Disease relevance of C02159

• Genes preferentially expressed in both placenta and hemangiomas were identified, including 17-beta hydroxysteroid dehydrogenase type 2 and tissue factor pathway inhibitor 2 [1].
• Animal studies indicate that maternal hypertension, excess glucocorticoids, and hydroxysteroid dehydrogenase inhibition program adult blood pressure [2].
• Effect of retinoic acid and palm oil carotenoids on oestrone sulphatase and oestradiol-17beta hydroxysteroid dehydrogenase activities in MCF-7 and MDA-MB-231 breast cancer cell lines [3].
• When maternal circulating B was maintained at the basal level by adrenalectomy and B supply, FR50 induced IUGR in pups and decreased placental 11beta- hydroxysteroid dehydrogenase type 2 expression at term, but did not disturb the offspring's HPA axis [4].
• The severity of intestinal disease in the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) (-/-) mice has been reported to co-segregate with gene loci which contain the genes for hydroxysteroid sulphotransferase (SULT) [5].

Psychiatry related information on C02159

• It binds an intracellular polypeptide known as ERAB, thought to be a hydroxysteroid dehydrogenase enzyme, which is expressed in normal tissues, but is overexpressed in neurons affected in Alzheimer's disease [6].
• This suggests that weight gain in the patient with anorexia nervosa could be associated with increased activity in the adrenal 17,20-lyase enzymes and a decrease in the activity of the 3-beta hydroxysteroid dehydrogenase [7].

High impact information on C02159

• The predicted amino acid sequence of the Ts2 protein shows significant similarity to short-chain alcohol dehydrogenases, particularly hydroxysteroid dehydrogenases [8].
• Molecular endocrinology of hydroxysteroid dehydrogenases [9].
• Our results suggest that bile acids did not reflux into the esophagus of patients with gastroesophageal reflux disease whom we studied and caution must be exercised in the use of enzymatic assay for bile acids in postprandial gastrointestinal fluids, as the commonly used hydroxysteroid dehydrogenase assay is not specific for bile acids alone [10].
• CRH was biologically active on human sebocytes: it induced biphasic increase in synthesis of sebaceous lipids with a maximum stimulation at 10(-7) M and up-regulated mRNA levels of 3 beta- hydroxysteroid dehydrogenase/Delta(5-4) isomerase, although it did not affect cell viability, cell proliferation, or IL-1 beta-induced IL-8 release [11].
• That the TAM-induced PR was indeed functional was evident from (a) increased activities of the progestin-sensitive enzyme, 17 beta-estradiol hydroxysteroid dehydrogenase and (b) histological appearance of subnuclear vacuolization in these tumors after progestin administration [12].

Chemical compound and disease context of C02159

• Enzyme histochemically, cortical cells showed weaker activity for 3 beta hydroxysteroid dehydrogenase and other enzymes than did usual cortisol-producing adenomas [13].
• Another abnormality in endometriosis, i.e. deficient hydroxysteroid dehydrogenase (17beta-HSD) type 2 expression, impairs the inactivation of estradiol to estrone [14].
• Oestradiol-17 beta hydroxysteroid dehydrogenase (E2DH) is present in normal and malignant breast tissues and also in cultured breast cancer cells [15].
• Demonstration of hydroxysteroid dehydrogenases and testosterone in the Sertoli-Leydig cell tumor (androblastoma) tissue of the human ovary: an enzyme histochemical and immunohistochemical study [16].
• Eznyme preparations from Pseudomonas testosteroni containing alpha- and beta- hydroxysteroid dehydrogenases catalyzed the oxidation of morphine and codeine by nicotinamide adenine dinucleotide [17].

Biological context of C02159

• We identified hydroxysteroid dehydrogenase-3beta isotype 4 and osteopontin as lead classifier genes in relation to the mesangial matrix expansion phenotype [18].
• Dehydroepiandrosterone sulfotransferase (STD) is a hydroxysteroid sulfo-conjugating enzyme with preferential substrate specificity for C-19 androgenic steroids and C-24 bile acids [19].
• A computer search of the protein data banks revealed significant homology with several sulfotransferases: 71% with bovine placental estrogen sulfotransferase, 52% with rat liver phenol sulfotransferase, 35% with rat liver hydroxysteroid sulfotransferase, and 36% with rat liver senescence marker protein 2 [20].
• The role of fish (estrogen, androgen, and progestogen) hormone receptors and invertebrate (ecdysone) hormone receptor, egg production (vtg and chorion) proteins, steroid biosynthesis enzymes (aromatase, sulfotransferase, and hydroxysteroid dehydrogenase), DNA damage, apoptosis, and their potential development as biomarkers are discussed in turn [21].
• A cluster of eight hydroxysteroid dehydrogenase genes belonging to the aldo-keto reductase supergene family on mouse chromosome 13 [22].

