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).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.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 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.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)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 1.1.1.62Sulfobromophthalein: A phenolphthalein that is used as a diagnostic aid in hepatic function determination.Clofibric Acid: An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.Protein O-Methyltransferase: An enzyme that catalyzes the transfer of methyl groups from S-adenosylmethionine to free carboxyl groups of a protein molecule forming methyl esters. EC 2.1.1.-.Clofibrate: A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Heliotropium: A plant genus in the family Boraginaceae, order Lamiales, subclass Asteridae. This is the True Heliotrope that should not be confused with an unrelated plant sometimes called Garden Heliotrope (VALERIAN).Gardenia: A plant genus of the family RUBIACEAE. Members contain genepin, from which geniposide is obtained for use as a crosslinking agent in ADHESIVES, and 3-caffeoyl-4-sinapoylquinic acid.Mice, Inbred AKRStructure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Fluids and Secretions: Liquid substances produced by living organisms to fulfill specific functions or excreted as waste.Mythology: A body of stories, the origins of which may be unknown or forgotten, that serve to explain practices, beliefs, institutions or natural phenomena. Mythology includes legends and folk tales. It may refer to classical mythology or to a body of modern thought and modern life. (From Webster's 1st ed)MEDLINE: The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).Otolaryngology: A surgical specialty concerned with the study and treatment of disorders of the ear, nose, and throat.Churg-Strauss Syndrome: Widespread necrotizing angiitis with granulomas. Pulmonary involvement is frequent. Asthma or other respiratory infection may precede evidence of vasculitis. Eosinophilia and lung involvement differentiate this disease from POLYARTERITIS NODOSA.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.Progesterone Reductase: An enzyme that catalyzes the reduction of a 3 beta-hydroxy-delta(5)-steroid to 3-oxo-delta(4)-steroid in the presence of NAD. It converts pregnenolone to progesterone and dehydroepiandrosterone to androstenedione. EC 1.1.1.145.Cortisone Reductase: An enzyme that catalyzes the interconversion of a ketone and hydroxy group at C-20 of cortisone and other 17,20,21-trihydroxy steroids. EC 1.1.1.53.Pregnanes: Saturated derivatives of the steroid pregnane. The 5-beta series includes PROGESTERONE and related hormones; the 5-alpha series includes forms generally excreted in the urine.Steroid Isomerases: Enzymes that catalyze the transposition of double bond(s) in a steroid molecule. EC 5.3.3.17-Ketosteroids: Steroids that contain a ketone group at position 17.Mandatory Testing: Testing or screening required by federal, state, or local law or other agencies for the diagnosis of specified conditions. It is usually limited to specific populations such as categories of health care providers, members of the military, and prisoners or to specific situations such as premarital examinations or donor screening.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Frameshift Mutation: A type of mutation in which a number of NUCLEOTIDES deleted from or inserted into a protein coding sequence is not divisible by three, thereby causing an alteration in the READING FRAMES of the entire coding sequence downstream of the mutation. These mutations may be induced by certain types of MUTAGENS or may occur spontaneously.Disorders of Sex Development: In gonochoristic organisms, congenital conditions in which development of chromosomal, gonadal, or anatomical sex is atypical. Effects from exposure to abnormal levels of GONADAL HORMONES in the maternal environment, or disruption of the function of those hormones by ENDOCRINE DISRUPTORS are included.Steroid 21-Hydroxylase: An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).Corpus Luteum: The yellow body derived from the ruptured OVARIAN FOLLICLE after OVULATION. The process of corpus luteum formation, LUTEINIZATION, is regulated by LUTEINIZING HORMONE.Progesterone: The major progestational steroid that is secreted primarily by the CORPUS LUTEUM and the PLACENTA. Progesterone acts on the UTERUS, the MAMMARY GLANDS and the BRAIN. It is required in EMBRYO IMPLANTATION; PREGNANCY maintenance, and the development of mammary tissue for MILK production. Progesterone, converted from PREGNENOLONE, also serves as an intermediate in the biosynthesis of GONADAL STEROID HORMONES and adrenal CORTICOSTEROIDS.Pregnancy, Unwanted: Pregnancy, usually accidental, that is not desired by the parent or parents.Luteal Phase: The period in the MENSTRUAL CYCLE that follows OVULATION, characterized by the development of CORPUS LUTEUM, increase in PROGESTERONE production by the OVARY and secretion by the glandular epithelium of the ENDOMETRIUM. The luteal phase begins with ovulation and ends with the onset of MENSTRUATION.Encephalomalacia: Softening or loss of brain tissue following CEREBRAL INFARCTION; cerebral ischemia (see BRAIN ISCHEMIA), infection, CRANIOCEREBRAL TRAUMA, or other injury. The term is often used during gross pathologic inspection to describe blurred cortical margins and decreased consistency of brain tissue following infarction. Multicystic encephalomalacia refers to the formation of multiple cystic cavities of various sizes in the cerebral cortex of neonates and infants following injury, most notably perinatal hypoxia-ischemic events. (From Davis et al., Textbook of Neuropathology, 2nd ed, p665; J Neuropathol Exp Neurol, 1995 Mar;54(2):268-75)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.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.Comamonas testosteroni: A species of gram-negative, aerobic rods formerly called Pseudomonas testosteroni. It is differentiated from other Comamonas species by its ability to assimilate testosterone and to utilize phenylacetate or maleate as carbon sources.Hydroxysteroids: Steroids in which one or more hydroxy groups have been substituted for hydrogen atoms either within the ring skeleton or on any of the side chains.Crystallography, X-Ray: The study of crystal structure using X-RAY DIFFRACTION techniques. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
(1/633) Luteinizing hormone inhibits conversion of pregnenolone to progesterone in luteal cells from rats on day 19 of pregnancy.

