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

Human brain short chain L-3-hydroxyacyl coenzyme A dehydrogenase is a single-domain multifunctional enzyme. Characterization of a novel 17beta-hydroxysteroid dehydrogenase. (1/334)

Human brain short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) was found to catalyze the oxidation of 17beta-estradiol and dihydroandrosterone as well as alcohols. Mitochondria have been demonstrated to be the proper location of this NAD+-dependent dehydrogenase in cells, although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB). This fatty acid beta-oxidation enzyme was identified as a novel 17beta-hydroxysteroid dehydrogenase responsible for the inactivation of sex steroid hormones. The catalytic rate constant of the purified enzyme was estimated to be 0.66 min-1 with apparent Km values of 43 and 50 microM for 17beta-estradiol and NAD+, respectively. The catalytic efficiency of this enzyme for the oxidation of 17beta-estradiol was comparable with that of peroxisomal 17beta-hydroxysteroid dehydrogenase type 4. As a result, the human SCHAD gene product, a single-domain multifunctional enzyme, appears to function in two different pathways of lipid metabolism. Because the catalytic functions of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase could weaken the protective effects of estrogen and generate aldehydes in neurons, it is proposed that a high concentration of this enzyme in brain is a potential risk factor for Alzheimer's disease.  (+info)

Unique multifunctional HSD17B4 gene product: 17beta-hydroxysteroid dehydrogenase 4 and D-3-hydroxyacyl-coenzyme A dehydrogenase/hydratase involved in Zellweger syndrome. (2/334)

Six types of human 17beta-hydroxysteroid dehydrogenases catalyzing the conversion of estrogens and androgens at position C17 have been identified so far. The peroxisomal 17beta-hydroxysteroid dehydrogenase type 4 (17beta-HSD 4, gene name HSD17B4) catalyzes the oxidation of estradiol with high preference over the reduction of estrone. The highest levels of 17beta-HSD 4 mRNA transcription and specific activity are found in liver and kidney followed by ovary and testes. A 3 kb mRNA codes for an 80 kDa (737 amino acids) protein featuring domains which are not present in the other 17beta-HSDs. The N-terminal domain of 17beta-HSD 4 reveals only 25% amino acid similarity with the other types of 17beta-HSDs. The 80 kDa protein is N-terminally cleaved to a 32 kDa enzymatically active fragment. Both the 80 kDa and the N-terminal 32 kDa (amino acids 1-323) protein are able to perform the dehydrogenase reaction not only with steroids at the C17 position but also with D-3-hydroxyacyl-coenzyme A (CoA). The enzyme is not active with L-stereoisomers. The central part of the 80 kDa protein (amino acids 324-596) catalyzes the 2-enoyl-acyl-CoA hydratase reaction with high efficiency. The C-terminal part of the 80 kDa protein (amino acids 597-737) facilitates the transfer of 7-dehydrocholesterol and phosphatidylcholine between membranes in vitro. The HSD17B4 gene is stimulated by progesterone, and ligands of PPARalpha (peroxisomal proliferator activated receptor alpha) such as clofibrate, and is down-regulated by phorbol esters. Mutations in the HSD17B4 lead to a fatal form of Zellweger syndrome.  (+info)

Enoyl-CoA hydratase deficiency: identification of a new type of D-bifunctional protein deficiency. (3/334)

D-bifunctional protein is involved in the peroxisomal beta-oxidation of very long chain fatty acids, branched chain fatty acids and bile acid intermediates. In line with the central role of D-bifunctional protein in the beta-oxidation of these three types of fatty acids, all patients with D-bifunctional protein deficiency so far reported in the literature show elevated levels of very long chain fatty acids, branched chain fatty acids and bile acid inter-mediates. In contrast, we now report two novel patients with D-bifunctional protein deficiency who both have normal levels of bile acid intermediates. Complementation analysis and D-bifunctional protein activity measurements revealed that both patients had an isolated defect in the enoyl-CoA hydratase domain of D-bifunctional protein. Subsequent mutation analysis showed that both patients are homozygous for a missense mutation (N457Y), which is located in the enoyl-CoA hydratase coding part of the D-bifunctional protein gene. Expression of the mutant protein in the yeast Saccharomyces cerevisiae confirmed that the N457Y mutation is the disease-causing mutation. Immunoblot analysis of patient fibroblast homogenates showed that the protein levels of full-length D-bifunctional protein were strongly reduced while the enoyl-CoA hydratase component produced after processing within the peroxisome was undetectable, which indicates that the mutation leads to an unstable protein.  (+info)

17beta-hydroxysteroid dehydrogenase (HSD)/17-ketosteroid reductase (KSR) family; nomenclature and main characteristics of the 17HSD/KSR enzymes. (4/334)

A number of enzymes possessing 17beta-hydroxysteroid dehydrogenase/17-ketosteroid reductase (17HSD/KSR) activities have been described and cloned, but their nomenclature needs specification. To clarify the present situation, descriptions of the eight cloned 17HSD/KSRs are given and guidelines for the classification of novel 17HSD/KSR enzymes are presented.  (+info)

Aromatase and sex steroid receptors in human vena cava. (5/334)

Among sex steroids, especially estrogen metabolism has been considered to play a role in the function and pathology of human veins. We investigated the expression and activity of the estrogen-producing enzyme aromatase and estrogen receptor (ER) in human vena cava to assess possible in situ biosynthesis of estrogens and their modes of action. We first examined aromatase expression by immunohistochemistry in human inferior vena cava obtained from 29 autopsy cases (11 males, 18 females, 63.6 +/- 3.0 years old). We then semiquantitated the level of aromatase mRNA by reverse transcriptase-polymerase chain reaction in 24 cases and aromatase activity by 3H-water assay in 15 cases to examine whether or not and in which cell types aromatase was expressed. We also studied alternative use of multiple exon 1s of its gene and immunolocalization of 17beta-hydroxysteroid dehydrogenase type I (17beta-HSD I), which converts estrone produced by aromatase to estradiol, a biologically active estrogen and ER. Aromatase and 17beta-HSD I immunoreactivity were both detected in smooth muscle cells (SMC) of the media in all the cases and in endothelial cells (EC) in 20 and 22 cases, respectively. ER immunoreactivity was detected in SMC of vena cava in 21 cases. The amount of aromatase mRNA was significantly greater in the cases utilizing 1c (I.3) or 1d (P.II) of exon 1 (9 cases, 191.1 +/- 26.3 attomol/ng total RNA) than those utilizing 1b (I.4) as the promoter (14 cases, 50.6 +/- 13.0 attomol/ng total RNA) (p < 0.01). Significant correlation (p < 0.05) was observed between the amount of aromatase mRNA and aromatase activity in 15 cases examined. No significant correlation was detected between the amount of aromatase mRNA or aromatase labeling index and the ER status. These results suggest that estrone and estradiol are produced in the human vena cava and that their production is mediated by aromatase and 17beta-HSD I, respectively but not all of these locally synthesized estrogens may not work directly in situ.  (+info)

Structure and activity of the murine type 5 17beta-hydroxysteroid dehydrogenase gene(1). (6/334)

