Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.
Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.
A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.
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).
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.
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.
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.
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.
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 1.1.1.62
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.
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)
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.
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).
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)
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)
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.
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.
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.
The rate dynamics in chemical or physical systems.
A metabolite of TESTOSTERONE or ANDROSTENEDIONE with a 3-alpha-hydroxyl group and without the double bond. The 3-beta hydroxyl isomer is epiandrosterone.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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.
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.
An enzymes that catalyzes the reversible reduction-oxidation reaction of 20-alpha-hydroxysteroids, such as from PROGESTERONE to 20-ALPHA-DIHYDROPROGESTERONE.
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.
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.
An enzyme that catalyzes the conversion of (S)-malate and NAD+ to oxaloacetate and NADH. EC 1.1.1.37.
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.
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.
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.
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.
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.
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)
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.
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.
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 1.1.1.14
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.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
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.
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.
Oxidoreductases that are specific for ALDEHYDES.
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.
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.
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.
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)
Enzymes that catalyze the first step in the beta-oxidation of FATTY ACIDS.
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.
An enzyme that catalyzes the dehydrogenation of inosine 5'-phosphate to xanthosine 5'-phosphate in the presence of NAD. EC 1.1.1.205.
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.
Alcohol oxidoreductases with substrate specificity for LACTIC ACID.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
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.
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.
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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).
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.
Oxidoreductases that are specific for KETONES.
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)
Inorganic salts of sulfuric acid.
An oxidoreductase involved in pyrimidine base degradation. It catalyzes the catabolism of THYMINE; URACIL and the chemotherapeutic drug, 5-FLUOROURACIL.
An enzyme that catalyzes the oxidation of UDPglucose to UDPglucuronate in the presence of NAD+. EC 1.1.1.22.
The facilitation of a chemical reaction by material (catalyst) that is not consumed by the reaction.
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.

Luteinizing hormone inhibits conversion of pregnenolone to progesterone in luteal cells from rats on day 19 of pregnancy. (1/633)

We have previously reported that intrabursal ovarian administration of LH at the end of pregnancy in rats induces a decrease in luteal progesterone (P4) synthesis and an increase in P4 metabolism. However, whether this local luteolytic effect of LH is exerted directly on luteal cells or on other structures, such as follicular or stromal cells, to modify luteal function is unknown. The aim of the present study was to determine the effect of LH on isolated luteal cells obtained on Day 19 of pregnancy. Incubation of luteal cells with 1, 10, 100, or 1000 ng/ml of ovine LH (oLH) for 6 h did not modify basal P4 production. The addition to the culture medium of 22(R)-hydroxycholesterol (22R-HC, 10 microgram/ml), a membrane-permeable P4 precursor, or pregnenolone (10(-2) microM) induced a significant increase in P4 accumulation in the medium in relation to the control value. When luteal cells were preincubated for 2 h with oLH, a significant (p < 0.01) reduction in the 22R-HC- or pregnenolone-stimulated P4 accumulation was observed. Incubation of luteal cells with dibutyryl cAMP (1 mM, a cAMP analogue) plus isobutylmethylxanthine (1 mM, a phosphodiesterase inhibitor) also inhibited pregnenolone-stimulated P4 accumulation. Incubation with an inositol triphosphate synthesis inhibitor, neomycin (1 mM), or an inhibitor of intracellular Ca2+ mobilization, (8,9-N, N-diethylamino)octyl-3,4,5-trimethoxybenzoate (1 mM), did not prevent the decrease in pregnenolone-stimulated P4 secretion induced by oLH. It was concluded that the luteolytic action of LH in late pregnancy is due, at least in part, to a direct action on the luteal cells and that an increase in intracellular cAMP level might mediate this effect.  (+info)

Luteinization and proteolysis in ovarian follicles of Meishan and Large White gilts during the preovulatory period. (2/633)

This experiment was conducted to determine why follicles luteinize faster in the Meishan breed than in the Large White breed of pig. Follicles were recovered during the late follicular phase from ovaries of both breeds before and after administration of hCG given to mimic the LH surge. First, the patterns of cholesterol transporters (high and low density lipoproteins: HDL and LDL) were compared. Cholesterol transporters detected in follicular fluid consisted of HDL only. Similar amounts of Apolipoprotein A-I were found in all samples. There was no obvious breed effect on minor lipoproteins found in the HDL-rich fraction, and this pattern was altered similarly by hCG in the two breeds. The LDL-rich samples of serum from both breeds contained similar amounts of protein. Second, three steroidogenic enzymes, adrenodoxin, 17 alpha-hydroxylase-lyase (P450(17) alpha) and 3 beta-hydroxysteroid-dehydrogenase (3 beta-HSD) were detected by immunohistochemistry and quantified by image analysis on sections of the two largest follicles. Before hCG treatment, theca interna cells demonstrated immunoreactivities for adrenodoxin (strong), P450(17) alpha and 3 beta-HSD (very strong), whereas granulosa cells displayed immunoreactivities for adrenodoxin only. After hCG treatment, the localization of the enzymes was unchanged but the staining intensity of adrenodoxin on granulosa cells and 3 beta-HSD on theca cells increased (P < 0.01 and P < 0.05, respectively). Breed effects were detected for the amounts of adrenodoxin in theca cells (Meishan > Large White; P < 0.05) and of 17 alpha-hydroxylase (Large White > Meishan, P < 0.01). Breed x treatment interactions were never detected. Finally, gelatinases, plasminogen activator, plasminogen activator inhibitor, tissue inhibitors of metalloproteases (TIMP-1 and TIMP-2) were visualized by direct or reverse zymography or western blotting. Whatever the stage relative to LH administration, follicular fluid from Large White gilts contained more TIMP-1, and TIMP-2 (P < 0.02 and P < 0.01, respectively). No breed effect was detected for the amounts of gelatinases and plasminogen activator inhibitor 1. However, for these parameters, a significant breed x time interaction was obvious, as the Meishan follicles had a greater response to hCG (P < 0.01). Since proteolysis plays a key role in the bioavailability of growth factors such as insulin-like growth factor 1, fibroblast growth factor and transforming growth factor beta, which have the ability to alter gonadotrophin-induced progesterone production in pigs, the differences observed in its control in the present study may explain, at least in part, the different patterns of luteinization observed in Meishan and Large White follicles.  (+info)

