Journal Article: On-column ligand exchange for structure-based drug design: a case study with human 11[beta]-hydroxysteroid dehydrogenase type 1 ...

The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is selectively expressed in aldosterone target tissues, conferring aldosterone selectivity for the mineralocorticoid receptor. A diminished activity causes salt-sensitive hypertension. The mechanism of the variable and distinct 11β-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) expression in the cortical collecting duct is poorly understood. Here, we analyzed for the first time whether the 11β-HSD2 expression is modulated by microRNAs (miRNAs). In silico analysis revealed 53 and 27 miRNAs with potential binding sites on human or rat HSD11B2 3′-untranslated region. A reporter assay demonstrated 3′-untranslated region-dependent regulation of human and rodent HSD11B2. miRNAs were profiled from cortical collecting ducts and proximal convoluted tubules. Bioinformatic analyses showed a distinct clustering for cortical collecting ducts and proximal convoluted tubules with 53 of 375 miRNAs, where 13 were predicted to bind to the ...

Looking for information on 3 beta hydroxysteroid dehydrogenase deficiency? Medigest has all you need to know about 3 beta hydroxysteroid dehydrogenase deficiency - Symptoms and Signs, Causes, Treatments and definition

TY - JOUR. T1 - Preparation of highly purified 3α- and 3β-hydroxysteroid dehydrogenases from Pseudomonas sp. AU - Shikita, Mikio. AU - Talalay, Paul. PY - 1979/5. Y1 - 1979/5. N2 - A method is described for preparing highly purified 3α- and 3β-hydroxysteroid dehydrogenases (EC 1.1.1.50 and EC 1.1.1.145, respectively), essentially uncontaminated with one another, from extracts of a steroid-induced Pseudomonas species. These enzymes are suitable for the microanalysis of 3α-hydroxy-, 3β-hydroxy-, and 3-ketosteroids.. AB - A method is described for preparing highly purified 3α- and 3β-hydroxysteroid dehydrogenases (EC 1.1.1.50 and EC 1.1.1.145, respectively), essentially uncontaminated with one another, from extracts of a steroid-induced Pseudomonas species. These enzymes are suitable for the microanalysis of 3α-hydroxy-, 3β-hydroxy-, and 3-ketosteroids.. UR - http://www.scopus.com/inward/record.url?scp=0018474352&partnerID=8YFLogxK. UR - ...

Achim Recktenwald, PhD (achim at ibex.ca) wrote: : Robert S. Strauss wrote: : , : , Maxy Mariasegaram ,mariaseg at HERCULES.CS.UREGINA.CA, wrote: : , : , ,Hello everyone, : , : , ,I have to write a paper on the above enzyme as part of the course : , ,requirements for a fourth year biochemistry class. : , : , ,I would appreciate any leads to literature that cover the structure, : , ,function, kinetics and recent development on 3-beta HSD, preferably some : , ,review articles. Failing which, what would be a good way to start this : , ,search? I tried looking up the Bio Abstracts, but that didnt help much. : , : , ,I look forward to hearing from people out there, and thank you very much : , ,for reading this message. : , : , ,cheers, : , ,Max Youll find a lot of information if you search medline with the words : short-chain dehydrogenases. In 1995 Jornvall et al. published a review in Biochemistry, it is pretty informative, although incomplete. Lluis ...

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 ...

TY - JOUR. T1 - The NGFI-B family of transcription factors regulates expression of 3β-hydroxysteroid dehydrogenase type 2 in the human ovary. AU - Havelock, Jon C.. AU - Smith, Allison L.. AU - Seely, Jeremiah B.. AU - Dooley, Christina A.. AU - Rodgers, Raymond J.. AU - Rainey, William E.. AU - Carr, Bruce R.. N1 - Funding Information: The authors would like to thank Bobbie Mayhew for her technical support. This work was supported by National Institutes of Health grant T32-HD007190 (BRC).. PY - 2005/2. Y1 - 2005/2. N2 - The nerve growth factor-induced clone B (NGFI-B) family of transcription factors are orphan members of the steroid hormone receptor superfamily. The NGFI-B expression was recently shown in the rat ovarian tissue and appears to be regulated by gonadotrophins. The purpose of our study was to investigate the role of the three members of this family [NGFI-B, Nur-related factor 1 (NURR1) and neuron derived orphan receptor 1 (NOR-1)] in the transcription of genes that encode key ...