17beta-Hydroxysteroid dehydrogenases (17beta-HSDs) play a crucial role in the control of active sex steroid intracellular levels. Seven types of 17beta-HSD have been described. In this study, we report the cloning and characterization of the mouse type 5 17beta-HSD belonging to the aldo-keto reductase superfamily, in contrast with types 1, 2, 3, 4, 6, and 7 17beta-HSD which belong to the short-chain alcohol dehydrogenase family. The gene spans 16 kb and contains 9 exons separated by 8 introns. Primer extension analysis identified a major transcription start site beginning 50 nucleotides upstream from the ATG initiation codon. Northern blot analysis showed a high mRNA expression level in the liver and a weaker signal in the kidney. To determine more precisely the substrate specificity of the enzyme, we established a stable cell line expressing mouse type 5 17beta-HSD in transformed human embryonic kidney (293) cells. The transfected cell line preferentially catalyzes the transformation of 4-androstenedione (4-dione) and androstanedione (A-dione) into testosterone (T) and dihydrotestosterone (DHT), respectively. This data is somewhat in contradiction with a previous study that described the enzyme as estradiol 17beta-dehydrogenase. Our results indicate that the rate of transformation of estradiol (E(2)) to estrone (E(1)) represents only 1% of the rate of transformation of 4-dione to T. Mouse type 5 17beta-HSD shares 76% amino acid sequence identity with human type 5 17beta-HSD; 71%, 76%, 76% with rat 3alpha-HSD and human types 1 and 3 3alpha-HSDs, respectively; and 71%, 69% and 77% with mouse, rat and human 20alpha-HSD, respectively.  (+info)

Determination of cDNA, gene structure and chromosomal localization of the novel human 17beta-hydroxysteroid dehydrogenase type 7(1). (7/334)

We have identified human 17beta-hydroxysteroid dehydrogenase type 7 (17beta-HSD 7). The novel human cDNA encodes a 37 kDa protein that shows 78 and 74% amino acid identity with rat and mouse 17beta-HSD 7, respectively. These enzymes are responsible for estradiol production in the corpus luteum during pregnancy, but are also present in placenta and several steroid target tissues (breast, testis and prostate) as revealed by RT-PCR. The human 17beta-HSD 7 gene (HSD17B7) consists of nine exons and eight introns, spanning 21. 8 kb and maps to chromosome 10p11.2 close to susceptibility loci for tumor progression, obesity and diabetes. The HSD17B7 promoter (1.2 kb) reveals binding sites for brain-specific and lymphoid transcription factors corresponding to additional expression domains in hematopoietic tissues and the developing brain as identified by in silico Northern blot.  (+info)

In vivo and in vitro expression of steroid-converting enzymes in human breast tumours: associations with interleukin-6. (8/334)

Enzymes modulating local steroid availability play an important role in the progression of human breast cancer. These include isoforms of 17beta-hydroxysteroid dehydrogenase (17-HSD), aromatase and steroid sulphatase (STS). The aim of this study was to investigate the expression, by reverse transcription polymerase chain reaction, of 17-HSD types I-IV, aromatase and steroid STS in a series of 51 human breast tumour biopsies and 22 primary cultures of epithelial and stromal cells derived from these tumours, giving a profile of the steroid-regulating network for individual tumours. Correlations between enzyme expression profiles and expression of the interleukin (IL)-6 gene were also sought. All except one tumour expressed at least one isoform of 17-HSD, either alone or in combination with aromatase and STS. Expression of 17-HSD isoforms I-IV were observed in nine tumours. Of the 15 tumours which expressed three isoforms, a combination of 17-HSD II, III and IV was most common (6/15 samples). The majority of tumours (n = 17) expressed two isoforms of 17-HSD with combinations of 17-HSD II and IV predominant (7/17 samples). Eight tumours expressed a single isoform and of these, 17-HSD I was in the majority (5/8 samples). In primary epithelial cultures, enzyme expression was ranked: HSD I (86%) > STS (77%) > HSD II (59%) > HSD IV (50%) = aromatase (50%) > HSD III (32%). Incidence of enzyme expression was generally reduced in stromal cultures which were ranked: HSD I (68%) > STS (67%) > aromatase (48%) > HSD II (43%) > HSD IV (28%) > HSD III (19%). Expression of IL-6 was associated with tumours that expressed > or = 3 steroid-converting enzymes. These tumours were of higher grade and tended to come from patients with family history of breast cancer. In conclusion, we propose that these enzymes work in tandem with cytokines thereby providing sufficient quantities of bioactive oestrogen from less active precursors which stimulates tumour growth.  (+info)

