating sterols (MAS) are substrates of SC4MOL and NSDHL in the cholesterol pathway and are important for normal organismal development. Oncogenic transformation by epidermal growth factor receptor (EGFR) or RAS increases the demand for cholesterol, suggesting a possibility for metabolic interference. To test this idea in vivo, we ablated Nsdhl in adult keratinocytes expressing KRAS(G12D). Strikingly, Nsdhl inactivation antagonized the growth of skin tumors while having little effect on normal skin. Loss of Nsdhl induced the expression of ATP-binding cassette (ABC) transporters ABCA1 and ABCG1, reduced the expression of low-density lipoprotein receptor (LDLR), decreased intracellular cholesterol, and was dependent on the liver X receptor (LXR) α. Importantly, EGFR signaling opposed LXRα effects on cholesterol homeostasis, whereas an EGFR inhibitor synergized with LXRα agonists in killing cancer cells. Inhibition of SC4MOL or NSDHL, or activation of LXRα by sterol metabolites, can ...
aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase 2; bile acid binding protein; 3-alpha hydroxysteroid dehydrogenase, type III ...
Cloning, Expression and Hormonal Regulation of Steroidogenic Acute Regulatory Protein Gene in Buffalo Ovary - StAR Gene;StAR mRNA;Semi-quantitative RT-PCR;Granulosa Cells;Ovary;Buffalo;
Buy our Recombinant Human NSDHL protein. Ab162360 is a full length protein produced in Wheat germ and has been validated in WB, ELISA. Abcam provides free…
Aldo-Keto Reductases and Toxicant Metabolism provides an overview of the rapidly growing Aldo-Keto Reductase (AKR) superfamily and its role in the metabolism of endogenous and exogenous toxicants. This book discusses the ability of AKRs to metabolize endogenous toxicants including: sugar aldehydes, advanced glycosylation end products, and lipid aldehydes (products of lipid peroxidation decomposition).
Distribution and activity of steroid producing enzymes have been studied in the central nervous system (CNS) of the frog Rana ridibunda. Cell bodies containing 3β-hydroxysteroid dehydrogenase (3β-HSD)-like immunoreactivity were exclusively observed in the preoptic nucleus, the dorsal infundibular nucleus and the dorsal aspect of the ventral infundibular nucleus. Identification of astrocytes with antisera raised against GFAP, and oligodendrocytes with antisera against galactocerebroside revealed that 3β-HSD is expressed in frog neurones. Biochemistry showed that hypothalamic slices can convert pregnenolone into Δ-3-ketosteroids including progesterone (P) and 17-hydroxyprogesterone (17OH-P); these steroids likely serve as precursors for other neurosteroids. This is the first immunocytochemical localisation of 3Β-HSD in the brain and the first evidence for neurosteroid biosynthesis in a nonmammalian vertebrate.
We show rat thymus to express several cytochrome P450 and other steroid-metabolizing enzymes and demonstrate tissue-specific metabolism of testosterone. We also demonstrate an age-dependent transcript expression of isoforms of P450 and 17β-HSDH, as well as the androgen receptor, in thymus tissue of fetal and adult rats. We thus extend earlier findings of a time-dependent P450 monooxygenase gene expression during liver organogenesis to the thymus (Borlakoglu et al., 1993; Yang et al., 1995; Juchau et al., 1998).. Importantly, steroid hormones are versatile signaling molecules and are metabolized via several enzyme systems, including P450 monooxygenases, hydroxysteroid dehydrogenases/reductases, and aromatases, and are usually bound reversibly to carrier proteins in the blood. Upon receptor-mediated endocytosis (Porto et al., 1995), they interact specifically with steroid-hormone-receptor proteins in the cytoplasm and nucleus (Becker et al., 1986). Binding of the hormone activates the receptor, ...
An exciting era is upon us in terms of new therapies for patients with diabetes, obesity, and metabolic syndrome. One such advance is the ability to selectively manipulate tissue levels of glucocorticoids through targeted inhibition of cortisol metabolic pathways. Perhaps the best paradigm for metabolic syndrome comes from patients with Cushings syndrome, with their characteristic central obesity, glucose intolerance, hypertension, and premature cardiovascular mortality. Although circulating cortisol concentrations are invariably normal in patients with obesity and metabolic syndrome (1), in vitro, in vivo, and clinical studies over the last decade have collectively shown the importance of local generation of cortisol, via 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in liver and fat, in mediating many facets of the metabolic syndrome (2). Major pharmaceutical companies are now engaged; over 50 patents have been issued detailing compounds and strategies for selective 11β-HSD1 ...