Opposing changes in 3alpha-hydroxysteroid dehydrogenase oxidative and reductive activities in rat leydig cells during pubertal development. (3/633)

The enzyme 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) has an important role in androgen metabolism, catalyzing the interconversion of dihydrotestosterone (DHT) and 5alpha-androstane-3alpha,17beta-diol (3alpha-DIOL). The net direction of this interconversion will affect the amount of biologically active ligand available for androgen receptor binding. We hypothesize that in Leydig cells, differential expression of 3alpha-HSD enzymes favoring one of the two directions is a mechanism by which DHT levels are controlled. In order to characterize 3alpha-HSD in rat Leydig cells, the following properties were analyzed: rates of oxidation (3alpha-DIOL to DHT) and reduction (DHT to 3alpha-DIOL) and preference for the cofactors NADP(H) and NAD(H) (i.e., the oxidized and reduced forms of both pyridine nucleotides) in Leydig cells isolated on Days 21, 35, and 90 postpartum. Levels of 3alpha-HSD protein were measured by immunoblotting using an antibody directed against the liver type of the enzyme. Levels of 3alpha-HSD protein and rates of reduction were highest on Day 21 and lowest on Day 90. The opposite was true for the rate of 3alpha-HSD oxidation, which was barely detectable on Day 21 and highest on Day 90 (59.08 +/- 6.35 pmol/min per 10(6) cells, mean +/- SE). Therefore, the level of 3alpha-HSD protein detectable by liver enzyme was consistent with reduction but not with oxidation. There was a clear partitioning of NADP(H)-dependent activity into the cytosolic fraction of Leydig cells, whereas on Days 35 and 90, Leydig cells also contained a microsomal NAD(H)-activated 3alpha-HSD. We conclude that 1) the cytosolic 3alpha-HSD in Leydig cells on Day 21 behaves as a unidirectional NADPH-dependent reductase; 2) by Day 35, a microsomal NAD(H)-dependent enzyme activity is present and may account for predominance of 3alpha-HSD oxidation over reduction and the resultant high capacity of Leydig cells on Day 90 to synthesize DHT from 3alpha-DIOL.  (+info)

Expression of 3beta-hydroxysteroid dehydrogenase type I and type VI isoforms in the mouse testis during development. (4/633)

Six isoforms of the enzyme 3beta-hydroxysteroid dehydrogenase (3betaHSD) have been identified in the mouse, each the product of a distinct gene. Two of these isoforms (type I and type VI) are detectable in the adult testis but changes in their expression during development are unknown. In this study we have examined changes in testicular expression and localization of mRNA encoding the type I and type VI isoforms of 3betaHSD. Total 3betaHSD (type I plus type VI) mRNA was measured by reverse transcription-polymerase chain reaction and showed a peak of expression at day 5 after birth followed by a decline and then a further rise after day 10 that continued up to adulthood. When each isoform was measured individually it was clear that the type I isoform was expressed at all ages from embryonic day 13 to adulthood. In contrast, the type VI isoform was only expressed at significant levels during fetal life on embryonic day 13 and then not again until after day 10 postnatally. Expression of the type VI isoform mRNA increased markedly after day 10 so that by adulthood it was the predominant 3betaHSD isoform present in the testis. Closer examination of the timing of type VI expression showed that the isoform mRNA was first detectable at a significant level on day 11. In-situ hybridization confirmed that the type I isoform is the only one expressed in the fetal/neonatal animal and showed that expression was limited to the interstitial tissue. In the adult, both type I and type VI expression was within the interstitial tissue. The timing of 3betaHSD type VI mRNA expression suggests, strongly, that this isoform is expressed only by adult-type Leydig cells in the mouse testis and that this development starts shortly before day 11. The limited expression of the type VI isoform means that it will be a useful marker in studies of adult Leydig cell development.  (+info)

Molecular cloning and characterization of hemolymph 3-dehydroecdysone 3beta-reductase from the cotton leafworm, Spodoptera littoralis. A new member of the third superfamily of oxidoreductases. (5/633)

The primary product of the prothoracic glands of last instar larvae of Spodoptera littoralis is 3-dehydroecdysone (3DE). After secretion, 3DE is reduced to ecdysone by 3DE 3beta-reductase in the hemolymph. We have previously purified and characterized 3DE 3beta-reductase from the hemolymph of S. littoralis. In this study, cDNA clones encoding the enzyme were obtained by reverse transcription-polymerase chain reaction, employing primers based on the amino acid sequences, in conjunction with 5'- and 3'-rapid amplification of cDNA ends. Multiple polyadenylation signals and AT-rich elements were found in the 3'-untranslated region, suggesting that this region may have a role in regulation of expression of the gene. Conceptual translation and amino acid sequence analysis suggest that 3DE 3beta-reductase from S. littoralis is a new member of the third superfamily of oxidoreductases. Northern analysis shows that 3DE 3beta-reductase mRNA transcripts are widely distributed, but are differentially expressed, in some tissues. The developmental profile of the mRNA revealed that the gene encoding 3DE 3beta-reductase is only transcribed in the second half of the last larval instar and that this fluctuation in expression accounts for the change in the enzyme activity during the instar. Southern analysis indicates that the 3DE 3beta-reductase is encoded by a single gene, which probably contains at least one intron.  (+info)