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

Title: Effect of Free and in Poly(η-caprolactone) Nanoparticles Incorporated New Type 1 17β -Hydroxysteroid Dehydrogenase Inhibitors on Cancer Cells. VOLUME: 6 ISSUE: 1. Author(s):Petra Kocbek, Karmen Teskac, Petra Brozic, Tea Lanisnik Rizner, Stanislav Gobec and Julijana Kristl. Affiliation:Askerceva 7, 1000 Ljubljana, Slovenia.. Keywords:Nanoparticles, enzyme inhibitors, T-47D cells, cellular uptake, drug delivery, breast cancer. Abstract: Development and progression of breast cancer can be caused by increased estradiol activity, which stimulates cell proliferation. Inhibitors of type 1 17β-hydroxysteroid dehydrogenase (17β-HSD) enzyme inhibit estradiol biosynthesis and therefore have potential anticancer activity. In this study two new trans-cinnamic acid esters were established as inhibitors of the human recombinant type 1 17β-HSD enzyme. Studied compounds are poorly water soluble and have low stability in aqueous medium. Free inhibitors were tested on T-47D cells, which express ...

Similar phenotypes in 46,XY DSD have different etiopathogenesis. Androgen (A) synthesis are rare respect to A action/metabolism defects. The most frequent cause in the former group is a mutation of HSD17B3, gene encoding for an enzyme (17BHSD3) converting delta4-androstenedione (D4) into testosterone (T). Homozygotes/compound heterozygotes have testes, male wolffian structures, completely female (F) or mildly virilized external genitalia (EG). Pts with not palpable testes may appear as F, but they virilize at puberty for the increase in serum T. Our patient (12-yrs-old. 46,XY) for FEG at birth was raised as girl until puberty, when clitoris enlargement (, 4 cm) and male pattern of body hair and timbre of voice appeared. The EG corresponded to Prader stage III. Pelvic echography: two hypoechogenic ovoid masses in inguinal regions, compatible with testes, no Müllerian structures, echogenic structure (20x5mm) like hypoplastic uterus, posteriorly to the bladder. T synthesis: reduced before (3.3 ...

Oestrogens play key roles in the development of the majority of breast tumours, a fact that has been exploited successfully in treating breast cancer with tamoxifen, which is a selective oestrogen receptor modulator. In post-menopausal women, oestrogens are synthesised in peripheral hormone-target tissues from adrenally derived precursors. Important in the peripheral fine-tuning of sex hormone levels are the 17β hydroxysteroid dehydrogenases (17βHSDs). These enzymes catalyse the oxidation/reduction of carbon 17β of androgens and oestrogens. Upon receptor binding, the 17β-hydroxy conformation of androgens and oestrogens (testosterone and oestradiol) triggers a greater biological response than the corresponding keto-conformation of the steroids (androstenedione and oestrone), and the 17βHSD enzymes are therefore important mediators in pre-receptor regulation of sex hormone action.. Breast tumours differ substantially with regards to molecular and/or biochemical signatures and thus clinical ...

Stolz, A., Sugiyama, Y., Kuhlenkamp, J., Osadchey, B., Yamada, T., Belknap, W., Balistreri, W. and Kaplowitz, N. (1986), Cytosolic bile acid binding protein in rat liver: Radioimmunoassay, molecular forms, developmental characteristics and organ distribution. Hepatology, 6: 433-439. doi: 10.1002/hep.1840060319 ...