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)

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

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)

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

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)

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

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)

(5/633) 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.

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)

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

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)

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

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)

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

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)

*  3-Hydroxysteroid dehydrogenase
... (3-HSD) may refer to: 3α-Hydroxysteroid dehydrogenase (3α-HSD) 3β-Hydroxysteroid dehydrogenase ( ...
*  3β-Hydroxysteroid dehydrogenase
Neville AM, Orr JC, Engel LL (1968). "Delta5-3beta-Hydroxy steroid dehydrogenase activities of bovine adrenal cortex". Biochem ... "Molecular biology of the 3beta-hydroxysteroid dehydrogenase/delta5-delta4 isomerase gene family". Endocr. Rev. 26 (4): 525-82. ... ene steroid dehydrogenase 3β-hydroxy steroid dehydrogenase/isomerase 3β-hydroxy-Δ5-C27-steroid dehydrogenase/isomerase 3β- ... 3β-HSD is also known as delta Δ5-4-isomerase, which catalyzes the oxidative conversion of Δ5-3β-hydroxysteroids to the Δ4-3- ...
*  3α-Hydroxysteroid dehydrogenase
... of 3alpha-hydroxysteroid/dihydrodiol dehydrogenase in human liver". Pharmacogenetics. 9 (6): 763-71. doi:10.1097/00008571- ... "Close kinship of human 20alpha-hydroxysteroid dehydrogenase gene with three aldo-keto reductase genes". Genes to Cells. 5 (2): ... of mirtazapine on plasma concentrations of neuroactive steroids in major depression and on 3alpha-hydroxysteroid dehydrogenase ... of mirtazapine on plasma concentrations of neuroactive steroids in major depression and on 3alpha-hydroxysteroid dehydrogenase ...
*  Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency
"Congenital adrenal hyperplasia due to 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase deficiency". Semin. Reprod ... Like the other forms of CAH, suspicion of severe 3β-HSD CAH is usually raised by the appearance of the genitalia at birth or by ... 3β-HSD II also mediates an alternate route of testosterone synthesis from androstenediol in the testes. 3β-HSD deficiency ... 3β-HSD II mediates three parallel dehydrogenase/isomerase reactions in the adrenals that convert Δ4 to Δ5 steroids: ...
*  3(or 17)a-hydroxysteroid dehydrogenase
... beta-hydroxysteroid dehydrogenase). Lau, P.C.K.; Layne, D.S.; Williamson, D.G. (1982). "A 3(17)α-hydroxysteroid dehydrogenase ... α-hydroxysteroid dehydrogenases of female rabbit kidney and liver". J. Biol. Chem. 257: 9450-9456. PMID 6955303. 3(or 17)alpha- ... alpha-hydroxysteroid dehydrogenase (EC 1.1.1.209, 3(17)alpha-hydroxysteroid dehydrogenase) is an enzyme with systematic name 3( ... hydroxysteroid dehydrogenase at the US National Library of Medicine Medical Subject Headings (MeSH) Molecular and Cellular ...
*  3β-Androstenol
... , also known as 5α-androst-16-en-3β-ol, is a naturally occurring mammalian pheromone known to be present in ... It is produced from androstenone via the enzyme 3β-hydroxysteroid dehydrogenase. Unlike its C3α epimer 3α-androstenol, 3β- ... 3α-androstenol, 3β-androstenol, skatole, and indole in pig fat by means of stable isotope dilution analysis-headspace solid- ...
*  Progesterone
Subsequently, 20α-hydroxysteroid dehydrogenase and 20β-hydroxysteroid dehydrogenase reduce these metabolites to form the ... Progesterone is highly susceptible to enzymatic reduction via reductases and hydroxysteroid dehydrogenases due to its double ... First, the 3β-hydroxyl group is oxidized to a keto group and second, the double bond is moved to C4, from C5 through a keto/ ... 27 (3): 229-39. doi:10.1055/s-0029-1216276. PMC 2675922 . PMID 19401954. Li Z, Wang B, Kan Z, Zhang B, Yang Z, Chen J, Wang D, ...
*  Δ4-Abiraterone
However, the initial 5α-reduced metabolite of D4A, 3-keto-5α-abiraterone, is an agonist of the AR, and has been found to ... D4A is specifically an inhibitor of CYP17A1 (17α-hydroxylase/17,20-lyase), 3β-HSD, and 5α-reductase. In addition, it has also ... Δ4-Abiraterone (D4A; code name CB-7627), also known as 17-(3-pyridyl)androsta-4,16-dien-3-one, is a steroidogenesis inhibitor ... 3β-HSD). It is said to be a more potent inhibitor of steroidogenesis than abiraterone, and is partially responsible for the ...