Trilostane is the chemical name for a medication that effectively treats Canine Cushings Disease. Worldwide, the only licensed veterinary version of trilostane is manufactured in the U.K. by the Dechra Group under the brand name of Vetoryl. Vetoryl is marketed in four dosage strengths: 10 mg., 30 mg., 60 mg., and 120 mg. capsules. Vetoryl is commonly used in the U.K. and Europe, and it is becoming more widely prescribed in the U.S. subsequent to FDA approval beginning in 2009. All dosage
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Cogent evidence points to the involvement of neurosteroids in the regulation of dopamine (DA) neurotransmission and signaling, yet the neurobiological bases of this link remain poorly understood. We previously showed that inhibition of 5α-reductase (5αR), a key neurosteroidogenic enzyme, attenuates the sensorimotor gating deficits induced by DA receptor activation, as measured by the prepulse inhibition (PPI) of the acoustic startle reflex. To extend these findings, the present study was aimed at the assessment of the role of other key neurosteroidogenic enzymes in PPI, such as 17α-hydroxylase/C17,20 lyase (CYP17A1), 3α- and 3β-hydroxysteroid dehydrogenase (HSD), in Sprague-Dawley rats. The PPI deficits induced by the DAergic non-selective agonist apomorphine (APO, 0.25 mg/kg, SC) were dose-dependently attenuated by the selective CYP17A1 inhibitor abiraterone (ABI, 10-50 mg/kg, IP) in a fashion akin to that of the 5αR inhibitor finasteride (FIN, 100 mg/kg, IP). These systemic effects were ...
The research in the Schlinger lab focuses on two questions: 1) How are steroids made available in active forms to distinct neural circuits at appropriate periods of the animals life? 2) How have some neural circuits, but not others, become sensitive to control by steroidal signalling molecules? Experimental Approaches: We study birds in the lab and in the field to explore these questions, examining species that have evolved unique behavioral strategies to optimize their reproductive potential. Techniques regularly used by members of the laboratory include: biochemical assays of steroidogenic enzyme activity, steroidogenic enzyme mRNA expression via Northern blots, rtPCR/Southern blots, in situ hybridization, protein expression via immunocytochemistry, Western blots, neuroanatomical measures via light and fluorescence microscopy and image analysis, and steroid-autoradiography. Please click on the links to learn more about our lab! ...
20α-Hydroxysteroid Dehydrogenase Activity in Rat Placenta  20α-Hydroxysteroid Dehydrogenase Activity in Rat Placenta
Thus, 20α-HSD activity was found in the tissues surrounding the fetus during pregnancy in the rat except for the specific ... 20α-HSD is therefore present in the decidual cells during placentation and in the visceral yolk sac throughout pregnancy. These ... 20α-HSD activity was not detected in the chorioallantoic placenta until day 20 and then increased dramatically on day 21. ... 20α-Hydroxysteroid dehydrogenase (20α-HSD) (EC.1.1.1.149) is the enzyme which catabolizes progesterone to 20α- ...
more infohttps://www.jstage.jst.go.jp/article/endocrj1993/40/6/40_6_673/_article
Regulation of T cell differentiation: in vitro induction of 20 alpha-hydroxysteroid dehydrogenase in splenic lymphocytes from...  Regulation of T cell differentiation: in vitro induction of 20 alpha-hydroxysteroid dehydrogenase in splenic lymphocytes from...
In vitro, 20 alpha SDH can be induced in splenic lymphocytes from nu/nu mice by conditioned media from mitogen- or alloantigen- ... The enzyme 20 alpha-hydroxysteroid dehydrogenase (20 alpha SDH) has previously been shown to be a specific enzyme marker of ... In vivo, the expression of 20 alpha SDH is thymus dependent, in that splenic lymphocytes from athymic mice have only low levels ... The factor responsible for 20 alpha SDH induction has been partially purified and is distinct from other known lymphokines in ...
more infohttps://www.jimmunol.org/content/126/6/2184
Characterization and functional analysis of the 5′-flanking region of the mouse 20α-hydroxysteroid dehydrogenase gene |...  Characterization and functional analysis of the 5′-flanking region of the mouse 20α-hydroxysteroid dehydrogenase gene |...