An inborn error of bile acid synthesis (3beta-hydroxy-delta5-C27-steroid dehydrogenase deficiency) presenting as malabsorption leading to rickets. (6/633)

Deficiency of 3beta-hydroxy-delta5-C27-steroid dehydrogenase (3beta-HSDH), the enzyme that catalyses the second reaction in the principal pathway for the synthesis of bile acids, has been reported to present with prolonged neonatal jaundice with the biopsy features of neonatal hepatitis. It has also been shown to present between the ages of 4 and 46 months with jaundice, hepatosplenomegaly, and steatorrhoea (a clinical picture resembling progressive familial intrahepatic cholestasis). This paper reports two children with 3beta-HSDH deficiency who developed rickets during infancy and did not develop clinically evident liver disease until the age of 3 years. Bile acid replacement resulted in considerable clinical and biochemical improvement. The importance of thorough investigation of fat soluble vitamin deficiencies in infancy is emphasised.  (+info)

Dynamics of periovulatory steroidogenesis in the rhesus monkey follicle after ovarian stimulation. (7/633)

The temporal relationships and regulation of events in the primate follicle during the periovulatory interval are poorly understood. This study was designed to elucidate the dynamics of steroid synthesis in the macaque follicle during ovarian stimulation cycles in which serum/follicular fluid aspirates were collected at precise intervals before (0 h) and after (up to 36 h) administration of the ovulatory human chorionic gonadotrophin (HCG) bolus. Serum concentrations of progesterone increased (P < 0.05) within 30 min, and follicular fluid progesterone concentrations were elevated 180-fold within 12 h, of HCG injection, and remained elevated until the time of ovulation. In contrast, 17beta-oestradiol concentrations increased initially, but then declined (P < 0.05) by 36 h post-HCG. Acute incubation of granulosa cells with and without steroidogenic substrates demonstrated that: (i) 3beta-hydroxysteroid dehydrogenase and aromatase activities were present in equivalent amounts before and after HCG; whereas (ii) P450 side-chain cleavage activity increased (P < 0.05) within 12 h of HCG; and (iii) exogenous low-density lipoprotein and cholesterol were not utilized for steroidogenesis. This model should be useful for further studies on ovulation and luteinization in primates, and enable elucidation of the local actions of progesterone and other steroids at specific time points during the periovulatory interval.  (+info)

Paracrine glucocorticoid activity produced by mouse thymic epithelial cells. (8/633)

Previous data have suggested that glucocorticoids (GCs) are involved in the differentiation of thymocytes into mature T cells. In this report we demonstrate that the mouse thymic epithelial cells (TEC) express the cytochrome P450 hydroxylases Cyp11A1, Cyp21, and Cyp11B1. These enzymes, in combination with 3beta-hydroxysteroid dehydrogenase (3betaHSD), convert cholesterol into corticosterone, the major GC in rodents. In addition, when TEC were cocultured with 'reporter cells' containing the glucocorticoid receptor (GR) and a GR-dependent reporter gene, a specific induction of reporter gene activity was observed. Induction of reporter gene activity was blocked when the TEC and reporter cells were incubated in the presence of the Cyp11B1 inhibitor metyrapone or the 3betaHSD inhibitor trilostane, as well as by the GR antagonist RU486. Coculturing of TEC with thymocytes induced apoptosis in the latter, which was partially blocked by the enzyme inhibitors and RU486. We conclude that TEC secrete a GC hormone activity and suggest a paracrine role for this in thymocyte development.  (+info)