*  3-Keto-5α-abiraterone
... , also known as 17-(3-pyridyl)-5α-androst-16-en-3-one, is an active metabolite of abiraterone acetate that ... 3-Keto-5α-abiraterone may counteract the clinical effectiveness of abiraterone acetate, and so inhibition of its formation ... It is formed as follows: abiraterone acetate to abiraterone by esterases; abiraterone to Δ4-abiraterone by 3β-hydroxysteroid ... dehydrogenase/Δ5-4 isomerase; and Δ4-abiraterone to 3-keto-5α-abiraterone by 5α-reductase. ...
*  3β-Dihydroprogesterone
Unlike 3α-dihydroprogesterone, 3β-DHP does not act as a positive allosteric modulator of the GABAA, which is in accordance with ... 3β-Dihydroprogesterone (3β-DHP), also known as 3β-hydroxyprogesterone or pregn-4-en-3β-ol-20-one (4-pregnenolone), is an ... 5α-Dihydroprogesterone 5β-Dihydroprogesterone 3β-Androstanediol Pregnenolone Quingestrone Kavaliers, Martin; Wiebe, John P.; ... It is biosynthesized by 3β-hydroxysteroid dehydrogenase from progesterone. ...
*  3α-Dihydroprogesterone
3α-DHP has been found to act as a positive allosteric modulator of the GABAA receptor and is described as being as active as ... 3α-Dihydroprogesterone (3α-DHP), also known as 3α-hydroxyprogesterone, as well as pregn-4-en-3α-ol-20-one, is an endogenous ... 3α-DHP has also been found to inhibit the secretion of follicle-stimulating hormone (FSH) from the rat pituitary gland, ... Unlike the case of most other inhibitory neurosteroids, 3α-DHP production is not blocked by 5α-reductase inhibitors like ...
*  3alpha(17beta)-hydroxysteroid dehydrogenase (NAD+)
17beta-hydroxy steroid dehydrogenase, 3alpha(17beta)-HSD, and 3alpha(17beta)-hydroxysteroid dehydrogenase (NAD+). This enzyme ... In enzymology, a 3alpha(17beta)-hydroxysteroid dehydrogenase (NAD+) (EC 1.1.1.239) is an enzyme that catalyzes the chemical ... hydroxysteroid dehydrogenase distinct from 3α-hydroxysteroid dehydrogenase in hamster liver". Biochem. J. 266 (2): 583-9. PMC ... The systematic name of this enzyme class is 3alpha(or 17beta)-hydroxysteroid:NAD+ oxidoreductase. Other names in common use ...
*  Gestrinone
Hydroxysteroid Dehydrogenase (3.BETA.-HSD), 17.ALPHA.-Hydroxylase and 17, 20 Lyase by Progestins and Danazol". Endocrinologia ... 141-. ISBN 978-3-319-14385-9. CS1 maint: Multiple names: authors list (link) Bromham, D. R.; Booker, M. W.; Rose, Gillian; ... ISBN 978-3-88763-075-1. Dr. Ian Morton; I.K. Morton; Judith M. Hall (31 October 1999). Concise Dictionary of Pharmacological ... 36 (3): 387-394. doi:10.1507/endocrj1954.36.387. ISSN 0013-7219. Tamaya T, Fujimoto J, Watanabe Y, Arahori K, Okada H (1986). " ...
*  Trilostane
Retrieved 3 April 2011. de Gier J; Wolthers CH; Galac S; Okkens AC; Kooistra HS (April 2011). "Effects of the 3β-hydroxysteroid ... dehydrogenase inhibitor trilostane on luteal progesterone production in the dog". Theriogenology. 75 (7): 1271-9. doi:10.1016/j ... Retrieved 3 April 2011. Braddock, JA, Church, DB, Robertson, ID, Watson, ADJ (October 2003). "Trilostane treatment in dogs with ... Retrieved 3 April 2011. (PDF) "Treating Cushing's Disease in Dogs". US Food and Drug Administration. Retrieved 3 April 2011. " ...
*  Medroxyprogesterone acetate
"The biological activity of 3alpha-hydroxysteroid oxido-reductase in the spinal cord regulates thermal and mechanical pain ... Less than 3% of a dose is excreted in unconjugated form. With intramuscular administration, the high levels of MPA in the blood ... MPA is described as extremely potent in its inhibition of rat 3α-HSD, with an IC50 of 0.2 μM and a Ki (in rat testicular ... ISBN 978-3-527-60749-5. Archived from the original on 2017-11-05. "WHO Model List of Essential Medicines (19th List)" (PDF). ...
*  3alpha-hydroxysteroid dehydrogenase (B-specific)
In enzymology, a 3alpha-hydroxysteroid dehydrogenase (B-specific) (EC 1.1.1.50) is an enzyme that catalyzes the chemical ... Marcus PI; Talalay P (1956). "Induction and purification of alpha- and beta-hydroxysteroid dehydrogenases". J. Biol. Chem. 218 ... more specifically it is part of the group of hydroxysteroid dehydrogenases. The systematic name of this enzyme class is 3alpha- ... hydroxysteroid:NAD(P)+ oxidoreductase (B-specific). Other names in common use include hydroxyprostaglandin dehydrogenase, ...
*  Zanoterone
