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Hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1

3 beta-hydroxysteroid dehydrogenase, 3 beta-HSD
Top mentioned proteins: P450scc, HAD, CAN, aromatase, HCG
Papers on 3 beta-hydroxysteroid dehydrogenase
ALPK1 affects testosterone mediated regulation of proinflammatory cytokines production.
Ko et al., Taiwan. In J Steroid Biochem Mol Biol, Nov 2015
Decreasing endogenous ALPK1 enhanced testosterone levels and transcripts of testosterone-regulated genes (P450scc, 3beta-HSD, P450C17, 17beta-HSD, StAR, and INSL3) in TM3 Leydig cells.
Cellular microenvironment dictates androgen production by murine fetal Leydig cells in primary culture.
Jorgensen et al., Madison, United States. In Biol Reprod, 2014
Fetal Leydig cell identity was validated using double-labeled immunohistochemistry against GFP and the steroidogenic enzyme 3beta-HSD, and cells were successfully isolated as indicated by qPCR results from sorted cell populations.
Wt1 is involved in leydig cell steroid hormone biosynthesis by regulating paracrine factor expression in mice.
Gao et al., Beijing, China. In Biol Reprod, 2014
In the present study, we found that Wt1 is also required for steroidogenesis in Leydig cells and that deletion of the Wt1 gene resulted in defects in testosterone biosynthesis and downregulation of steroidogenic gene expression, including cytochrome P450 side-chain cleavage (P450scc), steroidogenic acute regulatory protein (StAR), 3beta-hydroxysteroid dehydrogenase I (3beta-HSD), and cytochrome P450 17A1 (Cyp17a1).
[Differentiation of human bone marrow mesenchymal stem cells into Leydig or steroidogenic cells in vivo].
Dong et al., In Sichuan Da Xue Xue Bao Yi Xue Ban, 2014
The results were analyzed by microscopic observation, using 3beta-hydroxysteroid dehydrogenase (3beta-HSD) monoclonal antibody and mouse anti-human cell nucleus monoclonal antibody for immunofluorescence assay on the testis.
In vivo chronic and in vitro acute effects of di(2-ethylhexyl) phthalate on pseudopregnant rabbit corpora lutea: possible involvement of peroxisome proliferator-activated receptor gamma.
Zerani et al., Italy. In Biol Reprod, 2014
Immunohistochemistry provided evidence for the presence of PPARG, prostaglandin endoperoxide synthase 1 (PTGS1), PTGS2, prostaglandin E2-9-ketoreductase (PGE2-9-K), and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) in all the luteal cells during pseudopregnancy.
Genetic variation in the HSD3B1 gene and recurrent spontaneous abortions.
Lamnissou et al., Athens, Greece. In J Matern Fetal Neonatal Med, 2012
The HSD3B1 T/C polymorphism cannot be used as genetic marker for the risk for recurrent spontaneous abortions in our Caucasian population.
Expression of 3β-HSD1 and P450 Aromatase enzymes during mouse gonad differentiation.
Moreno-Mendoza et al., Mexico. In J Mol Histol, 2011
There is expression of 3beta-Hsd1 in XX gonads during gonad differentiation period.
Pharmacological doses of testosterone upregulated androgen receptor and 3-Beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase and impaired leydig cells steroidogenesis in adult rats.
Andric et al., Novi Sad, Serbia. In Toxicol Sci, 2011
The upregulation of AR and 3betaHSD in testosterone-impaired Leydig cells steroidogenesis could be the possible mechanism that maintains and prevents loss of steroidogenic function.
Association of HSD3B1 and HSD3B2 gene polymorphisms with essential hypertension, aldosterone level, and left ventricular structure.
Matsumoto et al., Tokyo, Japan. In Eur J Endocrinol, 2010
rs6203 and rs1047303 in the HSD3B1 gene are useful genetic markers for essential hypertension, while polymorphisms of HSD3B1 are associated with the BP and aldosterone level.
Salt-sensitive hypertension in circadian clock-deficient Cry-null mice involves dysregulated adrenal Hsd3b6.
Okamura et al., Kyoto, Japan. In Nat Med, 2010
In Cry-null mice, Hsd3b6 messenger RNA and protein levels are constitutively high, leading to a marked increase in 3beta-hydroxysteroid dehydrogenase-isomerase (3beta-HSD) enzymatic activity and, as a consequence, enhanced aldosterone production.