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TY - JOUR. T1 - The orphan nuclear receptor, liver receptor homolog-1, regulates cholesterol side-chain cleavage cytochrome P450 enzyme in human granulosa cells. AU - Kim, Joung W.. AU - Havelock, Jon C.. AU - Carr, Bruce R.. AU - Attia, George R.. PY - 2005/3/1. Y1 - 2005/3/1. N2 - After ovulation, there is a shift in ovarian steroidogenesis from an estrogen-producing ovarian follicle to a progesterone-producing corpus luteum. The first step in human ovarian steroidogenesis is catalyzed by cholesterol side-chain cleavage cytochrome P450 (CYP11A1) enzyme. Steroidogenic factor-1 is an orphan nuclear receptor that regulates several steroidogenic enzymes, including CYP11A1. Liver receptor homolog-1 (LRH-1) is another orphan nuclear receptor that is expressed in the human ovary. After ovulation there is a down-regulation in steroidogenic factor-1, which is associated with an up-regulation of LRH-1 expression. These changes coincide with increased level of CYP11A1 expression in human corpus luteum. ...
TY - JOUR. T1 - Preparation of highly purified 3α- and 3β-hydroxysteroid dehydrogenases from Pseudomonas sp. AU - Shikita, Mikio. AU - Talalay, Paul. PY - 1979/5. Y1 - 1979/5. N2 - A method is described for preparing highly purified 3α- and 3β-hydroxysteroid dehydrogenases (EC 1.1.1.50 and EC 1.1.1.145, respectively), essentially uncontaminated with one another, from extracts of a steroid-induced Pseudomonas species. These enzymes are suitable for the microanalysis of 3α-hydroxy-, 3β-hydroxy-, and 3-ketosteroids.. AB - A method is described for preparing highly purified 3α- and 3β-hydroxysteroid dehydrogenases (EC 1.1.1.50 and EC 1.1.1.145, respectively), essentially uncontaminated with one another, from extracts of a steroid-induced Pseudomonas species. These enzymes are suitable for the microanalysis of 3α-hydroxy-, 3β-hydroxy-, and 3-ketosteroids.. UR - http://www.scopus.com/inward/record.url?scp=0018474352&partnerID=8YFLogxK. UR - ...
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; ...
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 ...
Hydroxysteroid Dehydrogenase - Instruments Consumables Reagents Advanced BioMatrix,RANDOX,RANDOX ELISA,Biomedical, biochemical reagents, laboratory supplies, equipment, antibodies, ELISA kits, diagnostic reagents, methods of experimental techniques, general analytical instruments, material testing instruments and equipment, used laboratory equipment, instruments and equipment, life sciences, environmental monitoring equipment , measurement, measuring instruments, rotating wall bioreactor, three-dimensional tissue / stem cell culture system; microcapsule
1I5R: A concerted, rational design of type 1 17beta-hydroxysteroid dehydrogenase inhibitors: estradiol-adenosine hybrids with high affinity
17β-Hydroxysteroid dehydrogenases (HSD17Bs) comprise a large family of 15 members that are mainly involved in sex hormone metabolism. Some HSD17Bs enzymes also play key roles in cholesterol and fatty acid metabolism. Recent study showed that hydroxysteroid 17β-dehydrogenase 13 (HSD17B13), an enzyme …
The NSDHL gene provides instructions for making an enzyme that is involved in the production (synthesis) of cholesterol. Learn about this gene and related health conditions.
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
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 received FDA approval for sale in the U.S. beginning in 2009. Vetoryl is generally marketed in four dosage strengths: 10 mg., 30 mg., 60 mg., and 120 mg. capsules. In the U.S., 5 mg. capsules are also available. All dosage strengths of brand
The enzyme 20α-hydroxysteroid dehydrogenase (20α-HSD) catalyzes the conversion of progesterone to its inactive form, 20α-hydroxyprogesterone. This enzyme has been shown to play a critical role in the regulation of luteal function in experimental animals. In this study, we cloned and expressed the gene encoding elk deer 20α-HSD from reproductive placental ...
Complete information for HSDL1 gene (Protein Coding), Hydroxysteroid Dehydrogenase Like 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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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! ...
TY - JOUR. T1 - Structural and functional aspects of placental lactogens (PLs) and ovarian 20α-hydroxysteroid dehydrogenase (20α-HSD) in the rat. AU - Shiota, K.. AU - Hirosawa, M.. AU - Hattori, N.. AU - Itonori, S.. AU - Miura, R.. AU - Noda, K.. AU - Takahashi, M.. AU - Ogawa, T.. PY - 1994. Y1 - 1994. N2 - The placenta plays an essential role in fetal growth and the maintenance of pregnancy. Successful development and maturation of the embryo is totally dependent on placental function. The main endocrine participation of the placenta is attributed to placental lactogens (PLs). Progesterone is essential for pregnancy in all mammals and is secreted by the ovary and placenta, depending on the animal species. In the rat, the main source of progesterone throughout pregnancy is the ovary, and 20α-hydroxysteroid dehydrogenase (20α-HSD) is a key enzyme for ovarian progesterone secretion. The primary action of prolactin (PRL) in the maintenance of ovarian progesterone secretion is suppression of ...