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D-bifunctional enzyme deficiency (sometimes referred to as pseudo-Zellweger syndrome) is a genetic disorder typically characterized by hypotonia (low muscle tone) and seizures within the first month of life, vision and hearing problems, distinct facial features, and developmental delay. Some children with D-bifunctional enzyme deficiency also go on to develop liver disease and/or a progressive leukodystrophy. Most people who have D-bifunctional enzyme deficiency pass within the first 2 years of life; however, there have been a few reported cases of patients living beyond 2 years of life. Treatment is symptomatic and supportive. D-bifunctional enzyme deficiency is caused by mutations in the HSD17B4 gene and is believed to be inherited in an autosomal recessive fashion ...
The primary source of oestrogen in premenopausal women is the ovary but, after menopause, oestrogen biosynthesis in peripheral tissue is the exclusive site of formation. An enzyme group that affects the availability of active oestrogens is the 17β-hydroxysteroid dehydrogenase (17HSD) family. In breast cancer, 17HSD type 1 and type 2 have been mostly investigated and seem to be the principal 17HSD enzymes involved thus far. The question whether 17HSD type 1 or type 2 is of greatest importance in breast tumour development is still not clear. The aim of this study was to investigate how the loss of 17HSD type 2 expression, using siRNA in the non-tumour breast epithelial cells HMEC (human mammal epithelial cells) and MCF10A, and gain of 17HSD type 2 expression, using transient transfection in the breast cancer derived cell lines MCF7 and T47D, affect oestradiol conversion and proliferation rate measured as S-phase fraction. We further investigated how this was related to the endogenous expression ...
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Objective Increased glucocorticoid metabolite excretion and enhanced expression and activity of 11-hydroxysteroid dehydrogenase type 1 in adipose tissue are closely correlated with obesity and its detrimental consequences. Weight loss ameliorates the latter. The aim of this study was to explore whether increased glucocorticoid exposure in obesity is improved with substantial weight loss and thus is a consequence rather than a cause of obesity. Design and patients A prospective cohort study in 31 women. Measurements 11-HSD type 1 expression and activity, urinary glucocorticoid metabolite excretion, body composition including regional adipose tissue depots and insulin resistance by HOMA-IR before and 2years after gastric bypass surgery. Results After weight loss, excretion of cortisol and cortisone metabolites decreased. Both cortisol and cortisone metabolite excretion correlated with central obesity, where the intraabdominal fat depot showed the strongest association. Cortisol metabolites ...
17Beta-hydroxysteroid dehydrogenases (17beta-HSDs) catalyze the NAD(P)(H) dependent oxidoreduction at C17 oxo/beta-hydroxyl groups of androgen and estrogen hormones. This reversible reaction constitutes an important pre-receptor control mechanism for nuclear receptor ligands, since the conversion switches between the 17beta-OH receptor ligands and their inactive 17-oxo metabolites. At present, 14 mammalian 17beta-HSDs are described, of which at least 11 exist within the human genome, encoded by different genes. The enzymes differ in their expression pattern, nucleotide cofactor preference, steroid substrate specificity and subcellular localization, and thus constitute a complex system ensuring cell-specific adaptation and regulation of sex steroid hormone levels. Broad and overlapping substrate specificities with enzymes involved in lipid metabolism suggest interactions of several 17beta-HSDs with other metabolic pathways. Several 17beta-HSDs enzymes constitute promising drug targets, of particular
17Beta-hydroxysteroid dehydrogenases (17beta-HSDs) catalyze the NAD(P)(H) dependent oxidoreduction at C17 oxo/beta-hydroxyl groups of androgen and estrogen hormones. This reversible reaction constitutes an important pre-receptor control mechanism for nuclear receptor ligands, since the conversion switches between the 17beta-OH receptor ligands and their inactive 17-oxo metabolites. At present, 14 mammalian 17beta-HSDs are described, of which at least 11 exist within the human genome, encoded by different genes. The enzymes differ in their expression pattern, nucleotide cofactor preference, steroid substrate specificity and subcellular localization, and thus constitute a complex system ensuring cell-specific adaptation and regulation of sex steroid hormone levels. Broad and overlapping substrate specificities with enzymes involved in lipid metabolism suggest interactions of several 17beta-HSDs with other metabolic pathways. Several 17beta-HSDs enzymes constitute promising drug targets, of particular
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This gene encodes a member of the 17beta-hydroxysteroid dehydrogenase family of short-chain dehydrogenases/reductases. It has a dual function in estrogen activation and androgen inactivation and plays a major role in establishing the estrogen E2 concentration gradient between serum and peripheral tissues. The encoded protein catalyzes the last step in estrogen activation, using NADPH to convert estrogens E1 and E2 and androgens like 4-androstenedione, to testosterone. It has an N-terminal short-chain dehydrogenase domain with a cofactor binding site, and a narrow, hydrophobic C-terminal domain with a steroid substrate binding site. This gene is expressed primarily in the placenta and ovarian granulosa cells, and to a lesser extent, in the endometrium, adipose tissue, and prostate. Polymorphisms in this gene have been linked to breast and prostate cancer. A pseudogene of this gene has been identified. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Sep 2016 ...
Androgens are involved in prostate cancer (PCa) cell growth. Genes involved in androgen metabolism mediate key steps in sex steroid metabolism.
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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 ...
HSD17B2 - HSD17B2 - Human, 4 unique 29mer shRNA constructs in retroviral RFP vector shRNA available for purchase from OriGene - Your Gene Company.
The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is selectively expressed in aldosterone target tissues, conferring aldosterone selectivity for the mineralocorticoid receptor. A diminished activity causes salt-sensitive hypertension. The mechanism of the variable and distinct 11β-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) expression in the cortical collecting duct is poorly understood. Here, we analyzed for the first time whether the 11β-HSD2 expression is modulated by microRNAs (miRNAs). In silico analysis revealed 53 and 27 miRNAs with potential binding sites on human or rat HSD11B2 3′-untranslated region. A reporter assay demonstrated 3′-untranslated region-dependent regulation of human and rodent HSD11B2. miRNAs were profiled from cortical collecting ducts and proximal convoluted tubules. Bioinformatic analyses showed a distinct clustering for cortical collecting ducts and proximal convoluted tubules with 53 of 375 miRNAs, where 13 were predicted to bind to the ...
Journal Article: On-column ligand exchange for structure-based drug design: a case study with human 11[beta]-hydroxysteroid dehydrogenase type 1 ...