Enzymatic interconversion of active and inactive glucocorticoid hormone is important, and is carried out physiologically by 11β-hydroxysteroid dehydrogenase (11β-HSD) isoforms, explaining their role in cellular and toxicological processes. Two forms of the enzyme, 11β-HSD-1 and 11β-HSD-2, belonging to the protein superfamily of short-chain dehydrogenases/reductases, have been structurally and functionally characterised. Although displaying dehydrogenase and reductase activities in vitro, the dominant in vivo function of the type-1 enzyme might be to work as a reductase, thus generating active cortisol from inactive cortisone precursors. On the other hand, for adrenal glucocorticoids the type-2 enzyme seems to be exclusively a dehydrogenase and, by inactivating glucocorticoids, confers specificity to peripheral mineralocorticoid receptors.

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 ...

Regulation of 3β‐Hydroxysteroid Dehydrogenase Activity by Human Chorionic Gonadotropin, Androgens, and Antiandrogens in Cultured Testicular ...

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 ...

20α-Hydroxysteroid dehydrogenase (20α-HSD), which metabolizes progesterone to an inactive steroid in the corpus luteum of mice and rats but not of humans, is thought to play a crucial role in shortening the oestrous cycles in these rodent species. We determined the nucleotide sequence of the 5′-flanking region of the mouse 20α-HSD gene, and examined its promoter activity using a rat luteinized granulosa cell culture. A reporter assay, using reporter constructs of various lengths of the 5′-flanking region, revealed that the region between −83 and 60 bp upstream of the transcription start site was essential for transcriptional activity. Furthermore, mutational analysis demonstrated that a putative Sp1 site in this region was critical to the expression of the reporter gene. Electrophoretic mobility-shift assays showed that the interaction of proteins in a nuclear extract from rat luteinized granulosa cells with this region was inhibited by a competitor having the wild-type Sp1 sequence in ...

Hydroxysteroid Dehydrogenase - Instruments Consumables Reagents Advanced BioMatrix,RANDOX,RANDOX ELISA,Biomedical, biochemical reagents, laboratory supplies, equipment, antibodies, ELISA kits, diagnostic reagents, methods of experimental techniques, general analytical instruments, material testing instruments and equipment, used laboratory equipment, instruments and equipment, life sciences, environmental monitoring equipment , measurement, measuring instruments, rotating wall bioreactor, three-dimensional tissue / stem cell culture system; microcapsule

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 ...

aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase 2; bile acid binding protein; 3-alpha hydroxysteroid dehydrogenase, type III ...

Aldo-keto reductase family 1 member C1 also known as 20α-hydroxysteroid dehydrogenase, 3α-hydroxysteroid dehydrogenase, and dihydrodiol dehydrogenase 1/2 is an enzyme that in humans is encoded by the AKR1C1 gene.[1][2] This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reduction of progesterone to the inactive form 20-alpha-hydroxy-progesterone. This gene shares high sequence identity with three other gene members, and is clustered with those three genes at chromosome 10p15-p14.[2] ...

Testosterone is metabolized in various tissues by 5α-reductase into DHT, which is 3- to 10-fold more potent as an AR agonist, and by aromatase into estradiol, which is an estrogen and lacks significant AR affinity.[1] In addition, DHT is metabolized by 3α-hydroxysteroid dehydrogenase (3α-HSD) and 3β-hydroxysteroid dehydrogenase (3β-HSD) into 3α-androstanediol and 3β-androstanediol, respectively, which are metabolites with little or no AR affinity.[1] 5α-Reductase is widely distributed throughout the body, and is concentrated to various extents in skin (particularly the scalp, beard-area of the face, pubic area, and genital area (penis and scrotum)), prostate, seminal vesicles, liver, and the brain.[1] In contrast, expression of 5α-reductase in skeletal muscle is undetectable.[1] Aromatase is highly expressed in adipose tissue and the brain, and is also expressed significantly in skeletal muscle.[1] 3α-HSD is also highly expressed in skeletal muscle.[56]. Natural AAS like testosterone ...