Title: Effect of Free and in Poly(η-caprolactone) Nanoparticles Incorporated New Type 1 17β -Hydroxysteroid Dehydrogenase Inhibitors on Cancer Cells. VOLUME: 6 ISSUE: 1. Author(s):Petra Kocbek, Karmen Teskac, Petra Brozic, Tea Lanisnik Rizner, Stanislav Gobec and Julijana Kristl. Affiliation:Askerceva 7, 1000 Ljubljana, Slovenia.. Keywords:Nanoparticles, enzyme inhibitors, T-47D cells, cellular uptake, drug delivery, breast cancer. Abstract: Development and progression of breast cancer can be caused by increased estradiol activity, which stimulates cell proliferation. Inhibitors of type 1 17β-hydroxysteroid dehydrogenase (17β-HSD) enzyme inhibit estradiol biosynthesis and therefore have potential anticancer activity. In this study two new trans-cinnamic acid esters were established as inhibitors of the human recombinant type 1 17β-HSD enzyme. Studied compounds are poorly water soluble and have low stability in aqueous medium. Free inhibitors were tested on T-47D cells, which express ...
Abstract Interference with the pregnancy-maintaining influence of progesterone is the basis of most methods for termination of unwanted pregnancy in dogs. The currently available methods are based on induction of luteolysis or blocking of the progesterone receptor. Inhibition of progesterone synthesis using a competitive inhibitor of 3 -hydroxysteroid dehydrogenase (3 ... read more -HSD) could be another strategy to terminate unwanted pregnancies. In this study we investigated the effects of the 3 -HSD inhibitor trilostane on corpus luteum function in non-pregnant bitches. Trilostane was administered orally for seven consecutive days in either the pituitary-independent part of the luteal phase (PIP, start of treatment on D11 after ovulation, n 6) or the pituitary-dependent part (PDP, start of treatment on D31 after ovulation, n 6), in an oral dose of about 4.5 mg/kg bw, twice daily. Results were compared with those obtained in control bitches (n 6). ACTH stimulation tests were performed to ...
Musto, N; Hafiez, A A.; and Bartke, A, Prolactin increases 17beta-hydroxysteroid dehydrogenase activity in the testis. (1972). Subject Strain Bibliography 1972. 2710 ...
Regulation of 3β‐Hydroxysteroid Dehydrogenase Activity by Human Chorionic Gonadotropin, Androgens, and Antiandrogens in Cultured Testicular ...
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 ...
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.
The biosynthesis of steroid hormones in the gonads and adrenal glands requires the activities of the enzyme 3 beta-hydroxysteroid dehydrogenase/isomerase (3 beta HSD) which catalyzes the NAD(+)-dependent dehydrogenation and subsequent delta 5--|delta 4 isomerization of delta 5-3 beta-hydroxysteroids to delta 4-3-ketosteroids. The mouse expresses four isoforms of 3 beta HSD. 3 beta HSD I is expressed in gonads and adrenal glands and appears to be the major steroidogenic form, 3 beta HSDs II and III are expressed in both liver and kidneys, and 3 beta HSD IV has been detected only in kidneys. To determine the genetic relationship between the 3 beta HSD isoforms, we have mapped the chromosomal locations of the four genes by linkage analysis using gene-specific probes derived from the 3 untranslated regions of 3 beta HSD cDNA clones. The four 3 beta HSD structural genes (Hsd3b) are closely linked within a segment of chromosome 3 that is conserved on human chromosome 1. The order of markers on
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 ...
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 ...
Aldo-keto reductase family 1 member C1 also known as 20α-hydroxysteroid dehydrogenase, 3α-hydroxysteroid dehydrogenase, and dihydrodiol dehydrogenase 1/2 is an enzyme that in humans is encoded by the AKR1C1 gene.[1][2] This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reduction of progesterone to the inactive form 20-alpha-hydroxy-progesterone. This gene shares high sequence identity with three other gene members, and is clustered with those three genes at chromosome 10p15-p14.[2] ...
Circulating levels of the steroid hormone, progesterone (P), increase during development of the primate corpus luteum (CL) and then decline during luteal regres...
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 ...
Inderbinen SG, Zogg M, Kley M, Smieško M, Odermatt A Endocrine Disruption and Steroid Hormone Action Toxicology and Applied Pharmacology, 1 Feb 2021 ...
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. [...]
Homo sapiens aldo-keto reductase family 1, member C1 (dihydrodiol dehydrogenase 1; 20-alpha (3-alpha)-hydroxysteroid dehydrogenase) (AKR1C1), mRNA. (H00001645-R01) - Products - Abnova
aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase 2; bile acid binding protein; 3-alpha hydroxysteroid dehydrogenase, type III ...
To this day, a significant proportion of the human genome remains devoid of functional characterization. In this study, we present evidence that the previously functionally uncharacterized product of the human DHRS10 gene is endowed with 17beta-HSD (17beta-hydroxysteroid dehydrogenase) activity. 17beta-HSD enzymes are primarily involved in the metabolism of steroids at the C-17 position and also of other substrates such as fatty acids, prostaglandins and xenobiotics. In vitro, DHRS10 converts NAD+ into NADH in the presence of oestradiol, testosterone and 5-androstene-3beta,17beta-diol. Furthermore, the product of oestradiol oxidation, oestrone, was identified in intact cells transfected with a construct plasmid encoding the DHRS10 protein. In situ fluorescence hybridization studies have revealed the cytoplasmic localization of DHRS10. Along with tissue expression data, this suggests a role for DHRS10 in the local inactivation of steroids in the central nervous system and placenta. The crystal structure