11ß-hydroxysteroid dehydrogenase type1 (11β-HSD1) converts inactive glucocorticoids to active glucocorticoids which, in excess, leads to development of the various risk factors of the metabolic syndrome. Recent studies clearly suggest that both increased expression and activity of 11β-HSD1 in metabolically active tissues such as liver, muscle and adipose are implicated in tissue specific dysregulation which collectively contribute to the whole body pathology seen in metabolic syndrome. In the present study we have evaluated CNX-010-49, a highly potent, selective and pan tissue acting 11β-HSD1 inhibitor, for its potential to modulate multiple risk factors of the metabolic syndrome. Male C57B6/J mice on high fat diet (DIO mice) were orally dosed with CNX-010-49 (30 mg/kg twice daily; n = 8) or vehicle for 10 weeks. Fasting glucose, triglycerides, glycerol, free fatty acids, body weight and feed intake were measured at selected time points. At the end of the treatment an OGTT and subsequently organ
Bile acids (BAs) are important modulators of metabolic functions such as lipid, triglyceride and glucose homeostasis. Intrahepatic accumulation of BAs is known to cause liver injury in cholestatic conditions, where normal trans-hepatic BA flow is impaired due to pathological conditions or induced by toxic drugs. Therefore, it is important to understand the mechanisms of BA homeostasis regulation and to identify novel players and characterize their functions. The main goal of the present work was to investigate the impact of altered hepatic glucocorticoid activation by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) on BA homeostasis and to unravel the mechanisms of adaptations in a scenario of impaired 11β-HSD1 function. In order to achieve this goal, we developed and validated an ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) method for the quantification of a total of 24 BAs, including 11 unconjugated, 6 glycine-conjugated and 7 ...
Status of 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) immunoreactivity was significantly higher in invasive lobular carcinoma (ILC) than in invasive duc
11 beta-hydroxysteroid dehydrogenase (11 beta HSD) has both dehydrogenase (11 beta DH) and reductase (11 beta R) activities, which catalyse the interconversion of cortisol and cortisone, and prednisolone and prednisone. This enzyme confers specificity
KEE316Hu, HSD11b1L; SCDR10; HSD3; SDR26C2; 11-Beta Hydroxysteroid Dehydrogenase Type 1 Like Protein; Short chain dehydrogenase/reductase family 26C member 2 | Products for research use only!
There are increasing data on the central role of miRNAs in the development of various diseases, including some kidney and cardiovascular entities.27,32,33 Whether miRNAs and the 3′-UTR of specific players in the field of renal or blood pressure physiology are relevant is yet to be addressed specifically. The 11β-HSD2 is an essential enzyme for blood pressure control.3 Therefore, the mechanisms accounting for its regulation are a prerequisite for understanding blood pressure in health and disease states. Here, we present evidence that HSD11B2 mRNA fulfills the prerequisites to be modulated by miRNAs. Because a multitude of miRNAs directly or indirectly affect the expression of a protein, special emphasis was given to the miRNA expression profile in the CCD, the main site of 11β-HSD2 action.. To the best of our knowledge, the relationship between miRNA and 11β-HSD2 was reported previously only once.34 Shang et al34 starved a human placental cell line (BeWo) from amino acids and observed a ...
Estrogens play a central role in the development of breast cancer. Most breast carcinomas are detected after menopause and despite a low degree of ovarian estrogen production and low levels of serum estrogen these tumors show a high in situ level of estrogens. Enzymes modulating local steroid availability seem to play an important role in the progression of especially estrogen receptor positive breast cancer. The 17ß-hydroxysteroid dehydrogenase (17ß-HSD) enzymes are involved in the interconversion of biologically active and inactive sex steroids and are considered to play a critical role in the in situ metabolism of estrogen.. The aim of this thesis was to investigate the expression of 17ß-HSD type 1 and 2 in breast cancer and correlate this to prognosis, and to analyze if the gene encoding 17ßHSD type 1 exhibits altered gene copy number in breast cancer. We also wanted to examine if the protein levels of aromatase, 17ßHSD type 1 and 17ßHSD type 2 show association with the expression of ...
1JTV: Pseudo-symmetry of C19 steroids, alternative binding orientations, and multispecificity in human estrogenic 17beta-hydroxysteroid dehydrogenase.
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. [...]
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 …
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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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。
Peroxisomal beta-oxidation is an essential step in bile acid synthesis, since it is required for shortening of C27-bile acid intermediates to produce mature C24-bile acids. D-Bifunctional protein (DBP) is responsible for the second and third step of this beta-oxidation process. However, both patients and mice with a DBP deficiency still produce C24-bile acids, although C27-intermediates accumulate. An alternative pathway for bile acid biosynthesis involving the peroxisomal L-bifunctional protein (LBP) has been proposed. We investigated the role of LBP and DBP in bile acid synthesis by analyzing bile acids in bile, liver, and plasma from LBP, DBP, and LBP:DBP double knock-out mice. Bile acid biosynthesis, estimated by the ratio of C27/C24-bile acids, was more severely affected in double knock-out mice as compared with DBP-/- mice but was normal in LBP-/- mice. Unexpectedly, trihydroxycholestanoyl-CoA oxidase was inactive in double knock-out mice due to a peroxisomal import defect, preventing us ...
17 beta-hydroxysteroid dehydrogenases catalyze the oxidoreduction of hydroxy/oxo groups at position C17 of steroid hormones, thereby constituting a prereceptor control mechanism of hormone action. At present, 11 different mammalian 17 beta-hydroxysteroid dehydrogenases have been identified, catalyzing the cell- and steroid-specific activation and inactivation of estrogens and androgens. The human type 10 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD-10) is a multifunctional mitochondrial enzyme that efficiently catalyzes the oxidative inactivation at C17 of androgens and estrogens. However, it also mediates oxidation of 3 alpha-hydroxy groups of androgens, thereby reactivating androgen metabolites. Finally, it is involved in beta-oxidation of fatty acids by catalyzing the L-hydroxyacyl CoA dehydrogenase reaction of the beta-oxidation cycle. These features and expression profiles suggest a critical role of 17 beta-HSD-10 in neurodegenerative and steroid-dependent cancer forms. Since no three
The biological activity of steroid hormones is regulated at the pre-receptor level by several enzymes including 17 beta-hydroxysteroid dehydrogenases (17 beta -HSD). The latter are present in many microorganisms, invertebrates and vertebrates. Dysfunctions in human 17 beta-hydroxysteroid dehydrogenases result in disorders of biology of reproduction and neuronal diseases, the enzymes are also involved in the pathogenesis of various cancers. 17 beta-hydroxysteroid dehydrogenases reveal a remarkable multifunctionality being able to modulate concentrations not only of steroids but as well of fatty and bile acids. Current knowledge on genetics, biochemistry and medical implications is presented in this review.