Inderbinen SG, Zogg M, Kley M, Smieško M, Odermatt A Endocrine Disruption and Steroid Hormone Action Toxicology and Applied Pharmacology, 1 Feb 2021 ...

1I5R: A concerted, rational design of type 1 17beta-hydroxysteroid dehydrogenase inhibitors: estradiol-adenosine hybrids with high affinity

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 ...

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 ...

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 ...

TY - JOUR. T1 - 11-ketotestosterone is a major androgen produced in human gonads. AU - Imamichi, Yoshitaka. AU - Yuhki, Koh Ichi. AU - Orisaka, Makoto. AU - Kitano, Takeshi. AU - Mukai, Kuniaki. AU - Ushikubi, Fumitaka. AU - Taniguchi, Takanobu. AU - Umezawa, Akihiro. AU - Miyamoto, Kaoru. AU - Yazawa, Takashi. PY - 2016/10/1. Y1 - 2016/10/1. N2 - Context: 11-ketotestosterone (11-KT) is a novel class of active androgen. However, the detail of its synthesis remains unknown for humans. Objective: The objective of this study was to clarify the production and properties of 11-KT in human. Design, Participants, and Methods: Expression of cytochrome P450 and 11β-hydroxysteroid dehydrogenase types 1 and 2 (key enzymes involved in the synthesis of 11-KT) were investigated in human gonads. The production of 11-KT was investigated in Leydig cells. Plasma concentrations of testosterone and 11-KT were measured in 10 women and 10 men of reproductive age. Investigation of its properties was performed using ...

3-beta HSD2 / HSD3B2, 50 µg. 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.

Context: Estrogens impact the incidence and progression of colorectal cancer (CRC) although precise molecular mechanisms remain ill-defined. Objective: Pre-receptor estrogen metabolism through steroid sulphatase (STS) and 17-hydroxysteroid dehydrogenase activity and subsequent non-genomic estrogen signaling in human CRC tissue, in the TCGA COAD dataset, and in in vitro and in vivo CRC models was investigated. The study aimed to define and therapeutically target pathways through which estrogens alter CRC proliferation and progression. Design, Setting, Patients, and Interventions: Human CRC samples with normal tissue matched-controls were collected from post-menopausal female and age-matched male patients. Estrogen metabolism enzymes and non-genomic downstream signaling pathways were determined. CRC cell lines were transfected with STS and cultured for in vitro and in vivo analysis. Estrogen metabolism was determined through a novel uHPLC-MS/MS method. Primary Outcome Measure: The proliferative ...

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 …

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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 ...

Complete information for HSDL1 gene (Protein Coding), Hydroxysteroid Dehydrogenase Like 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

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To this day, a significant proportion of the human genome remains devoid of functional characterization. In this study, we present evidence that the previously functionally uncharacterized product of the human DHRS10 gene is endowed with 17beta-HSD (17beta-hydroxysteroid dehydrogenase) activity. 17beta-HSD enzymes are primarily involved in the metabolism of steroids at the C-17 position and also of other substrates such as fatty acids, prostaglandins and xenobiotics. In vitro, DHRS10 converts NAD+ into NADH in the presence of oestradiol, testosterone and 5-androstene-3beta,17beta-diol. Furthermore, the product of oestradiol oxidation, oestrone, was identified in intact cells transfected with a construct plasmid encoding the DHRS10 protein. In situ fluorescence hybridization studies have revealed the cytoplasmic localization of DHRS10. Along with tissue expression data, this suggests a role for DHRS10 in the local inactivation of steroids in the central nervous system and placenta. The crystal structure

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。

In 2 unrelated patients, Ulick et al. (1979) described a disorder in the peripheral metabolism of cortisol, manifested by hypertension, hypokalemia, low plasma renin activity, and responsiveness to spironolactone. Aldosterone levels were subnormal.