154 (3): 1060-1064. doi:10.1016/S0022-5347(01)66976-3. ISSN 0022-5347. Roberts, Alan E.; Ritz, Martha A.; Hoekstra, Susan; ... 11 (3): 101-110. doi:10.1002/(SICI)1522-7146(1996)11:3. 3.0.CO;2-O. ISSN 0887-2082. PMID 9029268. ... ISBN 978-0-8155-1856-3. Dr. Ian Morton; I.K. Morton; Judith M. Hall (31 October 1999). Concise Dictionary of Pharmacological ... Zanoterone does not inhibit 5α-reductase, aromatase, or 3α- or 3β-hydroxysteroid dehydrogenase in vitro. The drug significantly ...
*  AKR1C1
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 ... Aldo-keto reductase family 1 member C1 also known as 20α-hydroxysteroid dehydrogenase, 3α-hydroxysteroid dehydrogenase, and ... hydroxysteroid dehydrogenase)". Human AKR1C1 genome location and AKR1C1 gene details page in the UCSC Genome Browser. Human C9 ...
*  Genetic studies on Arabs
Rosler, A (August 2006). "17 beta-hydroxysteroid dehydrogenase 3 deficiency in the Mediterranean population". Pediatric ... glucose-6-phosphate dehydrogenase deficiency, and fragile X syndrome (FXS), which is an inherited genetic condition with ... glucose-6-phosphate dehydrogenase deficiency, alpha-thalassemia, molecular characterization, recessive osteoperosis, ... 16 (3): 374-86. doi:10.1038/sj.ejhg.5201934. PMID 17928816. Abu-Amero, KK; Hellani, A; González, AM; Larruga, JM; Cabrera, VM; ...
*  HSD17B3
17β-Hydroxysteroid dehydrogenase 3 (17β-HSD3) is an enzyme that in humans is encoded by the HSD17B3 gene and is involved in ... "Entrez Gene: HSD17B3 hydroxysteroid (17-beta) dehydrogenase 3". Ademola Akesode F, Meyer WJ, Migeon CJ (December 1977). "Male ... 17β-Hydroxysteroid dehydrogenase GRCh38: Ensembl release 89: ENSG00000130948 - Ensembl, May 2017 GRCm38: Ensembl release 89: ... Rösler A, Silverstein S, Abeliovich D (May 1996). "A (R80Q) mutation in 17 beta-hydroxysteroid dehydrogenase type 3 gene among ...
*  17β-Hydroxysteroid dehydrogenase III deficiency
"HSD17B3 hydroxysteroid 17-beta dehydrogenase 3 [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2017-03- ... 17β-Hydroxysteroid dehydrogenase III deficiency is a rare disorder of sexual development, or intersex condition, affecting ... A 2010 review put the risk of germ cell tumors at 17%. The management of 17β-hydroxysteroid dehydrogenase III deficiency can ... Hewitt and Warne state that, children with 17β-hydroxysteroid dehydrogenase III deficiency who are raised as girls often later ...
*  AKR1C3
Aldo-keto reductase family 1 member C3 (AKR1C3), also known as 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5, HSD17B5) is a ... Rheault P, Dufort I, Soucy P, Luu-The V (1999). "Assignment of HSD17B5 encoding type 5 17 beta-hydroxysteroid dehydrogenase to ... "Human 3alpha-hydroxysteroid dehydrogenase isoforms (AKR1C1-AKR1C4) of the aldo-keto reductase superfamily: functional ... "Close kinship of human 20alpha-hydroxysteroid dehydrogenase gene with three aldo-keto reductase genes". Genes to Cells. 5 (2): ...
*  Sertraline
9 (3): 151-7. doi:10.1007/s00737-005-0111-y. PMID 16292466. Hansen RA, Gaynes BN, Gartlehner G, Moore CG, Tiwari R, Lohr KN ( ... 25 (3): 193-200. doi:10.1002/hup.1106. PMID 20373470. Meyer JH, Wilson AA, Sagrati S, Hussey D, Carella A, Potter WZ, Ginovart ... Suppl 3: 22-34. PMID 11229450. Croft H, Settle E, Houser T, Batey SR, Donahue RM, Ascher JA (1999). "A placebo-controlled ... 3: 113-148. doi:10.1016/S1067-5698(06)80005-2. ISBN 978-1-55938-798-9. Sarges R, Tretter JR, Tenen SS, Weissman A (1973). "5,8- ...
*  Neurosteroidogenesis inhibitor
... of mirtazapine on plasma concentrations of neuroactive steroids in major depression and on 3alpha-hydroxysteroid dehydrogenase ... "The biological activity of 3alpha-hydroxysteroid oxido-reductase in the spinal cord regulates thermal and mechanical pain ... 29 (3): 339-54. doi:10.1016/s0306-4530(03)00033-7. PMID 14644065. de Wit H, Schmitt L, Purdy R, Hauger R (2001). "Effects of ... 11 (3): 261-72. doi:10.1038/sj.mp.4001782. PMID 16344854. Civic D, Scholes D, Ichikawa L, et al. (June 2000). "Depressive ...
*  Dihydrotestosterone
ISBN 978-0-323-29738-7. Jin Y, Penning TM (2001). "Steroid 5alpha-reductases and 3alpha-hydroxysteroid dehydrogenases: key ... It has an affinity (Kd) of 0.25 to 0.5 nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = ... 63-. ISBN 978-3-88763-075-1. List PH, Hörhammer L (12 March 2013). Chemikalien und Drogen: Teil B: R, S. Springer-Verlag. pp. ... 3α-Androstanediol is a potent positive allosteric modulator of the GABAA receptor, while 3β-androstanediol is a potent and ...