4FAL: Crystal structure of human 17beta-hydroxysteroid dehydrogenase type 5 in complex with 3-((3,4-dihydroisoquinolin-2(1H)-yl)sulfonyl)-N-methylbenzamide (80)
Musto, N; Hafiez, A A.; and Bartke, A, "Prolactin increases 17beta-hydroxysteroid dehydrogenase activity in the testis." (1972). Subject Strain Bibliography 1972. 2710 ...
Looking for the definition of 11-beta-hydroxysteroid dehydrogenases? Find out what is the full meaning of 11-beta-hydroxysteroid dehydrogenases on Abbreviations.com! Beta is one option -- get in to view more @ The Webs largest and most authoritative acronyms and abbreviations resource.
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 ...
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 ...
Q9EQC1: 3 beta-hydroxysteroid dehydrogenase type 7; 3 beta-hydroxysteroid dehydrogenase type VII; 3-beta-HSD VII; 3-beta-hydroxy-Delta(5)-C27 steroid oxidoreductase; C(27) 3-beta-HSD; 1.1.1.-; Cholest-5-ene-3-beta,7-alpha-diol 3-beta-dehydrogenase; 1.1. ...
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.
Human 17beta-hydroxysteroid dehydrogenase type 1 (17β-HSD1) is a steroid-converting enzyme that has long been known to play critical roles in estradiol synthesis and more recently in dihydrotestosterone (DHT) inactivation, showing a dual function that promotes breast cancer cell proliferation. Previously, we reported the first observation of the influence of the enzyme on endogenous estrogen-responsive gene expression. Here, we demonstrate the impact of 17β-HSD1 expression on the breast cancer cell proteome and investigate its role in cell migration. 17β-HSD1 was stably transfected in MCF7 cells and the proteome of the generated cells overexpressing 17β-HSD1 (MCF7-17βHSD1 cells) was compared to that of the wild type MCF7 cells. Proteomics study was performed using two-dimensional gel electrophoresis followed by mass spectrometry analysis of differentially expressed protein spots. Reverse transcription quantitative real-time PCR (RT-qPCR) was used to investigate the transcription of individual gene.
Glucocorticoid (GC) excess adversely affects skin integrity, inducing thinning and impaired wound healing. Aged skin, particularly that which has been photo-exposed, shares a similar phenotype. Previously, we demonstrated age-induced expression of the GC-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in cultured human dermal fibroblasts (HDFs). Here, we determined 11β-HSD1 levels in human skin biopsies from young and older volunteers and examined the aged 11β-HSD1 KO mouse skin phenotype. 11β-HSD1 activity was elevated in aged human and mouse skin and in PE compared with donor-matched photo-protected human biopsies. Age-induced dermal atrophy with deranged collagen structural organization was prevented in 11β-HSD1 KO mice, which also exhibited increased collagen density. We found that treatment of HDFs with physiological concentrations of cortisol inhibited rate-limiting steps in collagen biosynthesis and processing. Furthermore, topical 11β-HSD1 inhibitor treatment ...
Overnutrition, increased macronutritient intake, physical inactivity, and ageing are associated with expansion of adipose tissue mass and cytokines, favoring in genetically and metabolically susceptible subjects, the development of insulin resistance, metabolic syndrome and diabetes. Adipose tissue distribution in human is dependent on genetic and environmental factors. The control of the rate of filling of adipocytes seems to be the main factor determining the local, regional mass of adipose tissue. Causes of visceral fat accumulation include glucocorticoid excess or decreased estrogen/androgen ratio either in plasma or within adipose tissue. Intra-adipose sex steroid metabolism is a determinant of gynoid versus androgen patterns of body fat. Abdominal obesity is associated with greater risk for hypertension, dyslipidemia, type 2 diabetes and coronary heart disease, due to increased release of free fatty acids from visceral fat to the liver. Visceral fat is highly active metabolic and endocrine ...
An exciting era is upon us in terms of new therapies for patients with diabetes, obesity, and metabolic syndrome. One such advance is the ability to selectively manipulate tissue levels of glucocorticoids through targeted inhibition of cortisol metabolic pathways. Perhaps the best paradigm for metabolic syndrome comes from patients with Cushings syndrome, with their characteristic central obesity, glucose intolerance, hypertension, and premature cardiovascular mortality. Although circulating cortisol concentrations are invariably normal in patients with obesity and metabolic syndrome (1), in vitro, in vivo, and clinical studies over the last decade have collectively shown the importance of local generation of cortisol, via 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in liver and fat, in mediating many facets of the metabolic syndrome (2). Major pharmaceutical companies are now engaged; over 50 patents have been issued detailing compounds and strategies for selective 11β-HSD1 ...
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 ...
Life Sci. 2001 Jan 5;68(7):751-61. Links Chalcones are potent inhibitors of aromatase and 17beta-hydroxysteroid dehydrogenase activities.Le Bail JC,
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. ...
This highly specific HSD17B4 / 17-beta-Hydroxysteroid dehydrogenase 4 antibody is suitable for use in WB, IHC-P and is guaranteed to work as stated on the product data sheet. | R30817
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
3β-Hydroxysteroid dehydrogenase/Δ5-4 isomerase. 5.8 μM. Competitive. 4.3% ... 3β-hydroxysteroid dehydrogenase/Δ5-4 isomerase, 17α-hydroxylase, 17,20-lyase, 17β-hydroxysteroid dehydrogenase, 21-hydroxylase ... 1S,2R,13R,14S,17R,18S)-17-ethynyl-2,18-dimethyl-7-oxa-6-azapentacyclo[11.7.0.02,10.04,8.014,18]icosa-4(8),5,9-trien-17-ol ... Proligestone; 17α-Methylated: Medrogestone; Others: Haloprogesterone. *19-Norprogesterone derivatives: 17α-Hydroxylated: ...
Hydroxysteroid Dehydrogenase (3.BETA.-HSD), 17.ALPHA.-Hydroxylase and 17, 20 Lyase by Progestins and Danazol". Endocrinologia ... Gestrinone is the C18 methyl derivative of norgestrienone (17α-ethynyl-19-nor-δ9,11-testosterone) and the δ9,11 analogue of ... It is more specifically a derivative of norethisterone (17α-ethynyl-19-nortestosterone) and is a member of the gonane (18- ... The androgenic properties of gestrinone are more exploited in its derivative tetrahydrogestrinone (THG; 17α-ethyl-18-methyl-δ9, ...
PC Pyruvate dehydrogenase deficiency; 312170; PDHA1 Pyruvate dehydrogenase E2 deficiency; 245348; DLAT Pyruvate dehydrogenase ... SCARB2 Acyl-CoA dehydrogenase, long chain, deficiency of; 201460; ACADL Acyl-CoA dehydrogenase, medium chain, deficiency of; ... TMPRSS6 Isobutyryl-CoA dehydrogenase deficiency; 611283; ACAD8 Isovaleric acidemia; 243500; IVD IVIC syndrome; 147750; SALL4 ... DCX Succinic semialdehyde dehydrogenase deficiency; 271980; ALDH5A1 Succinyl-CoA:3-oxoacid CoA transferase deficiency; 245050; ...
1998). "Characterization of Ke 6, a new 17beta-hydroxysteroid dehydrogenase, and its expression in gonadal tissues". J. Biol. ... 2007). "Transcriptional regulation of the human type 8 17beta-hydroxysteroid dehydrogenase gene by C/EBPbeta". J. Steroid ... 2006). "Expression of aromatase and 17beta-hydroxysteroid dehydrogenase types 1, 7 and 12 in breast cancer. An ... "Entrez Gene: HSD17B8 hydroxysteroid (17-beta) dehydrogenase 8". Kikuti YY, Tamiya G, Ando A, et al. (1997). "Physical mapping ...