TY - JOUR. T1 - Structural and functional aspects of placental lactogens (PLs) and ovarian 20α-hydroxysteroid dehydrogenase (20α-HSD) in the rat. AU - Shiota, K.. AU - Hirosawa, M.. AU - Hattori, N.. AU - Itonori, S.. AU - Miura, R.. AU - Noda, K.. AU - Takahashi, M.. AU - Ogawa, T.. PY - 1994. Y1 - 1994. N2 - The placenta plays an essential role in fetal growth and the maintenance of pregnancy. Successful development and maturation of the embryo is totally dependent on placental function. The main endocrine participation of the placenta is attributed to placental lactogens (PLs). Progesterone is essential for pregnancy in all mammals and is secreted by the ovary and placenta, depending on the animal species. In the rat, the main source of progesterone throughout pregnancy is the ovary, and 20α-hydroxysteroid dehydrogenase (20α-HSD) is a key enzyme for ovarian progesterone secretion. The primary action of prolactin (PRL) in the maintenance of ovarian progesterone secretion is suppression of ...

Looking for online definition of 3-beta (beta)-hydroxysteroid sulfatase in the Medical Dictionary? 3-beta (beta)-hydroxysteroid sulfatase explanation free. What is 3-beta (beta)-hydroxysteroid sulfatase? Meaning of 3-beta (beta)-hydroxysteroid sulfatase medical term. What does 3-beta (beta)-hydroxysteroid sulfatase mean?

Bile-acid 7alpha-dehydroxylase (EC 1.17.99.5, cholate 7alpha-dehydroxylase, 7alpha-dehydroxylase, bile acid 7-dehydroxylase) is an enzyme with systematic name deoxycholate:NAD+ oxidoreductase. This enzyme catalyses the following chemical reaction (1) deoxycholate + NAD+ + H2O ⇌ {\displaystyle \rightleftharpoons } cholate + NADH + H+ (2) lithocholate + NAD+ + H2O ⇌ {\displaystyle \rightleftharpoons } chenodeoxycholate + NADH + H+ Bile-acid 7alpha-dehydroxylase is highly specific for bile acid substrates. White, B.A.; Cacciapuoti, A.F.; Fricke, R.J.; Whitehead, T.R.; Mosbach, E.H.; Hylemon, P.B. (1981). Cofactor requirements for 7α-dehydroxylation of cholic and chenodeoxycholic acid in cell extracts of the intestinal anaerobic bacterium, Eubacterium species V.P.I. 12708. J. Lipid Res. 22 (6): 891-898. PMID 7276750. White, B.A.; Paone, D.A.; Cacciapuoti, A.F.; Fricke, R.J.; Mosbach, E.H.; Hylemon, P.B. (1983). Regulation of bile acid 7-dehydroxylase activity by NAD+ and NADH in cell ...

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 ...

Evidence is reported for the existence of a structurally and functionally related and probably evolutionarily conserved class of membrane-bound liver carbonyl reductases/hydroxysteroid dehydrogenases involved in steroid and xenobiotic carbonyl metabolism. Carbonyl reduction was investigated in liver microsomes of 8 vertebrate species, as well as in insect larvae total homogenate and in purified 3 alpha-hydroxysteroid dehydrogenase preparations of the procaryont Pseudomonas testosteroni, using the ketone compound 2-methyl-1,2 di-(3-pyridyl)-1-propanone (metyrapone) as substrate. The enzyme activities involved in the metyrapone metabolism were screened for their sensitivity to several steroids as inhibitors. In all fractions tested, steroids of the adrostane or pregnane class strongly inhibited xenobiotic carbonyl reduction, whereas only in the insect and procaryotic species could ecdysteroids inhibit this reaction. Immunoblot analysis with antibodies against the respective microsomal mouse liver

Alterations in glucocorticoid (GC) biosynthesis and metabolism are associated with a variety of pathophysiological disorders including cholestasis, diabetes and other metabolic disorders. Bile acids (BA) are also important modulators of metabolic functions and regulate cholesterol, triglyceride and glucose homeostasis as well as being critical for dietary fat digestion, enterohepatic function, and postprandial thermogenesis. In intact cells and in vivo, the 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme converts inactive GC precursors (cortisone in humans, and 11-dehydrocorticosterone in mice and rats) into their active forms (cortisol and corticosterone, respectively) thereby amplifying local intracellular GC levels. Interconversion by 11β-HSD1 of other sterols has also been described. These include conversions of 7keto-cholesterol to 7β-hydroxycholesterol, 7-oxodehydroepiandrosterone (7-oxo-DHEA) to 7α-hydroxy- and 7β-hydroxy DHEA, 7- oxo-lithocholic acid (LCA, a bile acid; ...