20α-Hydroxysteroid dehydrogenase (20α-HSD), which metabolizes progesterone to an inactive steroid in the corpus luteum of mice ... Characterization and functional analysis of the 5′-flanking region of the mouse 20α-hydroxysteroid dehydrogenase gene. Keiji ... We determined the nucleotide sequence of the 5′-flanking region of the mouse 20α-HSD gene, and examined its promoter activity ... Characterization and functional analysis of the 5′-flanking region of the mouse 20α-hydroxysteroid dehydrogenase gene ...
more infohttp://www.biochemj.org/content/382/3/975
Changes in Ovarian and Placental 20α-hydroxysteroid Dehydrogenase Activity during the Pregnancy in the Rat | Korea Science  Changes in Ovarian and Placental 20α-hydroxysteroid Dehydrogenase Activity during the Pregnancy in the Rat | Korea Science
Changes in Ovarian and Placental 20α-hydroxysteroid Dehydrogenase Activity during the Pregnancy in the Rat - $20{\alpha ... TEX>-HSD Activity;Progesterone;$20{\alpha}$-dihydroprogesterone;Rat Ovary; ... hydroxysteroid dehydrogenase activity in spontaneous Neoplasms in the dog and cat. J. Vet. Med. Sci. 53:549-552. ... hydroxysteroid dehydrogenase (. -HSD) catabolizes progesterone to -dihydroprogesterone (. -OHP), and is appeared in rat corpora ...
more infohttp://www.koreascience.or.kr/article/ArticleFullRecord.jsp?cn=E1DMBP_2003_v16n3_342
The transcription factor Ap-1 regulates monkey 20α-hydroxysteroid dehydrogenase promoter activity in CHO cells | BMC...  The transcription factor Ap-1 regulates monkey 20α-hydroxysteroid dehydrogenase promoter activity in CHO cells | BMC...
Monkey 20α-HSD was highly abundant in ovarian and placental tissues during the pre-ovulation and pre-parturition phase and was ... Thus, we demonstrated that monkey 20α-HSD promoter activity is regulated by the transcription factor Ap-1 in CHO-K1 cells. ... Monkey 20α-hydroxysteroid dehydrogenase (20α-HSD) is a catabolic enzyme responsible for converting progesterone into ... In this study, we focused on the molecular characterization of the monkey 20α-HSD promoter region by conducting reporter assays ...
more infohttps://bmcbiotechnol.biomedcentral.com/articles/10.1186/1472-6750-14-71
The transcription factor Ap-1 regulates monkey 20α-hydroxysteroid dehydrogenase promoter activity in CHO cells - pdf descargar  The transcription factor Ap-1 regulates monkey 20α-hydroxysteroid dehydrogenase promoter activity in CHO cells - pdf descargar
The transcription factor Ap-1 regulates monkey 20α-hydroxysteroid dehydrogenase promoter activity in CHO cells. . Biblioteca ... Monkey 20α-HSD was highly abundant in ovarian and placental tissues during the pre-ovulation and pre-parturition phase and was ... KeywordsMacaque monkey 20α-HSD Transcription factor Ap-1 Sp-1 CHO-K1 cells Electronic supplementary materialThe online version ... Thus, we demonstrated that monkey 20α-HSD promoter activity is regulated by the transcription factor Ap-1 in CHO-K1 cells.. ...
more infohttp://libros.duhnnae.com/2017/jul4/14991136040-The-transcription-factor-Ap-1-regulates-monkey-20-hydroxysteroid-dehydrogenase-promoter-activity-in-CHO-cells.php
20alpha-hydroxysteroid dehydrogenase - Wikipedia  20alpha-hydroxysteroid dehydrogenase - Wikipedia
Other names in common use include 20alpha-hydroxy steroid dehydrogenase, 20alpha-hydroxy steroid dehydrogenase, 20alpha-HSD, ... "Expression of 17beta-hydroxysteroid dehydrogenase type 1 and type 2, P450 aromatase, and 20alpha-hydroxysteroid dehydrogenase ... Hershkovitz L, Beuschlein F, Klammer S, Krup M, Weinstein Y (March 2007). "Adrenal 20alpha-hydroxysteroid dehydrogenase in the ... Weinstein Y (October 1977). "20alpha-hydroxysteroid dehydrogenase: a T lymphocyte-associated enzyme". J. Immunol. 119 (4): 1223 ...