"Deleterious missense mutations and silent polymorphism in the human 17beta-hydroxysteroid dehydrogenase 3 gene (HSD17B3)". The ... "Phenotypic variability in 17beta-hydroxysteroid dehydrogenase-3 deficiency and diagnostic pitfalls". Clinical Endocrinology. 67 ... "Entrez Gene: HSD17B3 hydroxysteroid (17-beta) dehydrogenase 3". Ademola Akesode F, Meyer WJ, Migeon CJ (December 1977). "Male ... short-chain dehydrogenase/reductase and related enzymes) nomenclature initiative". Chemico-Biological Interactions. 178 (1-3): ...
In addition, it has been found to inhibit aldehyde dehydrogenase and estrogen sulfotransferase in vitro (Ki = 35 μM and 1-3 μM ... 17 (3): 249-54. doi:10.1089/rej.2013.1519. PMID 24325271. Zhang Z, Liu X, Schroeder JP, Chan CB, Song M, Yu SP, Weinshenker D, ... Unlike many other flavonoids, 7,8-DHF does not show any inhibitory activity on 17β-hydroxysteroid dehydrogenase. 7,8-DHF has ... Le Bail, J.C; Laroche, T; Marre-Fournier, F; Habrioux, G (1998). "Aromatase and 17β-hydroxysteroid dehydrogenase inhibition by ...
... 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, ... 87 (1): 17-25. doi:10.1016/j.ajhg.2010.05.018. PMC 2896773 . PMID 20579625. Al-Zahery, N; Pala, M; Battaglia, V; Grugni, V; ... Retrieved 17 May 2015. Brenna M. Henn; Laura R. Botigué; Simon Gravel; Wei Wang; Abra Brisbin; Jake K. Byrnes; Karima Fadhlaoui ...
17β-Hydroxysteroid dehydrogenase type 14 also known as 17β-HSD type 14 or 17βHSD14 is an enzyme that in humans is encoded by ... 17βHSD14 catalyzes the stereospecific oxidation and reduction of the 17β carbon atom of androgens and estrogens using NAD(P)(H ... 257-. ISBN 978-1-118-84985-9. Sivik T, Vikingsson S, Gréen H, Jansson A (2012). "Expression patterns of 17β-hydroxysteroid ... dehydrogenase 14 in human tissues". Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et ...
17beta-hydroxysteroid dehydrogenase 4 and D-3-hydroxyacyl-coenzyme A dehydrogenase/hydratase involved in Zellweger syndrome". J ... 1999). "17Beta-hydroxysteroid dehydrogenases in human bone cells". J. Bone Miner. Res. 13 (10): 1539-46. doi:10.1359/jbmr. ... 1999). "17Beta-hydroxysteroid dehydrogenase type 1, 2, 3, and 4 expression and enzyme activity in human anterior pituitary ... 1999). "Structure of the gene for the human 17beta-hydroxysteroid dehydrogenase type IV". Mamm. Genome. 9 (12): 1036-41. doi: ...
Aka JA, Mazumdar M, Chen CQ, Poirier D, Lin SX (Apr 2010). "17beta-hydroxysteroid dehydrogenase type 1 stimulates breast cancer ... "Structural basis of the multispecificity demonstrated by 17beta-hydroxysteroid dehydrogenase types 1 and 5". Molecular and ... "Entrez Gene: HSD17B1 Hydroxysteroid (17-beta) dehydrogenase 1". Saloniemi T, Jokela H, Strauss L, Pakarinen P, Poutanen M (2012 ... This enzyme contains a short-chain dehydrogenase domain that contains a characteristic 3-layer (αβα) sandwich known as a ...
"Cloning and expression of a novel tissue specific 17beta-hydroxysteroid dehydrogenase". Endocrine Research. 24 (3-4): 663-7. ... "Entrez Gene: HSD17B11 hydroxysteroid (17-beta) dehydrogenase 11". Li KX, Smith RE, Krozowski ZS (1999). " ... Haeseleer F, Palczewski K (2000). "Short-chain dehydrogenases/reductases in retina". Methods in Enzymology. 316: 372-83. doi: ... short-chain dehydrogenase/reductase and related enzymes) nomenclature initiative". Chemico-Biological Interactions. 178 (1-3): ...
Peltoketo H, Nokelainen P, Piao YS, Vihko R, Vihko P (Aug 1999). "Two 17beta-hydroxysteroid dehydrogenases (17HSDs) of ... Ohnesorg T, Adamski J (2005). "Promoter analyses of human and mouse 17beta-hydroxysteroid dehydrogenase type 7". J. Steroid ... 2003). "Production, purification, and functional analysis of recombinant human and mouse 17beta-hydroxysteroid dehydrogenase ... gene structure and chromosomal localization of the novel human 17beta-hydroxysteroid dehydrogenase type 7(1)". FEBS Lett. 460 ( ...
"Characterization of type 12 17beta-hydroxysteroid dehydrogenase, an isoform of type 3 17beta-hydroxysteroid dehydrogenase ... 2006). "Systemic distribution and tissue localizations of human 17beta-hydroxysteroid dehydrogenase type 12". J. Steroid ... 2005). "Platelets express steroidogenic 17beta-hydroxysteroid dehydrogenases. Distinct profiles predict the essential ... "Entrez Gene: HSD17B12 hydroxysteroid (17-beta) dehydrogenase 12". Maruyama K, Sugano S (1994). "Oligo-capping: a simple method ...
"Chalcones are potent inhibitors of aromatase and 17β-hydroxysteroid dehydrogenase activities". Life Sciences. 68 (7): 751-61. ...
MPA has been found to act as a competitive inhibitor of rat 3α-hydroxysteroid dehydrogenase (3α-HSD). This enzyme is essential ... MPA has been identified as a competitive inhibitor of human 3β-hydroxysteroid dehydrogenase/Δ5-4 isomerase II (3β-HSDII). This ... Penning TM, Sharp RB, Krieger NR (December 1985). "Purification and properties of 3 alpha-hydroxysteroid dehydrogenase from rat ... "The biological activity of 3alpha-hydroxysteroid oxido-reductase in the spinal cord regulates thermal and mechanical pain ...
2001). "Further characterization of human microsomal 3alpha-hydroxysteroid dehydrogenase". Arch. Biochem. Biophys. 386 (1): 1- ... 2007). "Role of microsomal retinol/sterol dehydrogenase-like short-chain dehydrogenases/reductases in the oxidation and ... and 3alpha-hydroxysteroid dehydrogenases from rat and human prostate". J. Biol. Chem. 272 (25): 15959-66. doi:10.1074/jbc. ... "Evolution of 17beta-hydroxysteroid dehydrogenases and their role in androgen, estrogen and retinoid action". Mol Cell ...
... blocks production of all steroid hormones from cholesterol 3β-Hydroxysteroid dehydrogenase type 2 deficiency: impairs ... causes androgen deficiency in males and androgen excess in females Combined 17α-hydroxylase/17,20-lyase deficiency: impairs ... results in mineralocorticoid excess 17β-Hydroxysteroid dehydrogenase deficiency: impairs androgen and estrogen metabolism; ... progestogen metabolism; prevents androgen, estrogen, and glucocorticoid synthesis; causes mineralocorticoid excess Isolated 17, ...
Subsequently, 20α-hydroxysteroid dehydrogenase and 20β-hydroxysteroid dehydrogenase reduce these metabolites to form the ... This is followed by the further reduction of these metabolites via 3α-hydroxysteroid dehydrogenase and 3β-hydroxysteroid ... This reaction is catalyzed by 3β-hydroxysteroid dehydrogenase/δ5-4-isomerase. Progesterone in turn is the precursor of the ... Progesterone is highly susceptible to enzymatic reduction via reductases and hydroxysteroid dehydrogenases due to its double ...
Many people regard the term "sex reassignment surgery" as preferable to "sex change".[17] Sex in humans is usually determined ... Cohen-Kettenis, Peggy T. (2005). "Gender Change in 46,XY Persons with 5α-Reductase-2 Deficiency and 17β-Hydroxysteroid ... Dehydrogenase-3 Deficiency". Archives of Sexual Behavior. 34 (4): 399-410. doi:10.1007/s10508-005-4339-4. PMID 16010463.. ... Bertelloni, Silvano; Maggio, M. Cristina; Federico, Giovanni; Baroncelli, Giampiero; Hiort, Olaf (2006). "17β-Hydroxysteroid ...
... dehydrogenase 2". Moeller G, Adamski J (2006). "Multifunctionality of human 17beta-hydroxysteroid dehydrogenases". Mol. Cell. ... Dong Y, Qiu QQ, Debear J, Lathrop WF, Bertolini DR, Tamburini PP (Oct 1998). "17Beta-hydroxysteroid dehydrogenases in human ... ISBN 978-0-12-803608-2. Moeller G, Adamski J (2009). "Integrated view on 17beta-hydroxysteroid dehydrogenases". Mol. Cell. ... "17Beta-hydroxysteroid dehydrogenase-2 deficiency and progesterone resistance in endometriosis". Semin. Reprod. Med. 28 (1): 44- ...
D4A is formed from abiraterone by 3β-hydroxysteroid dehydrogenase/Δ5-4 isomerase (3β-HSD). It is said to be a more potent ... 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 ...