Anatomical context of C02159

• The number of Leydig cells per testis was determined after immunohistochemical staining for 3-beta hydroxysteroid dehydrogenase in experiment 2 [23].
• Additionally, appreciable immunohistochemical staining for p-nitrophenol UDP-glucuronosyltransferase, but not for the two hydroxysteroid UDP-glucuronosyltransferases, was detected within the epithelium of the hepatic bile duct and the endothelium of the hepatic artery and portal vein [24].
• The activity of 17 beta hydroxysteroid dehydrogenase (170HSD) was measured in adipose tissue adjacent to benign or malignant breast tumours [25].
• Estrogen and hydroxysteroid sulfotransferases in guinea pig adrenal cortex: cellular and subcellular distributions [26].
• Age and sex differences in the distribution of lipids, tetrazolium reductases and hydroxysteroid dehydrogenases in the gonads and adrenals of the bank vole (Clethrionomys glareoulus): a histochemical study [27].

Associations of C02159 with other chemical compounds

• However, in contrast to the 3-ketosteroid reductase activity of the enzymes, their hydroxysteroid oxidase activity was potently inhibited by low micromolar concentrations of the opposing cofactor (NADPH) [28].
• The temporal expression patterns of the fetal LC marker gene, thrombospondin 2, and those of adult LCs, hydroxysteroid dehydrogenase-6, delta5-3-beta and prostaglandin D synthase, were similar in wild-type and hCG+ males [29].
• Purified STa was classified as a hydroxysteroid ST because the 5-HCR- and DHA-sulfating activities were inseparable from each other throughout the purification steps [30].
• With progesterone and testosterone as substrate, all variants of CYP1A1 exhibited high, but different steroid hydroxylation activities (8-40 pmol hydroxysteroid/min/pmol CYP1A1, i.e. approximately 800-4000 pmol/min/mg microsomal protein) [31].
• The hydroxysteroid dehydrogenase activities of testes from 124 rats between the ages of 15 and 138 days were determined using as substrates, 3beta-hydroxy-5beta-androstan-17-one, 3beta-hydroxy-5alpha-androstan-17-one, 3beta,17beta-dihydroxy-5alpha-androstane, dehydroepiandrosterone and pregnenolone [32].

Gene context of C02159

• Several hydroxysteroid dehydrogenases of the AKR1C subfamily catalyzed the reduction of HNE with higher activity than aldehyde reductase (AKR1A1) [33].
• Both cDNAs appeared, on the basis of amino acid sequence analysis, to be members of the hydroxysteroid SULT "family, " SULT2, but they were only 48% identical in amino acid sequence with the single known member of that family in humans, SULT2A1 (also referred to as DHEA ST) [34].
• The nucleotide base sequence of the ST-40 cDNA shared a strong homology of 94.4% with that of ST-20 cDNA encoding a hydroxysteroid ST which had been reported by us [35].
• The SULT2 or hydroxysteroid SULT isoforms, SULT2A1 and SULT2B1b, did not show reactivity with any of the compounds [36].
• Molecular docking simulations of steroid substrates into human cytosolic hydroxysteroid dehydrogenases (AKR1C1 and AKR1C2): Insights into positional and stereochemical preferences [37].

Analytical, diagnostic and therapeutic context of C02159

• In addition, sequence alignment and subsequent homology modelling of mouse liver 17beta-hydroxysteroid dehydrogenase and rat ovary 20alpha-hydroxysteroid dehydrogenase indicate that three loops on the C-terminal side of the barrel play potential roles in determining the positional and stereo-specificity of the hydroxysteroid dehydrogenases [38].
• Human Hydroxysteroid (17-{beta}) Dehydrogenase 1 Expression Enhances Estrogen Sensitivity of MCF-7 Breast Cancer Cell Xenografts [39].
• We have examined the expression of hydroxysteroid sulphotransferase, an enzyme which inactivates many steroids, in particular androgens, in normal breast tissue and in six ductal-type mammary carcinomas using immunohistochemistry [40].
• Molecular cloning of the alcohol/hydroxysteroid form (mSTa1) of sulfotransferase from mouse liver [41].
• Free and conjugated bile acids in human sera were analyzed by micro high-performance liquid chromatography with detection by an immobilized hydroxysteroid dehydrogenase postcolumn reaction and a spectrofluorometer [42].

References