more infohttps://en.wikipedia.org/wiki/20alpha-hydroxysteroid_dehydrogenase
Study of Protein Translocation in Patients With Beta-Oxidation Disorders  Study of Protein Translocation in Patients With Beta-Oxidation Disorders
Acyl-coa Dehydrogenases. Enzymes that catalyze the first step in the beta-oxidation of FATTY ACIDS. ... 20-hydroxysteroid Dehydrogenases. A group of enzymes that catalyze the reversible reduction-oxidation reaction of 20- ... Eighty female mice were randomly assigned to four groups of 20 mice each: one contro... ... such as from a 20-ketosteroid to a 20-alpha-hydroxysteroid (EC 1.1.1.149) or to a 20-beta-hydroxysteroid (EC 1.1.1.53). ...
more infohttps://www.bioportfolio.com/resources/trial/125597/Study-of-Protein-Translocation-in-Patients-With-Beta-Oxidation-Disorders.html
Zeitschrift für Naturforschung C  Zeitschrift für Naturforschung C
Nucleoside Triphosphate Levels in Streptomyces hydrogenans during Growth and Induction of 20β-Hydroxysteroid Dehydrogenase. ...
more infohttps://www.degruyter.com/view/j/znc.1976.31.issue-7-8/issue-files/znc.1976.31.issue-7-8.xml
3alpha(or 20beta)-hydroxysteroid dehydrogenase - Wikipedia  3alpha(or 20beta)-hydroxysteroid dehydrogenase - Wikipedia
20beta-hydroxysteroid dehydrogenase, 3alpha,20beta-hydroxysteroid:NAD+-oxidoreductase, NADH-20beta-hydroxysteroid dehydrogenase ... In enzymology, a 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53) is an enzyme that catalyzes the chemical reaction ... The systematic name of this enzyme class is 3alpha(or 20beta)-hydroxysteroid:NAD+ oxidoreductase. Other names in common use ... dehydrogenase, 20beta-hydroxy steroid, Delta4-3-ketosteroid hydrogenase, ...
more infohttps://en.wikipedia.org/wiki/3alpha(or_20beta)-hydroxysteroid_dehydrogenase
HSD17B1 antibody [EP1682Y] Recombinant (ab51045) | Abcam  HSD17B1 antibody [EP1682Y] Recombinant (ab51045) | Abcam
Hydroxysteroid (17 beta) dehydrogenase 1 antibody. *MGC13814 antibody. *Placental 17 beta hydroxysteroid dehydrogenase antibody ... Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles. ... PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific ...
more infohttp://www.abcam.com/hsd17b1-antibody-ep1682y-ab51045.html
KAKEN - Research Projects | Development of new in vivo systems for the evaluation of growth factors function. (KAKENHI-PROJECT...  KAKEN - Research Projects | Development of new in vivo systems for the evaluation of growth factors function. (KAKENHI-PROJECT...
... hydroxysteroid dehydrogenase. Biochemca et Biophysica Acta. 1079. 112-118 (1991). *. Description. 「研究成果報告書概要(欧文)」より ... hydroxysteroid dehydrogenase in luteotrophic and luteolytic processes during rat pseudopregnancy. Journal of Reproduction and ... Publications] K. Noda, K. Shiota and M. Takahashi: Purification and characterization of rat ovarian 20 alpha- ... Publications] J. Matsuda, K. Noda, K. Shiota and M. Takahashi: Participation of ovarian 20 alpah - ...
more infohttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-01860040/
AKR1C4 Gene - GeneCards | AK1C4 Protein | AK1C4 Antibody  AKR1C4 Gene - GeneCards | AK1C4 Protein | AK1C4 Antibody
Chlordecone Reductase; 3-Alpha Hydroxysteroid Dehydrogenase, Type I; Dihydrodiol Dehydrogenase 4 2 3 ... Close kinship of human 20alpha-hydroxysteroid dehydrogenase gene with three aldo-keto reductase genes. (PMID: 10672042) ... aldo-keto reductase family 1,member C4 (3-alpha hydroxysteroid dehydrogenase,type I),with high affinity for dihydrotestosterone ... Molecular cloning of two human liver 3 alpha- hydroxysteroid/dihydrodiol dehydrogenase isoenzymes that are identical with ...
more infohttp://www.genecards.org/cgi-bin/carddisp.pl?gene=AKR1C4
GO Gene List  GO Gene List
... hydroxysteroid dehydrogenase). NM_001353. Gene Info. AKR1C2. Aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase ... Alcohol dehydrogenase 5 (class III), chi polypeptide. NM_000671. Gene Info. ADH7. Alcohol dehydrogenase 7 (class IV), mu or ... Aldehyde dehydrogenase 1 family, member A1. NM_000689. Gene Info. ALDH1A2. Aldehyde dehydrogenase 1 family, member A2. NM_ ... 3-alpha hydroxysteroid dehydrogenase, type III). NM_001354. NM_205845. NM_001135241. Gene Info. ...
more infohttps://cgap.nci.nih.gov/Genes/GoGeneQuery?PAGE=1&ORG=Hs&GOID=0008289
GO Gene List  GO Gene List
... hydroxysteroid dehydrogenase). NM_001353. Gene Info. AKR1C2. Aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase ... Aldo-keto reductase family 1, member C3 (3-alpha hydroxysteroid dehydrogenase, type II). NM_003739. NM_001253908. NM_001253909 ... 3-alpha hydroxysteroid dehydrogenase, type III). NM_001354. NM_205845. NM_001135241. Gene Info. ... Aldehyde dehydrogenase 1 family, member A1. NM_000689. Gene Info. ALK. Anaplastic lymphoma receptor tyrosine kinase. NM_004304 ...
more infohttps://cgap.nci.nih.gov/Genes/GoGeneQuery?PAGE=1&ORG=Hs&GOID=0009966
AKR1C4 gene - Genetics Home Reference - NIH  AKR1C4 gene - Genetics Home Reference - NIH
Also has some 20-alpha-hydroxysteroid dehydrogenase activity. The biotransformation of the pesticide chlordecone (kepone) to ...
more infohttps://ghr.nlm.nih.gov/gene/AKR1C4
Recombinant human HSD3a protein (ab109831) | Abcam  Recombinant human HSD3a protein (ab109831) | Abcam
3-alpha-hydroxysteroid dehydrogenase type I. *AK1C4_HUMAN. *AKR1C4. *Aldo keto reductase family 1 member C4 ... Store at -20°C or -80°C. Avoid freeze / thaw cycle.. Preservative: None. Constituents: 20% Glycerol, 0.58% Sodium chloride, ... Also has some 20-alpha-hydroxysteroid dehydrogenase activity. The biotransformation of the pesticide chlordecone (kepone) to ...
more infohttps://www.abcam.com/recombinant-human-hsd3a-protein-ab109831.html
EC 1.1.1.210  EC 1.1.1.210
... hydroxysteroid dehydrogenase. Reaction: 5α-androstan-3β,17β-diol + NADP+ = 17β-hydroxy-5α-androstan-3-one + NADPH + H+. Other ... hydroxysteroid:NADP+ oxidoreductase. Comments: Also acts on 20α-hydroxysteroids.. Links to other databases: BRENDA, EXPASY, ... name(s): progesterone reductase; dehydrogenase, 3β,20α-hydroxy steroid; 3β,20α-hydroxysteroid oxidoreductase. Systematic name: ... 1. Sharaf, M.A. and Sweet, F. Dual activity at an enzyme active site: 3β,20α-hydroxysteroid oxidoreductase from fetal blood. ...