2004). "11Beta-hydroxysteroid dehydrogenase inhibition improves cognitive function in healthy elderly men and type 2 diabetics ... inhibits the conversion of cortisol to the inactive metabolite cortisone by blocking 11β-hydroxysteroid dehydrogenase (11β-HSD ... U.S.A. 101 (17): 6734-9. doi:10.1073/pnas.0306996101. PMC 404114 . PMID 15071189. ...
Marcus, P.I. & Talalay, P. (1956). „Induction and purification of α- and β-hydroxysteroid dehydrogenases". J. Biol. Chem. 218: ... Talalay, P. & Dobson, M.M. (1953). „Purification and properties of a α-hydroxysteroid dehydrogenase". J. Biol. Chem. 205: 823- ... β-Hydroxysteroid dehydrogenase of Pseudomonas testosteroni. A convenient purification and demonstration of multiple molecular ... 3(ili 17)b-hidroksisteroid dehidrogenaza (EC 1.1.1.51, beta-hidroksi steroidna dehidrogenaza, 17-ketoreduktaza, 17beta-hidroksi ...
These precursors are not further converted in the adrenal cortex if the cells lack 17Beta Hydroxysteroid dehydrogenase. Instead ... In humans the reticularis layer does contain 17 alpha-hydroxylase; this hydroxylates pregnenolone, which is then converted to ...
... a possible modulator of 17 beta-hydroxysteroid dehydrogenase". J. Clin. Endocrinol. Metab. 86 (6): 2721-7. doi:10.1210/jc.86.6. ...
17 March 2006. Archived from the original on 5 August 2007.. *^ a b c d e "Diagnosis of Diabetes and Prediabetes". National ... 172 (17): 1296-303. doi:10.1001/archinternmed.2012.3147. PMID 22868819.. *^ Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M ... 2011). "Chapter 17: Pancreatic hormones & diabetes mellitus". Greenspan's basic & clinical endocrinology (9th ed.). New York: ... Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity.[17] As of 2015 there were approximately ...
... natural steroids androstanediol via17β-hydroxysteroid dehydrogenase or from androstanedione via 3β-hydroxysteroid dehydrogenase ... and can also be converted from the natural steroids androstanediol via 17β-hydroxysteroid dehydrogenase or from androstanedione ... via 3β-hydroxysteroid dehydrogenase.It was first isolated in 1931 and has been shown to naturally occur in most mammals ...
... from 3-hydroxysteroid dehydrogenase and -hydroxysteroid dehydrogenase, bypassing conventional intermediates such as and ... Synonyms: 3-Hydroxy-5-androstan-17-one;5-Androstan-3-ol-17-one. CAS No.: 53-41-8. M.F.& ...
... metabolism in pig liver microsomes was determined by the level of expression of hepatic 3β-hydroxysteroid dehydrogenase. They ... Sinclair PA, Squires EJ: Testicular sulfoconjugation of the 16-androstene steroids by hydroxysteroid sulfotransferase: Its ... 17.. Doran E, Whittington FM, Wood J, Mc Giwan JD: Cytochrome P450IIE1 (CYP2E1) is induced by skatole and this induction is ... 17] found that skatole induced CYP2E1 protein expression while androstenone antagonised this effect in isolated hepatocytes. ...
17beta-Hydroxysteroid dehydrogenase-3 deficiency: from pregnancy to adolescence. J Endocrinol Invest. 2009 Sep;32(8):666-70. ... and molecular findings in 17beta-hydroxysteroid dehydrogenase type 3 deficiency. J Endocrinol Invest. 2008 Jan;31(1):85-91. ... Most people with 17-beta hydroxysteroid dehydrogenase 3 deficiency are born with external genitalia that appear female. In some ... Children with 17-beta hydroxysteroid dehydrogenase 3 deficiency are often raised as girls. About half of these individuals ...
dehydrogenase/reductase SDR family member 8. retinal short-chain dehydrogenase/reductase 2. short chain dehydrogenase/reductase ... 17beta-hydroxysteroid dehydrogenase type 11 (Pan1b) expression in human prostate cancer. Nakamura Y, et al. Neoplasma, 2009. ... Cloning and expression of a novel tissue specific 17beta-hydroxysteroid dehydrogenase. Li KX, et al. Endocr Res, 1998 Aug-Nov. ... Identification and characterization of the ER/lipid droplet-targeting sequence in 17beta-hydroxysteroid dehydrogenase type 11. ...
Moeller G, Adamski J (2009). "Integrated view on 17beta-hydroxysteroid dehydrogenases". Mol. Cell. Endocrinol. 301 (1-2): 7-19 ... Talalay P, Dobson MM (December 1953). "Purification and properties of a beta-hydroxysteroid dehydrogenase". The Journal of ... Marcus PI, Talalay P (February 1956). "Induction and purification of alpha- and beta-hydroxysteroid dehydrogenases". The ... a new 17beta-hydroxysteroid dehydrogenase, and its expression in gonadal tissues". The Journal of Biological Chemistry. 273 (35 ...
Aka JA, Mazumdar M, Chen CQ, Poirier D, Lin SX (April 2010). "17beta-hydroxysteroid dehydrogenase type 1 stimulates breast ... Talalay P, Dobson MM (December 1953). "Purification and properties of a beta-hydroxysteroid dehydrogenase". The Journal of ... ISBN 978-0-12-803608-2. Moeller G, Adamski J (2009). "Integrated view on 17beta-hydroxysteroid dehydrogenases". Mol. Cell. ... Marcus PI, Talalay P (February 1956). "Induction and purification of alpha- and beta-hydroxysteroid dehydrogenases". The ...
... 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 ...
Dehydrogenase 4 antibody validated for WB and tested in Human. Immunogen corresponding to recombinant fragment ... dehydrogenase 4 antibody. See all Hydroxysteroid (17-beta) Dehydrogenase 4 primary antibodies. ... 17beta estradiol dehydrogenase type IV antibody. *3 alpha 7 alpha12 alpha trihydroxy 5 beta cholest 24 enoyl CoA hydratase ... Anti-hydroxysteroid (17-beta) dehydrogenase 4 antibody (ab97971) at 1/1000 dilution + HeLa whole cell lysate at 30 µg. ...
Dehydrogenase 4 antibody validated for WB, IHC, ICC/IF and tested in Human and Rat. Immunogen corresponding to… ... Dehydrogenase 4 antibody. See all Hydroxysteroid (17-beta) Dehydrogenase 4 primary antibodies. ... Anti-Hydroxysteroid (17-beta) Dehydrogenase 4 antibody (ab97975) at 1/3000 dilution + Rat heart lysate at 20 µg. Secondary. HRP ... 17beta estradiol dehydrogenase type IV antibody. *3 alpha 7 alpha12 alpha trihydroxy 5 beta cholest 24 enoyl CoA hydratase ...
TYPE 1 17-BETA HYDROXYSTEROID DEHYDROGENASE EQUILIN COMPLEXED WITH NADP+ ... Human estrogenic 17beta-hydroxysteroid dehydrogenase type 1 (17beta-HSD1), which catalyzes the reduction of inactive estr ... ... Human estrogenic 17beta-hydroxysteroid dehydrogenase type 1 (17beta-HSD1), which catalyzes the reduction of inactive estrone ( ... Structure of the ternary complex of human 17beta-hydroxysteroid dehydrogenase type 1 with 3-hydroxyestra-1,3,5,7-tetraen-17-one ...
... rational design of type 1 17beta-hydroxysteroid dehydrogenase inhibitors: estradiol-adenosine hybrids with high affinity ...
View mouse Hsd17b11 Chr5:103989765-104021796 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
Shop a large selection of Proteins A-Z products and learn more about Novus Biologicals hydroxysteroid (17-beta) dehydrogenase ... dehydrogenase 11 Protein is derived from E. coli. The Recombinant Human hydroxysteroid (17-beta) dehydrogenase 11 Protein has ... A recombinant protein with a N-Terminal His-tag and corresponding to the amino acids 20-285 of Human hydroxysteroid (17-beta) ...
... and 17β-hydroxysteroid dehydrogenase-3 deficiency (17β-HSD-3) are often raised as girls. Over the past number of years, this ... Gender role changes were reported in 56-63% of cases with 5α-RD-2 and 39-64% of cases with 17β-HSD-3 who were raised as girls. ... Lanes, R., Brown, T. R., Gruber de Bustos, E., Valverde, B., Pieretti, R. B., Bianco, N., et al. (1983). Sibship with 17- ... Millán, M., Audi, L., Martinez-Mora, J., Martinez de Osaba, M. J., Viguerra, J., Esmatjes, E., et al. (1983). 17-Ketosteroid ...