CP001022.PE374 Location/Qualifiers FT CDS_pept 400861..401859 FT /codon_start=1 FT /transl_table=11 FT /locus_tag=Exig_0378 FT /product=UDP-glucose 4-epimerase FT /note=TIGRFAM: UDP-glucose 4-epimerase; PFAM: FT NAD-dependent epimerase/dehydratase; short-chain FT dehydrogenase/reductase SDR; 3-beta hydroxysteroid FT dehydrogenase/isomerase; polysaccharide biosynthesis FT protein CapD; dTDP-4-dehydrorhamnose reductase; Male FT sterility domain; KEGG: bld:BLi04283 hypothetical protein FT /db_xref=EnsemblGenomes-Gn:Exig_0378 FT /db_xref=EnsemblGenomes-Tr:ACB59862 FT /db_xref=GOA:B1YIH9 FT /db_xref=InterPro:IPR001509 FT /db_xref=InterPro:IPR005886 FT /db_xref=InterPro:IPR036291 FT /db_xref=UniProtKB/TrEMBL:B1YIH9 FT /protein_id=ACB59862.1 FT /translation=MAVLVVGGAGYIGSHAVYQLVDAGQDVVVIDHLKSGHREAVHPKA FT RFYEGDIRDRAFLDTVFEKETIDQVVHFAAFSLVGESMEHPLAYFDNNVYGTQVLLEAM FT MAHDVKQIVFSSTAATYGEQEQMPILETATTNPTNAYGETKLMMEKMMRWCETAYGLNY FT ...
Life Sci. 2001 Jan 5;68(7):751-61. Links Chalcones are potent inhibitors of aromatase and 17beta-hydroxysteroid dehydrogenase activities.Le Bail JC,
Shop Inactive hydroxysteroid dehydrogenase-like protein ELISA Kit, Recombinant Protein and Inactive hydroxysteroid dehydrogenase-like protein Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
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The IUPHAR/BPS Guide to Pharmacology. hydroxysteroid 11-beta dehydrogenase 1 - 1.-.-.- Oxidoreductases. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
The IUPHAR/BPS Guide to Pharmacology. trilostane ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Kit Component:- KN307977G1, Hsd3b2 gRNA vector 1 in pCas-Guide vector- KN307977G2, Hsd3b2 gRNA vector 2 in pCas-Guide vector- KN307977D, donor vector…
Hydroxysteroid (17-beta) Dehydrogenase 4兔多克隆抗体(ab97971)可与人样本反应并经WB实验严格验证。所有产品均提供质保服务,中国75%以上现货。
Harris Brake is the third largest lake owned by the AGFC. Located adjacent Harris Brake Wildlife Management Area, this multi-use recreation site is one of the states most popular outdoor destinations thanks to its close proximity to Little Rock, Conway and Russellville. Here visitors can enjoy a relaxing day fishing, hunting or just taking in the beauty of the Ouachita Mountain foothills.. Harris Brake Lake has cover and structure galore - shoreline brush, sunken timber, cypress trees, underwater points and islands, creek channel drop-offs, old docks and artificial fish structures. Visiting anglers land plenty of big bluegills, redear sunfish, crappies, channel catfish and largemouth bass. Sportsmen may want to plan their fishing trip to coincide with hunting season. The bottomlands of Harris Brake WMA, just north of Arkansas Highway 300, offer good hunting for ducks, squirrels, rabbits, raccoons and other game animals. Additional hunting opportunities are available on nearby Winona Wildlife ...
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
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
Enzymatic interconversion of active and inactive glucocorticoid hormone is important, and is carried out physiologically by 11β-hydroxysteroid dehydrogenase (11β-HSD) isoforms, explaining their role in cellular and toxicological processes. Two forms of the enzyme, 11β-HSD-1 and 11β-HSD-2, belonging to the protein superfamily of short-chain dehydrogenases/reductases, have been structurally and functionally characterised. Although displaying dehydrogenase and reductase activities in vitro, the dominant in vivo function of the type-1 enzyme might be to work as a reductase, thus generating active cortisol from inactive cortisone precursors. On the other hand, for adrenal glucocorticoids the type-2 enzyme seems to be exclusively a dehydrogenase and, by inactivating glucocorticoids, confers specificity to peripheral mineralocorticoid receptors.
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 ...
Testosterone is metabolized in various tissues by 5α-reductase into DHT, which is 3- to 10-fold more potent as an AR agonist, and by aromatase into estradiol, which is an estrogen and lacks significant AR affinity.[1] In addition, DHT is metabolized by 3α-hydroxysteroid dehydrogenase (3α-HSD) and 3β-hydroxysteroid dehydrogenase (3β-HSD) into 3α-androstanediol and 3β-androstanediol, respectively, which are metabolites with little or no AR affinity.[1] 5α-Reductase is widely distributed throughout the body, and is concentrated to various extents in skin (particularly the scalp, beard-area of the face, pubic area, and genital area (penis and scrotum)), prostate, seminal vesicles, liver, and the brain.[1] In contrast, expression of 5α-reductase in skeletal muscle is undetectable.[1] Aromatase is highly expressed in adipose tissue and the brain, and is also expressed significantly in skeletal muscle.[1] 3α-HSD is also highly expressed in skeletal muscle.[56]. Natural AAS like testosterone ...
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.