*  List of diseases (C)
X-linked type 3, recessive Charcot-Marie-Tooth disease Charcot-Marie-Tooth peroneal muscular atrophy, X-linked CHARGE syndrome ... monosomy 3q27 Chromosome 3, trisomy 3p Chromosome 3, trisomy 3p25 Chromosome 3, trisomy 3q Chromosome 3, trisomy 3q13 2 q25 ... monosomy 3p Chromosome 3, monosomy 3p14 p11 Chromosome 3, monosomy 3p2 Chromosome 3, monosomy 3p25 Chromosome 3, monosomy 3q13 ... trisomy 5pter p13 3 Chromosome 5, trisomy 5q Chromosome 5, uniparental disomy Chromosome 6 - Chromosome 7 Chromosome 6 ring ...
3-Hydroxysteroid dehydrogenase - Wikipedia  3-Hydroxysteroid dehydrogenase - Wikipedia
3-Hydroxysteroid dehydrogenase (3-HSD) may refer to: 3α-Hydroxysteroid dehydrogenase (3α-HSD) 3β-Hydroxysteroid dehydrogenase ( ...
more infohttps://en.wikipedia.org/wiki/3-Hydroxysteroid_dehydrogenase
3β-Hydroxysteroid dehydrogenase - Wikipedia  3β-Hydroxysteroid dehydrogenase - Wikipedia
Neville AM, Orr JC, Engel LL (1968). "Delta5-3beta-Hydroxy steroid dehydrogenase activities of bovine adrenal cortex". Biochem ... "Molecular biology of the 3beta-hydroxysteroid dehydrogenase/delta5-delta4 isomerase gene family". Endocr. Rev. 26 (4): 525-82. ... ene steroid dehydrogenase 3β-hydroxy steroid dehydrogenase/isomerase 3β-hydroxy-Δ5-C27-steroid dehydrogenase/isomerase 3β- ... 3β-HSD is also known as delta Δ5-4-isomerase, which catalyzes the oxidative conversion of Δ5-3β-hydroxysteroids to the Δ4-3- ...
more infohttps://en.wikipedia.org/wiki/3%CE%B2-Hydroxysteroid_dehydrogenase
3-beta-hydroxysteroid dehydrogenase deficiency - Genetics Home Reference  3-beta-hydroxysteroid dehydrogenase deficiency - Genetics Home Reference
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 ... Simard J, Moisan AM, Morel Y. Congenital adrenal hyperplasia due to 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) ... Carboxyl-terminal mutations in 3beta-hydroxysteroid dehydrogenase type II cause severe salt-wasting congenital adrenal ...
more infohttps://ghr.nlm.nih.gov/condition/3-beta-hydroxysteroid-dehydrogenase-deficiency
IJMS  | Free Full-Text | Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4 Isomerase: A Review | Notes  IJMS | Free Full-Text | Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4 Isomerase: A Review | Notes
3β-HSD is often associated with steroidogenesis, but its function in the metabolism of both steroids and xenobiotics is more ... 3β-HSD is involved in the synthesis of a number of natural steroid hormones, including progesterone and testosterone, and the ... Much of the research conducted on porcine 3β-HSD is motivated by its importance for the occurrence of the boar taint phenomenon ... This review focuses on the expression and regulation of 3β-hydroxysteroid dehydrogenase/Δ5-Δ4 isomerase (3β-HSD), with emphasis ...
more infohttp://www.mdpi.com/1422-0067/14/9/17926/notes
3 beta-hydroxysteroid dehydrogenase deficiency - wikidoc  3 beta-hydroxysteroid dehydrogenase deficiency - wikidoc
"Newly proposed hormonal criteria via genotypic proof for type II 3beta-hydroxysteroid dehydrogenase deficiency". J. Clin. ... 21 (3): 245-91. doi:10.1210/edrv.21.3.0398. PMID 10857554.. *↑ Hohl A, Ronsoni MF, Oliveira M (2014). "Hirsutism: diagnosis and ... "3-beta-hydroxysteroid dehydrogenase deficiency - Genetics Home Reference".. *↑ Simard J, Rheaume E, Mebarki F, Sanchez R, New ... 3 beta-hydroxysteroid dehydrogenase deficiency must be differentiated from diseases that cause ambiguous genitalia:[2][3] ...
more infohttps://www.wikidoc.org/index.php/Congenital_adrenal_hyperplasia_due_to_3_beta-hydroxysteroid_dehydrogenase_deficiency
Browsing  by subject 3-Hydroxysteroid Dehydrogenases  Browsing by subject "3-Hydroxysteroid Dehydrogenases"
Paracrine interactions between adipose fibroblasts and malignant epithelial cells are essential for structural and hormonal support of breast tumors. Factors derived from malignant epithelial cells inhibit adipogenic ...
more infohttps://repository.icr.ac.uk/browse?value=3-Hydroxysteroid+Dehydrogenases&type=subject
Activation of Human Liver 3α-Hydroxysteroid Dehydrogenase by Clofibrate Derivatives | Journal of Pharmacology and Experimental...  Activation of Human Liver 3α-Hydroxysteroid Dehydrogenase by Clofibrate Derivatives | Journal of Pharmacology and Experimental...