Placental steroids in cattle: hormones, placental growth factors or by-products of trophoblast giant cell differentiation?
Hoffmann et al., Gießen, Germany. In Exp Clin Endocrinol Diabetes, 2008
The down-regulation of P450scc and P450c17 and the up-regulation of 3beta-HSD and aromatase during the differentiation of TGC from UTC in parallel with the up-regulation of ER beta and estrogen sulfotransferase in maturing TGC suggests a function of placental estrogens primarily as autoor intracrine regulators during this process and assigns to conjugated placental estrogens a role as inactivated by-products of TGC differentiation intended for excretion.
Expression of steroidogenic enzymes and sex-steroid receptors in human prostate.
Pelletier, Québec, Canada. In Best Pract Res Clin Endocrinol Metab, 2008
The enzymes 3beta-hydroxysteroid dehydrogenase (3beta-HSD), which converts dehydroepiandrosterone (DHEA) into androstenedione, and type 5 17beta-HSD, which catalyzes the reduction of androstenedione to testosterone, have been localized in basal cells of alveoli as well as in stromal cells and endothelial cells of blood vessels.
Neuroprogesterone: key to estrogen positive feedback?
Sinchak et al., Los Angeles, United States. In Brain Res Rev, 2008
In support of the idea that estradiol induces neuroprogesterone, estradiol increased expression of the progesterone-synthesizing enzyme 3beta-hydroxysteroid dehydrogenase (3beta-HSD) in the hypothalamus before the LH surge.
3beta-HSD activates DHEA in the songbird brain.
Soma et al., Los Angeles, United States. In Neurochem Int, 2008
Over the past decade, we have obtained considerable evidence from avian studies demonstrating that (1) DHEA is an important circulating prohormone in songbirds and (2) the enzyme 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD), responsible for converting DHEA into a more active androgen, is expressed at high levels in the songbird brain.
[Medical treatment for Cushing's syndrome].
Omura et al., Yokohama, Japan. In Nihon Rinsho, 2008
We rarely use trilostane which is an inhibitor against 3beta-hydroxysteroid dehydrogenase (3beta-HSD).
Molecular biology of the 3beta-hydroxysteroid dehydrogenase/delta5-delta4 isomerase gene family.
Melner et al., Québec, Canada. In Endocr Rev, 2005
The 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase (3beta-HSD) isoenzymes are responsible for the oxidation and isomerization of Delta(5)-3beta-hydroxysteroid precursors into Delta(4)-ketosteroids, thus catalyzing an essential step in the formation of all classes of active steroid hormones.
Total biosynthesis of hydrocortisone from a simple carbon source in yeast.
Dumas et al., Gif-sur-Yvette, France. In Nat Biotechnol, 2003
Biosynthesis involves eight mammalian proteins (mature forms of CYP11A1, adrenodoxin (ADX), and adrenodoxin reductase (ADR); mitochondrial forms of ADX and CYP11B1; 3beta-HSD, CYP17A1, and CYP21A1).
Actions of placental and fetal adrenal steroid hormones in primate pregnancy.
Albrecht et al., Norfolk, United States. In Endocr Rev, 1995
As a result of this cascade of events, there is an increase in expression of pituitary POMC/ACTH and key enzymes, e.g. 3 beta-HSD and P-450 17 alpha-hydroxylase, important for de novo cortisol formation by, and consequently maturation of, the fetal adrenal gland.
Regulation of expression of 3β-hydroxysteroid dehydrogenase is mediated by cAMP in rat Leydig cells and H540 rat Leydig tumor cells.
Mason et al., Dallas, United States. In J Steroid Biochem Mol Biol, 1992
Data suggest that cAMP mediates transcriptional regulation of Hsd3b1 in Leydig cells (i.e., both normal Leydig cells and Leydig tumor cells); luteinizing hormone may be required to maintain expression of testicular Hsd3b1.
Congenital adrenal hyperplasia due to point mutations in the type II 3 beta-hydroxysteroid dehydrogenase gene.
Labrie et al., Québec, Canada. In Nat Genet, 1992
Classical 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4-isomerase (3 beta-HSD) deficiency is an autosomal recessive form of congenital adrenal hyperplasia characterized by a severe impairment of steroid biosynthesis in both the adrenals and the gonads.
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