DISCUSSION. Our baseline CON values for the E:F ratio were similar to those previously reported by others (6). The short term GFJ treatment in the present study lowered enzyme activity by 44% (Figure 3), which compares favorably to the ~40% inhibition estimated from the urinary-E/F ratio obtained in a pilot study (10) and to the ~60% obtained in a patient presenting with edema and hypokalemia associated with the habitual oral intake of 1 liter/day of GFJ (5). Taken together, our findings suggest that Sal effluents are a cost-effective and convenient matrix (compared to plasma/urine) for probing alterations in 11β-HSD2 activity induced by GFJ ingestion. In our study, the decrease in enzyme activity induced by GFJ at baseline was mainly driven by a significant decrease (~30%) in Sal-E concentration. This is in line with a decrease in F oxidation to E, a reaction that is mediated by 11β-HSD2 (1,9,10) and likely inhibited by one or more flavonoids found in GFJ (naringenin, quercetin, hesperetin, ...
trans-1,2-dihydrobenzene-1,2-diol dehydrogenase: rat liver cytosol enzyme also catalyzes 3alpha-hydroxysteroid dehydrogenase activity (EC 1.1.1.50); GenBank AH009074 (rat); RefSeq NM_001818 (human)
1. Actions of CRH on the Fetal Adrenal Gland As discussed in Chapter 3 (see Fetal Adrenal Glands), the human fetal adrenal glands are morphologically, functionally, and physiologically remarkable organs. At term, the fetal adrenal glands weigh the same as those in the adult and are similar in size to the adjacent fetal kidney. The…
Macdonald, I.A., Mahony, D.E., Jellett, J.F. and Meier, C.E. (1977). NAD-dependent 3α- and 12α-hydroxysteroid dehydrogenase activities from Eubacterium lentum ATCC no. 25559. Biochim. Biophys. Acta 489: 466-476. PMID 201289. ...
1J96: Structure of the human 3alpha-hydroxysteroid dehydrogenase type 3 in complex with testosterone and NADP at 1.25-A resolution.
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 ...
... hydroxysteroid dehydrogenase (HSD) deficiency is an inherited disorder that affects hormone-producing glands including the ... Pan Y, Zhong S, Hu RM, Gong W. Mutation of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) at the 3-untranslated region is ... A novel nonstop mutation in the stop codon and a novel missense mutation in the type II 3beta-hydroxysteroid dehydrogenase ( ... Carriers for type II 3beta-hydroxysteroid dehydrogenase (HSD3B2) deficiency can only be identified by HSD3B2 genotype study and ...
3-beta-hydroxysteroid dehydrogenase (3BHSD) deficiency is a rare genetic disorder of steroid biosynthesis that results in ... decreased production of all 3 groups of adrenal steroids, which include mineralocorticoids, glucocorticoids, and sex steroids. ... 3alpha-Hydroxysteroid dehydrogenase type III deficiency: a novel mechanism for hirsutism. J Clin Endocrinol Metab. 2008 Apr. 93 ... 3beta-Hydroxysteroid dehydrogenase in human aorta. Endocr J. 2005 Feb. 52(1):111-5. [QxMD MEDLINE Link]. ...
3-Hydroxysteroid dehydrogenase (3-HSD) may refer to: 3α-Hydroxysteroid dehydrogenase (3α-HSD) 3β-Hydroxysteroid dehydrogenase ( ... 3β-HSD) This set index page lists enzyme articles associated with the same name. If an internal link led you here, you may wish ...
3-beta-hydroxysteroid dehydrogenase (3BHSD) deficiency is a rare genetic disorder of steroid biosynthesis that results in ... decreased production of all 3 groups of adrenal steroids, which include mineralocorticoids, glucocorticoids, and sex steroids. ... 3alpha-Hydroxysteroid dehydrogenase type III deficiency: a novel mechanism for hirsutism. J Clin Endocrinol Metab. 2008 Apr. 93 ... 3beta-Hydroxysteroid dehydrogenase in human aorta. Endocr J. 2005 Feb. 52(1):111-5. [QxMD MEDLINE Link]. ...
3α-Hydroxysteroid Dehydrogenase, recombinant from bacteria (r3 α-HSDH). Download Datasheets Request a Quote ...
Omega-3 fatty acid supplementation decreases liver fat content in polycystic ovary syndrome: a randomized controlled trial ...
NADH-dependent dehydrogenase. Putative functions. 26. NA. nmrA. Putative nmrA negative transcriptional regulator family protein ... 3hydroxysteroid dehydrogenase/isomerase. Steroid metabolism. 17. (26). group_273. Recombinase/resolvase. Mobile genetic ... Volume 27, Number 3-March 2021 Research. Foodborne Origin and Local and Global Spread of Staphylococcus saprophyticus Causing ...
... hydroxysteroid:NAD+ oxidoreductase also known as 3\xCE\xB1(or 20\xCE\xB2)-hydroxysteroid dehydrogenase ... hydroxysteroid dehydrogenase:. *1hdc: Mechanism of Inhibition of 3alpha,20beta-hydroxysteroid Dehydrogenase by a Licorice- ... Hydroxysteroid Dehydrogenase and Possible Roles of The Residues Conserved in Short-chain Dehydrogenases ... 1n5d: Crystal Structure of Porcine Testicular Carbonyl Reductase/ 20beta-hydroxysteroid Dehydrogenase. *1nff: Crystal Structure ...
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The specific crossreaction of antibodies directed against mammalian liver type I 11 beta-hydroxysteroid dehydrogenase (11 beta- ... No dihydrodiol dehydrogenase activity towards trans- or cis-benzene-dihydrodiols could be detected, thus distinguishing it from ... It belongs to the protein superfamily of short-chain dehydrogenases/reductases (SDR) as established by N-terminal sequence ... Along with the 3 alpha-hydroxysteroid dehydrogenase and 3-oxo-reductase activities towards a variety of cis or trans fused A/B ...
Timeline for Protein 11-beta-hydroxysteroid dehydrogenase 1 from c.2.1.2: Tyrosine-dependent oxidoreductases: *Protein 11-beta- ... Lineage for Protein: 11-beta-hydroxysteroid dehydrogenase 1. *Root: SCOPe 2.08 *. Class c: Alpha and beta proteins (a/b) [51349 ... Protein 11-beta-hydroxysteroid dehydrogenase 1 from c.2.1.2: Tyrosine-dependent oxidoreductases appears in SCOPe 2.07. ... More info for Protein 11-beta-hydroxysteroid dehydrogenase 1 from c.2.1.2: Tyrosine-dependent oxidoreductases. ...