A ligand-based 17β-HSD2 pharmacophore model was applied to screen a cosmetic chemicals database, followed by in vitro testing ... Ethylparaben and ethyl vanillate inhibited 17β-HSD2 with IC50 values of 4.6 ± 0.8 and 1.3 ± 0.3 µM, respectively. Additionally ... All tested parabens and paraben-like compounds, except their common metabolite p-hydroxybenzoic acid, inhibited 17β-HSD2. ... Low micromolar concentrations of hexyl- and heptylparaben decreased 17β-HSD1 activity, and ethylparaben and ethyl vanillate ...
... Sivik, Tove Linköping University, Department of ... A role for 17βHSD14 in sex steroid metabolism is supported by the finding that 17HSD14 oxidizes both estradiol and testosterone ... The 17βHSD14 protein was expressed in several classical steroidogenic tissues such as breast, ovary and testis which supports ... 17βHSD enzymes catalyze the stereospecific oxidation/reduction at carbon 17β of androgens and estrogens, and are important ...
... beta-hydroxysteroid dehydrogenase: acts on both 3 beta or 17 beta hydroxysteroids; 17 beta type 1 is probably ESTRADIOL ... DEHYDROGENASES; for 3 or 17 alpha-hydroxysteroids see EC 1.1.1.209; was mapped to TESTOSTERONE DEHYDRONGENASES (85-93) (see ... on-line search 17-HYDROXYSTEROID DEHYDROGENASES (85-93), Index Medicus search TESTOSTERONE DEHYDROGENASES (91-93), 17- ... 17HSD1; 17beta HSD1; 17beta-HSD 7; 17beta-HSD7; 17beta-hydroxysteroid dehydrogenase; 17beta-hydroxysteroid dehydrogenase type 7 ...
Dysfunctions in human 17 beta-hydroxysteroid dehydrogenases result in disorders of biology of reproduction and neuronal ... 17 beta-hydroxysteroid dehydrogenases reveal a remarkable multifunctionality being able to modulate concentrations not only of ... The biological activity of steroid hormones is regulated at the pre-receptor level by several enzymes including 17 beta- ... hydroxysteroid dehydrogenases (17 beta -HSD). The latter are present in many microorganisms, invertebrates and vertebrates. ...
The second goal of this thesis was to further study the role of hydroxysteroid 17β dehydrogenase enzymes in breast cancer, and ... The role of the androgen receptor and hydroxysteroid 17β dehydrogenase in breast cancer: Impact on tamoxifen treatment(1043 kB) ... The role of the androgen receptor and hydroxysteroid 17β dehydrogenase in breast cancer: Impact on tamoxifen treatment. Hilborn ... The modulation of the members of the hydroxysteroid 17β dehydrogenase in breast cancer is associated with changes in the local ...
... and aromatase and 17 beta-hydroxysteroid dehydrogenase (E2DH) activities were determined in normal glandular and cancerous ... Aromatase, 17 beta-hydroxysteroid dehydrogenase and intratissular sex hormone concentrations in cancerous and normal glandular ... 17 beta-diol (5-Adiol), estrone (E1), estradiol (E2) and progesterone (P) were significantly higher than plasma concentrations ... and aromatase and 17 beta-hydroxysteroid dehydrogenase (E2DH) activities were determined in normal glandular and cancerous ...
Keywords:enzyme, hydroxysteroid dehydrogenase, 4-aza-steroids, sar, inhibitors, steroidogenesis. Abstract: We present the SAR ... hydroxysteroid dehydrogenase (17β-HSD). The conversion of E1 into E2 is reduced by nearly 90 % by 17β-(Nalkylformamido)- 4- ... hydroxysteroid dehydrogenase (17β-HSD). The conversion of E1 into E2 is reduced by nearly 90 % by 17β-(Nalkylformamido)- 4- ... First Inhibitors of the Steroidogenic Enzyme Type 7 17β-Hydroxysteroid Dehydrogenase. Author(s): E. Bellavance, V. Luu-The, D. ...
Status of 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) immunoreactivity was significantly higher in invasive lobular ... 17βHSD5, 17β-hydroxysteroid dehydrogenase type 5; 5αRed1, 5α-reductase type 1. Mentions: It was previously reported that 17 ... a) 17βHSD2 mRNA expression in four IDC and four ILC cases was analyzed using RT2 quantitative PCR. (b) Representive ... a) 17βHSD2 mRNA expression in four IDC and four ILC cases was analyzed using RT2 quantitative PCR. (b) Representive ...
The 17βHSD14 protein was expressed in several classical steroidogenic tissues such as breast, ovary and testis which supports ... 1. Elucidating the role of 17β hydroxysteroid dehydrogenase type 14 in normal physiology and in breast cancer. Åpne denne ... This thesis focuses on 17βHSD14, which is one such proposed marker, aiming to learn more of properties of the enzyme in breast ... 17β-hydroxysteroid dehydrogenase type 14 is a predictive marker for tamoxifen response in oestrogen receptor positive breast ...
Avhandling: The role of the androgen receptor and hydroxysteroid 17β dehydrogenase in breast cancer Impact on tamoxifen ... The second goal of this thesis was to further study the role of hydroxysteroid 17β dehydrogenase enzymes in breast cancer, and ... The role of the androgen receptor and hydroxysteroid 17β dehydrogenase in breast cancer Impact on tamoxifen treatment. Detta är ... The modulation of the members of the hydroxysteroid 17β dehydrogenase in breast cancer is associated with changes in the local ...
  • These features and expression profiles suggest a critical role of 17 beta-HSD-10 in neurodegenerative and steroid-dependent cancer forms. (ox.ac.uk)
  • Not expressed in the ovaries, where another 17β-HSD subtype, likely HSD17B5, is expressed instead. (wikipedia.org)
  • HSD17B5: Has 3α-HSD and 20α-HSD activity in addition to 17β-HSD activity. (wikipedia.org)
  • Belongs to the short-chain dehydrogenases/reductases (SDR) family. (abcam.com)
  • The active site contains a Ser-Tyr-Lys triad, typical for short-chain dehydrogenases/reductases (SDR). (diva-portal.org)
  • Conversely, hepatic 11β-HSD1 activity, assessed by measuring plasma cortisol after oral administration of cortisone, is reduced in obesity ( 17 , 19 , 21 ), although it is uncertain whether increased inactivation of cortisone and cortisol by A-ring reductases in the liver ( 22 ) contributes to the difference in plasma cortisol. (diabetesjournals.org)
  • No prognostic importance of 17βHSD14 was seen for systemically untreated patients. (diva-portal.org)
  • The importance of 17β-estradiol (E2) in the prevention of large bowel tumorigenesis has been shown in many epidemiological studies. (beds.ac.uk)
  • Fomepizole is an alcohol dehydrogenase inhibitor used for the treatment of ethylene glycol and methanol poisonings in adults. (adooq.com)
  • It inhibits adione-stimulated proliferation of 17β-HSD3-expressing androgen receptor-positive LNCaP(HSD3) prostate cancer cells in vitro. (ox.ac.uk)
  • Human estrogenic 17beta-hydroxysteroid dehydrogenase type 1 (17beta-HSD1), which catalyzes the reduction of inactive estrone (E1) to the active 17beta-estradiol in breast tissues, is a key enzyme responsible for elevated levels of E2 in breast tumor tissues. (rcsb.org)
  • It catalyzes the reversible reduction/ dehydrogenation of the oxo/beta-hydroxy groups at positions 3 and 17 of steroid compounds, including hormones and isobile acids. (diva-portal.org)
  • Similarly, mutation of Asn87 to Ala results in an 80% reduction of kcat/Km in the dehydrogenase direction but also unchanged 3-oxoreductase properties. (ox.ac.uk)
  • In euglycemic obesity, numerous studies ( 17 - 19 ) have shown that 11β-HSD1 mRNA and activity in subcutaneous adipose tissue is increased, which has been corroborated in vivo using microdialysis ( 20 ). (diabetesjournals.org)
  • RU486 (mifepristone, 11β-[p-(dimethylamino)phenyl]-17β-hydroxy-17-(1-propynyl)estra-4,9-dien-3-one), a glucocorticoid receptor antagonist, decreased adipose mRNA levels of 11β-HSD1 as well as adipose triglyceride lipase. (sigmaaldrich.com)
  • A ligand-based 17β-HSD2 pharmacophore model was applied to screen a cosmetic chemicals database, followed by in vitro testing of selected paraben compounds for inhibition of 17β-HSD1 and 17β-HSD2 activities. (mdpi.com)