... is identified with human liver dihydrodiol dehydrogenase isoform 1 that exhibits high 20α-hydroxysteroid dehydrogenase and very ... hydroxysteroid dehydrogenase from human prostatic cytosol. J Steroid Biochem Mol Biol 42:321-327. ... Lineweaver-Burk analysis of the dual effects of clofibric acid on the dehydrogenase activity of AKR 1C4. In A and B, the ... 1990) Purification and properties of multiple forms of dihydrodiol dehydrogenase from human liver. J Biochem (Tokyo) 108:250- ...
more infohttp://jpet.aspetjournals.org/content/285/3/1096
Hsd3b5 - 3 beta-hydroxysteroid dehydrogenase type 5 - Rattus norvegicus (Rat) - Hsd3b5 gene & protein  Hsd3b5 - 3 beta-hydroxysteroid dehydrogenase type 5 - Rattus norvegicus (Rat) - Hsd3b5 gene & protein
The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. HSD V can only ... Exhibits only 3-ketosteroid reductase activity in the presence of NADPH and does not function as an isomerase. ... steroid dehydrogenase activity Source: RGD ,p>Traceable Author Statement,/p> ,p>Used for information from review articles where ... 3 beta-hydroxysteroid dehydrogenase type 5Add BLAST. 373. Amino acid modifications. Feature key. Position(s). Description ...
more infohttps://www.uniprot.org/uniprot/P27364
BRENDA - 1.1.1.50: 3alpha-hydroxysteroid 3-dehydrogenase (Si-specific)  BRENDA - 1.1.1.50: 3alpha-hydroxysteroid 3-dehydrogenase (Si-specific)
3alpha-hydroxy steroid, type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase, type 3 3alpha- ... 3alpha-hydroxysteroid dehydrogenase, 3alpha-hydroxysteroid dehydrogenase/carbonyl reductase, 3alpha-hydroxysteroid oxido- ... hydroxyprostaglandin dehydrogenase, More, NAD(P)+-3alpha-hydroxysteroid dehydrogenase, NAD+-dependent 3alpha-HSD, NADP(H)- ... 3alpha/3beta-hydroxysteroid dehydrogenase, 3alphaHSD, 3HSD, 5alpha-dihydroprogesterone 3alpha-hydroxysteroid oxidoreductase, ...
more infohttp://www.brenda-enzymes.org/all_enzymes.php?ecno=1.1.1.50&table=Storage_Stability
BRENDA - 1.1.1.50: 3alpha-hydroxysteroid 3-dehydrogenase (Si-specific)  BRENDA - 1.1.1.50: 3alpha-hydroxysteroid 3-dehydrogenase (Si-specific)
3alpha-hydroxy steroid, type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase, type 3 3alpha- ... 3alpha-hydroxysteroid dehydrogenase, 3alpha-hydroxysteroid dehydrogenase/carbonyl reductase, 3alpha-hydroxysteroid oxido- ... hydroxyprostaglandin dehydrogenase, More, NAD(P)+-3alpha-hydroxysteroid dehydrogenase, NAD+-dependent 3alpha-HSD, NADP(H)- ... 3alpha/3beta-hydroxysteroid dehydrogenase, 3alphaHSD, 3HSD, 5alpha-dihydroprogesterone 3alpha-hydroxysteroid oxidoreductase, ...
more infohttp://www.brenda-enzymes.org/all_enzymes.php?ecno=1.1.1.50&table=pH_Stability
Info required on 3-beta-hydroxy steroid dehydrogenase  Info required on 3-beta-hydroxy steroid dehydrogenase
cheers, : , ,Max You'll find a lot of information if you search medline with the words : short-chain dehydrogenases. In 1995 ... I would appreciate any leads to literature that cover the structure, : , ,function, kinetics and recent development on 3-beta ... Info required on 3-beta-hydroxy steroid dehydrogenase. Lluis Ribas lluis at aars.mit.edu Thu Sep 26 10:06:28 EST 1996 *Previous ...
more infohttp://www.bio.net/bionet/mm/proteins/1996-September/004670.html
Hsd3b2 - 3 beta-hydroxysteroid dehydrogenase/Delta 5--|4-isomerase type 2 - Mus musculus (Mouse) - Hsd3b2 gene & protein  Hsd3b2 - 3 beta-hydroxysteroid dehydrogenase/Delta 5--|4-isomerase type 2 - Mus musculus (Mouse) - Hsd3b2 gene & protein
3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the ... The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. ... 3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta5-ene-3-beta-hydroxy steroid, and the ... The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. ...
more infohttp://www.uniprot.org/uniprot/P26149
3 Beta Hydroxysteroid Dehydrogenase Deficiency: What Is 3 Beta Hydroxysteroid Dehydrogenase Deficiency?  3 Beta Hydroxysteroid Dehydrogenase Deficiency: What Is 3 Beta Hydroxysteroid Dehydrogenase Deficiency?
Read about 3 beta hydroxysteroid dehydrogenase deficiency medical facts: what is the definition of 3 beta hydroxysteroid ... Read about 3 beta hydroxysteroid dehydrogenase deficiency medical facts: what is the definition of 3 beta hydroxysteroid ... dehydrogenase deficiency, pathophysiology, medical care, frequency, mortality or morbidity, and related 3 beta hydroxysteroid ... dehydrogenase deficiency, pathophysiology, medical care, frequency, mortality or morbidity, and related 3 beta hydroxysteroid ...
more infohttps://signssymptoms.org/definition-for-disease-signs-symptoms-and-treatment/?3_beta_hydroxysteroid_dehydrogenase_deficiency-8
Sequence Similarity 