3-beta (β)-hydroxysteroid dehydrogenase (HSD) deficiency is an inherited disorder that affects hormone-producing glands including the gonads (ovaries in females and testes in males) and the adrenal glands. Explore symptoms, inheritance, genetics of this condition.

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 ...

HSD17B1: Referred to as estrogenic. Major subtype for activation of estrogens from weaker forms (estrone to estradiol and 16α-hydroxyestrone to estriol). Catalyzes the final step in the biosynthesis of estrogens. Highly selective for estrogens; 100-fold higher affinity for estranes over androstanes. However, also catalyzes the conversion of DHEA into androstenediol.[10] Recently, has been found to inactivate DHT into 3α- and 3β-androstanediol.[10][11] Expressed primarily in the ovaries and placenta but also at lower levels in the breast epithelium.[12][10] Major isoform of 17β-HSD in the granulosa cells of the ovaries.[13] Mutations and associated deficiency have not been reported in humans.[14] Knockout mice show altered ovarian sex steroid production, normal puberty, and severe subfertility due to defective luteinization and ovarian progesterone production.[15] ...

Circulating levels of the steroid hormone, progesterone (P), increase during development of the primate corpus luteum (CL) and then decline during luteal regres...

DISCUSSION. Our baseline CON values for the E:F ratio were similar to those previously reported by others (6). The short term GFJ treatment in the present study lowered enzyme activity by 44% (Figure 3), which compares favorably to the ~40% inhibition estimated from the urinary-E/F ratio obtained in a pilot study (10) and to the ~60% obtained in a patient presenting with edema and hypokalemia associated with the habitual oral intake of 1 liter/day of GFJ (5). Taken together, our findings suggest that Sal effluents are a cost-effective and convenient matrix (compared to plasma/urine) for probing alterations in 11β-HSD2 activity induced by GFJ ingestion. In our study, the decrease in enzyme activity induced by GFJ at baseline was mainly driven by a significant decrease (~30%) in Sal-E concentration. This is in line with a decrease in F oxidation to E, a reaction that is mediated by 11β-HSD2 (1,9,10) and likely inhibited by one or more flavonoids found in GFJ (naringenin, quercetin, hesperetin, ...

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. [...]

|i|Background|/i|. Glucocorticoid excess has been linked to clinical observations associated with the pathophysiology of metabolic syndrome. The intracellular glucocorticoid levels are primarily modulated by 11|i|β|/i|-hydroxysteroid dehydrogenase type 1 (11|i|β|/i|-HSD1) enzyme that is highly expressed in key metabolic tissues including fat, liver, and the central nervous system.|i| Methods|/i|. In this study we synthesized a set of novel tetrahydrothiazolopyridine derivatives, TR-01–4, that specifically target 11|i|β|/i|-HSD1 and studied their ability to interfere with the glucocorticoid and lipid metabolism in the 3T3-L1 adipocytes.|i| Results|/i|. Based on the docking model and structure-activity relationships, tetrahydrothiazolopyridine derivatives TR-02 and TR-04 showed the highest potency against 11|i|β|/i|-HSD1 by dose-dependently inhibiting conversion of cortisone to cortisol (IC|sub|50|/sub| values of 1.8 |i|μ|/i|M and 0.095 |i|μ|/i|M,