more infohttps://www.qmul.ac.uk/sbcs/iubmb/enzyme/EC1/1/1/210.html
EC 1.1.1.101 to EC 1.1.1.150  EC 1.1.1.101 to EC 1.1.1.150
... β-hydroxysteroid dehydrogenase; 11β-hydroxy steroid dehydrogenase; corticosteroid 11-reductase; dehydrogenase, 11β-hydroxy ... Δ5-3β-hydroxysteroid dehydrogenase; 3β-hydroxy-5-ene steroid dehydrogenase; 3β-hydroxy steroid dehydrogenase/isomerase; 3β- ... EC 1.1.1.146 11β-hydroxysteroid dehydrogenase. EC 1.1.1.147 16α-hydroxysteroid dehydrogenase. EC 1.1.1.148 estradiol 17α- ... Other name(s): 17α-estradiol dehydrogenase; 17α-hydroxy steroid dehydrogenase; 17α-hydroxy steroid oxidoreductase; 17α- ...
more infohttps://www.qmul.ac.uk/sbcs/iubmb/enzyme/EC1/0101c.html
  • The 20α-HSD protein was intensively localized in the large luteal cells and placental cytotrophoblast villus, glandular epithelial cells of the endometrium, syncytiotrophoblast of the placenta, the isthmus cells of the oviduct, and the basal part of the primary chorionic villi and chorionic stem villus of the placenta and large luteal cells of the CL in many mammalian species. (rdb.or.kr)
  • 20α-HSD activity was not detected in the chorioallantoic placenta until day 20 and then increased dramatically on day 21. (go.jp)
  • Monkey 20α-HSD was highly abundant in ovarian and placental tissues during the pre-ovulation and pre-parturition phase and was primarily localized in the syncytiotrophoblast of the placenta. (biomedcentral.com)
  • In enzymology, a 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53) is an enzyme that catalyzes the chemical reaction androstan-3alpha,17beta-diol + NAD+ ⇌ {\displaystyle \rightleftharpoons } 17beta-hydroxyandrostan-3-one + NADH + H+ Thus, the two substrates of this enzyme are androstan-3alpha,17beta-diol and NAD+, whereas its 3 products are 17beta-hydroxyandrostan-3-one, NADH, and H+. (wikipedia.org)
  • In vivo, the expression of 20 alpha SDH is thymus dependent, in that splenic lymphocytes from athymic mice have only low levels of activity, although the levels of enzyme activity increase gradually with age. (jimmunol.org)
  • The phenotype of both the precursor and the induced lymphocyte populations is Thy 1.2-, Lyt 1-, 2-, suggesting that induction of 20 alpha SDH expression is an early step in T cell differentiation. (jimmunol.org)
  • Finally, promoter activity was elevated by the co-transfection of an Sp1 expression vector, and, to a lesser extent, by an Sp3 expression vector, supporting further the involvement of these factors in the expression of the 20α-HSD gene. (biochemj.org)
  • Placental lactogen (PL) is another suppressor of 20α-HSD gene expression. (biomedcentral.com)
  • We have studied the molecular expression and regulation of 20α-HSD in cows, pigs, deer, and monkeys. (rdb.or.kr)
  • The specific antibody against bovine 20α-HSD was generated in a rabbit immunized with the purified recombinant protein. (rdb.or.kr)
  • In vitro, 20 alpha SDH can be induced in splenic lymphocytes from nu/nu mice by conditioned media from mitogen- or alloantigen-stimulated normal lymphocytes. (jimmunol.org)
  • Eighty female mice were randomly assigned to four groups of 20 mice each: one contro. (bioportfolio.com)
  • 20α-HSD is therefore present in the decidual cells during placentation and in the visceral yolk sac throughout pregnancy. (go.jp)
  • HSD activities were high detected from days 8 to 10 of pregnancy, not detectable from days 11 to 20 of pregnancy, but again very high at the time of parturition. (koreascience.or.kr)
  • Further studies are needed to determine the functional significance of the 20α- HSD molecule during ovulation, pregnancy, and parturition. (rdb.or.kr)
  • KeywordsMacaque monkey 20α-HSD Transcription factor Ap-1 Sp-1 CHO-K1 cells Electronic supplementary materialThe online version of this article doi:10.1186-1472-6750-14-71 contains supplementary material, which is available to authorized users. (duhnnae.com)
  • Analysis of DEAE column chromatography revealed that these tissues contain two different types of 20α-HSD (HSD-1 and HSD-2). (go.jp)
  • Our results indicate that the Ap-1 site (-281 → -274) (5′-TGTCTCAT-3′) plays a crucial role in the activation of the monkey 20α-HSD gene. (biomedcentral.com)