- 1AFS: RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH...  Sequence Similarity - 1AFS: RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH...
... crystal structure of testosterone and NADP+ bound to 3 alpha-hydroxysteroid/dihydrodiol dehydrogenase. ... 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE protein, length: 323 (BLAST) Sequence Similarity Cutoff. Rank. Chains in Cluster. Cluster ... RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH NADP AND TESTOSTERONE. ...
more infohttp://www.rcsb.org/pdb/explore/sequenceCluster.do?structureId=1AFS
RCSB PDB 









- 1AFS: RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH NADP AND...  RCSB PDB - 1AFS: RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH NADP AND...
... crystal structure of testosterone and NADP+ bound to 3 alpha-hydroxysteroid/dihydrodiol dehydrogenase. ... 3-alpha-hydroxysteroid dehydrogenase Rat (Rattus norvegicus) [TaxId: 10116] B. d1afsb_. Alpha and beta proteins (a/b) TIM beta/ ... RECOMBINANT RAT LIVER 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE (3-ALPHA-HSD) COMPLEXED WITH NADP AND TESTOSTERONE. ...
more infohttp://www.rcsb.org/pdb/explore/derivedData.do?structureId=1AFS
Gender Change in 46,XY Persons with 5α-Reductase-2 Deficiency and 17β-Hydroxysteroid Dehydrogenase-3 Deficiency | SpringerLink  Gender Change in 46,XY Persons with 5α-Reductase-2 Deficiency and 17β-Hydroxysteroid Dehydrogenase-3 Deficiency | SpringerLink
... and 17β-hydroxysteroid dehydrogenase-3 deficiency (17β-HSD-3) are often raised as girls. Over the past number of years, this ... Individuals with 5α-reductase-2 deficiency (5α-RD-2) and 17β-hydroxysteroid dehydrogenase-3 deficiency (17β-HSD-3) are often ... Rösler, A., Silverstein, S., & Abeliovich, D. (1996). A (R80Q) mutation in 17 β-hydroxysteroid dehydrogenase type 3 gene among ... Gender Change in 46,XY Persons with 5α-Reductase-2 Deficiency and 17β-Hydroxysteroid Dehydrogenase-3 Deficiency. ...
more infohttps://link.springer.com/article/10.1007%2Fs10508-005-4339-4
17-Beta hydroxysteroid dehydrogenase 3 deficiency  17-Beta hydroxysteroid dehydrogenase 3 deficiency
... Common Name(s). 17-Beta hydroxysteroid dehydrogenase 3 deficiency, 17-Beta ... 17-beta hydroxysteroid dehydrogenase 3 deficiency is caused by mutations in the HSD17B3 gene and is inherited in an autosomal ... 17-beta hydroxysteroid dehydrogenase 3 deficiencyis an inherited condition that affects male sexual development. People with ... Please click this link to visit the PubMed website for results on "17-Beta hydroxysteroid dehydrogenase 3 deficiency". ...
more infohttp://diseaseinfosearch.org/17-Beta+hydroxysteroid+dehydrogenase+3+deficiency/5
Most recent papers with the keyword 3 beta-hydroxysteroid dehydrogenase deficiency | Read by QxMD  Most recent papers with the keyword "3 beta-hydroxysteroid dehydrogenase deficiency" | Read by QxMD
CONCURRENT 3-BETA-HYDROXYSTEROID DEHYDROGENASE DEFICIENCY IN ADRENAL AND SCLEROCYSTIC OVARY.. L R AXELROD, J W GOLDZIEHER, S D ... Steroid 3-beta hydroxysteroid dehydrogenase type II (3β-HSD2) deficiency is a rare autosomal recessive form of congenital ... 3 beta-hydroxysteroid dehydrogenase deficiency is a disorder of steroid biosynthesis resulting in decreased production of all 3 ... The structures of the highly homologous type I and II 3 beta-HSD genes have been analyzed in three male pseudohermaphrodite 3 ...
more infohttps://www.readbyqxmd.com/keyword/109579
Genetic variation of 3β-hydroxysteroid dehydrogenase type II in three racial/ethnic groups: Implications for prostate cancer...  Genetic variation of 3β-hydroxysteroid dehydrogenase type II in three racial/ethnic groups: Implications for prostate cancer...
Devgan, S.A.,Reichardt, J.K.V.,Henderson, B.E.,Yu, M.C.,Pike, M.C.,Ross, R.K.,Shi, C.-Y. (1997). Genetic variation of 3β- ... hydroxysteroid dehydrogenase type II in three racial/ethnic groups: Implications for prostate cancer risk. Prostate 33 (1) : 9- ... Genetic variation of 3β-hydroxysteroid dehydrogenase type II in three racial/ethnic groups: Implications for prostate cancer ...
more infohttp://scholarbank.nus.edu.sg/handle/10635/31836
Mitochondrial 3 beta-hydroxysteroid dehydrogenase (HSD) is essential for the synthesis of progesterone by corpora lutea: An...  Mitochondrial 3 beta-hydroxysteroid dehydrogenase (HSD) is essential for the synthesis of progesterone by corpora lutea: An...