BARNARD L. The Biosynthesis of Adrenal C11-Oxy C21 Steroids, Implicated in 21-Hydroxylase Deficiency - Desoxycortisol and Desoxycortisone and Their Downstream Metabolism. MSc, 2017. 105 pp. Studieleier: SWART AC.. BARNARD M. The characterization of 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) activity towards novel C19 substrates. MSc, 2017. 104 pp. Studieleier: STORBECK K.. BARRY CJ. Modelling the glucocorticoid receptor dimerisation cycle. MSc, 2017. 123 pp. Studieleier: ROHWER JM. Medestudieleier: LOUW A.. BURGER R. Flux balance analysis of Plasmodium falciparum growth and energy metabolism. MSc, 2017. 100 pp. Studieleier: SNOEP JL. Medestudieleier: EICHER JJ.. JOHNSTONE E. Comparative secretome analysis of normal prostate and prostate cancer cell models. MSc, 2017. 134 pp. Studieleier: STORBECK K. Medestudieleier: VLOK NM.. JONKER HI. Evaluation of DNA vaccines against Mycoplasma nasistruthionis sp. nov. str. Ms03 infections in ostriches and the production of IgA heavy chain proteins. ...

Background Impaired corticosteroid action caused by genetic and environmental influence, including exposure to hazardous xenobiotics, contributes to the development and progression of metabolic diseases, cardiovascular complications and immune disorders. Novel strategies are thus needed for identifying xenobiotics that interfere with corticosteroid homeostasis. 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) and mineralocorticoid receptors (MR) are major regulators of corticosteroid action. 11β-HSD2 converts the active glucocorticoid cortisol to the inactive cortisone and protects MR from activation by glucocorticoids. 11β-HSD2 has also an essential role in the placenta to protect the fetus from high maternal cortisol concentrations. Methods and Principal Findings We employed a previously constructed 3D-structural library of chemicals with proven and suspected endocrine disrupting effects for virtual screening using a chemical feature-based 11β-HSD pharmacophore. We tested several in silico

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 ...

Other lines of investigation have demonstrated that aldose reductase exhibits broad substrate specificity for both hydrophilic and hydrophobic aldehydes. Aldose reductase and the structurally related enzyme in the aldo-keto reductase family, aldehyde reductase, both catalyze the reduction of biogenic aldehydes derived from the catabolism of the catecholamines and serotonin by the action of monoamine oxidase (Turner and Tipton, 1972; Tabakoff et al., 1973;Wermuth et al., 1982). These two enzymes also catalyze the reduction of isocorticosteroids, intermediates in the catabolism of the corticosteroid hormones (Wermuth and Monder, 1983). Recently, aldose reductase in the adrenal gland was reported to be a major reductase for isocaproaldehyde, a product of sidechain cleavage of cholesterol (Matsuura et al., 1996).. Apart from these findings, molecular cloning of bovine testicular 20α-hydroxysteroid dehydrogenase cDNA incidentally revealed that the deduced amino acid sequence of the enzyme is ...

Homo sapiens aldo-keto reductase family 1, member C1 (dihydrodiol dehydrogenase 1; 20-alpha (3-alpha)-hydroxysteroid dehydrogenase) (AKR1C1), mRNA. (H00001645-R01) - Products - Abnova

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The IUPHAR/BPS Guide to Pharmacology. hydroxysteroid 11-beta dehydrogenase 1 - 1.-.-.- Oxidoreductases. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.

Mouse polyclonal antibody raised against a partial recombinant NSDHL. NSDHL (NP_057006, 1 a.a. ~ 110 a.a) partial recombinant protein with GST tag. (H00050814-A01) - Products - Abnova

Rabbit polyclonal Hydroxysteroid (17-beta) Dehydrogenase 4 antibody validated for WB and tested in Human. Immunogen corresponding to recombinant fragment

ERAB antibody, C-term (hydroxysteroid (17-beta) dehydrogenase 10) for WB. Anti-ERAB pAb (GTX89602) is tested in Human samples. 100% Ab-Assurance.

ERAB antibody (hydroxysteroid (17-beta) dehydrogenase 10) for WB. Anti-ERAB pAb (GTX50767) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.