Beta-hydroxysteroid dehydrogenase deficiency of 3-beta-hidroxiesteriode, (3-hydroxysteroid dehydrogenase deficiency beta) - Gen ... Genetic Testing - Beta-hydroxysteroid dehydrogenase deficiency 3 -... (3-hydroxysteroid dehydrogenase deficiency beta) - Gen ... People with 3?-HSD deficiency lack many of the hormones that are synthesized in these glands. This disease is one of a group of ... In general, women with 3?-HSD deficiency are infertile. This process is due to mutations in the gene HSD3B2, located on the ...
3Beta-hydroxysteroid dehydrogenase type-2 (3β-HSD 2) deficiency *Congenital lipoid adrenal hyperplasia (lipoid CAH) (StAR ...
Compound: 3alpha-hydroxysteroid dehydrogenase type 3. Species: Homo sapiens [TaxId:9606]. Database cross-references and ... Compound: 3alpha-hydroxysteroid dehydrogenase type 3. Species: Homo sapiens [TaxId:9606]. Database cross-references and ... Description: Human 3alpha-HSD type 3 in Ternary Complex with NADP and Testosterone. Class: oxidoreductase. Keywords: Aldo-keto ...
Type I pseudohypoaldosteronism (PHAI) can be caused by an inactivating mutation of 1 of 3 encoding subunits of the epithelial ... Maintenance of serum potassium with sodium zirconium cyclosilicate (ZS-9) in heart failure patients: results from a phase 3 ... Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities. Nature. 2012 Jan 22. 482(7383):98-102 ... 11-Beta hydroxylase deficiency, 3-beta hydroxysteroid dehydrogenase deficiency, and 17 alpha-hydroxylase/17,20-lyase deficiency ...
3-β-hydroxysteroid dehydrogenase. rare. Males virilized; female virilization mild. Salt-wasting may be seen. ...
Dickson, A., Yutuc, E., Thornton, C., Dunford, J., Oppermann, U., Wang, Y., & Griffiths, W. (n.d.) HSD3B1 is an Oxysterol 3β- ... Hydroxysteroid Dehydrogenase in Human Placenta. bioRxiv. https://doi.org/10.1101/2022.04.01.486576, SU Repository: https:// ... Dickson, A., Yutuc, E., Thornton, C., Dunford, J., Oppermann, U., Wang, Y., & Griffiths, W. (n.d.) HSD3B1 is an Oxysterol 3β- ... Hydroxysteroid Dehydrogenase in Human Placenta. bioRxiv. https://doi.org/10.1101/2022.04.01.486576, SU Repository: https:// ...
3 beta-hydroxysteroid dehydrogenase type 7. Q9H2F3 HSD3B7. 16p11.2. Unknown. Not Available. ...
20 alpha-hydroxysteroid dehydrogenase,OTTHUMP00000018992,aldo-keto reductase C,aldo-keto reductase family 1, member C1, ... dihydrodiol dehydrogenase isoform DD1,hepatic dihydrodiol dehydrogenase,trans- ... High NRF2 level mediates cancer stem cell-like properties of aldehyde dehydrogenase (ALDH)-high ovarian cancer cells: ... aldo-keto reductase family 1, member C1 (dihydrodiol dehydrogenase 1; 20-alpha (3-alpha)-hydroxysteroid dehydrogenase) ...
Involvement of a 3β-hydroxysteroid dehydrogenase activity in ecdysteroid biosynthesis. *C. Dauphin-Villemant, D. Böcking, C. ...
... and 17-beta-hydroxysteroid dehydrogenase type II. These enzymes metabolize relatively weak circulating androgens, such as ... 3] scrotum, [4] foreskin, [5] shaft of penis, [6] and vulva. [7, 8, 9] Rarely reported variants have included a giant form, [10 ... Sebocytes contain androgen-metabolizing enzymes, including 5-alpha-reductase type I, 3-beta-hydroxysteroid dehydrogenase, ...
Oxidation and epimerization are catalyzed by hydroxysteroid dehydrogenase. Epimerization is a reversible stereochemical change ... 3. Fontana J, Trnka J, Mada P, Ivák P, Lavríková P, Nováková L, et al. Functions of Cells and Human Body. Prague: Karlovy ... 3). (B) Bile acids can be conjugated with either glycine or taurine. In this example, cholic acid becomes either taurocholic ... Growth of S. enterica in the presence of DOC is also associated with a decrease in 3-3 crosslinks between the sugar components ...
Genes for hydroxysteroid dehydrogenases (HSDs) 3β-HSD and 11β-HSD and cytochrome P450 aromatase A-isoform (CYP19A) were not ... hydroxysteroid dehydrogenases (HSDs) 3β-HSD [85] and 11β-HSD [86], inhibin (INHB) and cytochrome P450 aromatase A-isoform ( ... hydroxysteroid dehydrogenases including 3β-HSD and 11β-HSD. ... Figure 3. Comparison of overall gene regulation. (A) 5 ng EE2/L ... The Q-PCR conditions were 95°C for 3 min and 40 cycles at 95°C for 15 sec and 60°C for 1 min in an iCycler Thermal Cycler (Bio- ...
HSD is hydroxysteroid dehydrogenase.. *P450scc is cytochrome P450 side chain cleavage enzyme. ... The corona was 3 cm long and 8 cm in circumference. There was an ample prepuce. There was a first grade hypospadias… There were ... 3β-HSD CAH. 3βHSD II. 1p13. pregnenolone→17OH-pregnenolone→DHEA→. progesterone. 17OH-progesterone. androstenedione. ... Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency. *Congenital adrenal hyperplasia due to 11β- ...
Pitfalls in hormonal diagnosis of 17-beta hydroxysteroid dehydrogenase III deficiency. Ahmed Khattab, Tony Yuen, Mabel Yau, ... Dive into the research topics of Pitfalls in hormonal diagnosis of 17-beta hydroxysteroid dehydrogenase III deficiency. ...
3alpha(or 20beta)-hydroxysteroid dehydrogenase / testosterone dehydrogenase (NAD+) activity / androsterone dehydrogenase ... hydroxysteroid dehydrogenase / 15-hydroxyprostaglandin-D dehydrogenase (NADP+) activity / 3alpha(17beta)-hydroxysteroid ... 17-beta-hydroxysteroid dehydrogenase (NAD+) activity / NAD-retinol dehydrogenase activity / aldo-keto reductase (NADP) activity ... 3beta(or 20alpha)-hydroxysteroid dehydrogenase .... prostaglandin D2 11-ketoreductase activity / cellular response to ...

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