... the enzyme 3 beta-hydroxysteroid dehydrogenase (HSD) is distributed between microsomes and mitochondria. Throughout the ... Thomas JL, Mason JI, Blanco G, Veisaga ML: The engineered, cytosolic form of human type I β-hydroxysteroid dehydrogenase/ ... The enzymes that catalyze the latter reaction are NADP+-linked isocitrate dehydrogenase and NADP+-linked malate dehydrogenase. ... The role of nicotinamide-adenine dinucleotide phosphate-dependent malate dehydrogenase and isocitrate dehydrogenase in the ...
more infohttps://rbej.biomedcentral.com/articles/10.1186/1477-7827-3-11
  • 3β-HSD is also known as delta Δ5-4-isomerase, which catalyzes the oxidative conversion of Δ5-3β-hydroxysteroids to the Δ4-3-keto configuration and is, therefore, essential for the biosynthesis of all classes of hormonal steroids, namely progesterone, glucocorticoids, mineralocorticoids, androgens, and estrogens. (wikipedia.org)
  • The 3β-HSD complex is responsible for the conversion of: Pregnenolone to progesterone 17α-Hydroxypregnenolone to 17α-hydroxyprogesterone DHEA to androstenedione Androstenediol to testosterone Androstadienol to androstadienone 3β-HSD belongs to the family of oxidoreductases, to be specific, those acting on the CH-OH group with NAD+ or NADP+ as acceptor. (wikipedia.org)
  • The enzymatic activity of 3 beta-hydroxysteroid dehydrogenase (3 beta HSD/I) constitutes an essential step in the biosynthesis of active steroid hormones such as progesterone, mineralo- and gluco-corticoids, estrogens, and androgens. (semanticscholar.org)
  • As a result of cortisol absence, corticotropin ( ACTH ) secretion increases and leads to produce 3-hydroxy-delta-5-steroids pregnenolone, 17-hydroxypregnenolone , and dehydroepiandrosterone ( DHEA ), also their sulfates. (wikidoc.org)
  • Symptoms of 3 beta-hydroxysteroid dehydrogenase deficiency may include symptoms of both cortisol and aldosterone deficiency such as feeding difficulties , vomiting , volume depletion , undervirilization in newborn males , and mild virilization and clitoromegaly in newborn female . (wikidoc.org)
  • As a result of cortisol absence, corticotropin ( ACTH ) secretion increases the production of 3-hydroxy-delta-5-steroids pregnenolone , 17-hydroxypregnenolone , and dehydroepiandrosterone ( DHEA ). (wikidoc.org)
  • The glucocorticoid hypothesis is affirmed by studies that have shown that elevated maternal cortisol is associated with heightened HPA activity [ 2 ] and alterations in brain structure [ 3 ] in affected offspring. (hindawi.com)
  • Medroxyprogesterone acetate and medrogestone are weak inhibitors of 3β-HSD which may substantially inhibit it at high dosages. (wikipedia.org)
  • The type I isoenzyme is expressed in placenta and peripheral tissues, whereas the type II 3β-HSD isoenzyme is expressed in the adrenal gland, ovary, and testis. (wikipedia.org)
  • With the exception of 3β-hydroxysteroid dehydrogenase (HSD), the enzymes involved in the conversion of cholesterol to steroid hormones are located in either the mitochondria or the endoplasmic reticulum. (biomedcentral.com)
  • 17beta-Hydroxysteroid dehydrogenases (17beta-HSDs) are responsible for the pre-receptor reduction/oxidation of steroids at the 17-position into active/inactive hormones, and the 15 known enzymes vary in their substrate specificity, localisation, and directional activity. (ox.ac.uk)
  • We report the genetic basis of 3β-HSD2 deficiency arising from uniparental isodisomy (UPD) of chromosome 1. (readbyqxmd.com)
  • There are three types of 3β-HSD deficiency: the salt-wasting, non-salt-wasting, and non-classic types. (nih.gov)
  • People with the non-salt-wasting type of 3β-HSD deficiency produce enough hormone to allow sodium reabsorption in the kidneys. (nih.gov)
  • Elevated LH of 24 mIU/L and FSH of 36 mIU/mL with elevated testosterone of 3 ng/mL (normal range for male, 2.4 8.3) were found. (eurospe.org)
  • On examination, she had a male appearance with severe hirsutism, male hair balding, clitoromegaly of 3 cm and bilateral palpable inguinal mass of 2 mL. (eurospe.org)
  • People with 3β-HSD deficiency lack many of the hormones that are made in these glands. (nih.gov)
  • In males with any type of 3β-HSD deficiency, problems with male sex hormones lead to abnormalities of the external genitalia. (nih.gov)