Dehydroepiandrosterone sulfate, abbreviated as DHEA sulfate or DHEA-S, also known as androstenolone sulfate, is an endogenous androstane steroid that is produced by the adrenal cortex. It is the 3β-sulfate ester and a metabolite of dehydroepiandrosterone (DHEA) and circulates in far greater relative concentrations than DHEA. The steroid is hormonally inert and is instead an important neurosteroid and neurotrophin.
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InChI=1S/C19H28O5S/c1-18-9-7-13(24-25(21,22)23)11-12(18)3-4-14-15-5-6-17(20)19(15,2)10-8-16(14)18/h3,13-16H,4-11H2,1-2H3,(H,21,22,23)/t13-,14-,15-,16-,18-,19-/m0/s1 |
CZWCKYRVOZZJNM-USOAJAOKSA-N |
C1[C@@]2([C@@]([C@@]3(C(C[C@@H](OS(O)(=O)=O)CC3)=C1)C)(CC[C@]4([C@]2(CCC4=O)[H])C)[H])[H] |
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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See:
PubMed
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EC 2.7.1.33 (pantothenate kinase) inhibitor
An EC 2.7.1.* (phosphotransferases with an alcohol group as acceptor) inhibitor that interferes with the action of pantothenate kinase (EC 2.7.1.33).
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
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View more via ChEBI Ontology
17-oxoandrost-5-en-3β-yl hydrogen sulfate
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(3-beta)-3-(Sulfooxy)androst-5-en-17-one
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ChemIDplus
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17-Ketoandrost-5-en-3beta-yl sulfate
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ChemIDplus
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17-oxoandrost-5-en-3β-yl hydrogen sulphate
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ChEBI
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3-O-Sulfodehydroepiandrosterone
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ChemIDplus
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3beta-Hydroxyandrost-5-en-17-one 3-sulfate
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KEGG COMPOUND
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3beta-hydroxyandrost-5-en-17-one 3-sulfate
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ChEBI
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3beta-Hydroxyandrost-5-en-17-one 3-sulfate
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KEGG COMPOUND
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Androst-5-en-17-on-3beta-yl sulfuric acid
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ChemIDplus
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Dehydroepiandrosterone 3-sulfate
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ChemIDplus
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Dehydroepiandrosterone monosulfate
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ChemIDplus
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Dehydroepiandrosterone sulfate
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KEGG COMPOUND
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Dehydroepiandrosterone sulphate
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ChemIDplus
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Dehydroisoandrosterone sulfate
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ChemIDplus
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Dehydroisoandrosterone-3-sulfate
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ChemIDplus
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DHEA sulfate
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ChemIDplus
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DHEA sulfate
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KEGG COMPOUND
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DHEA-S
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ChEBI
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DHEAS
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ChemIDplus
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Prasterone sulfate
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ChemIDplus
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2227078
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Reaxys Registry Number
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Reaxys
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651-48-9
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CAS Registry Number
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ChemIDplus
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Roux A, Xu Y, Heilier JF, Olivier MF, Ezan E, Tabet JC, Junot C (2012) Annotation of the human adult urinary metabolome and metabolite identification using ultra high performance liquid chromatography coupled to a linear quadrupole ion trap-Orbitrap mass spectrometer. Analytical chemistry 84, 6429-6437 [PubMed:22770225] [show Abstract] Metabolic profiles of biofluids obtained by atmospheric pressure ionization mass spectrometry-based technologies contain hundreds to thousands of features, most of them remaining unknown or at least not characterized in analytical systems. We report here on the annotation of the human adult urinary metabolome and metabolite identification from electrospray ionization mass spectrometry (ESI-MS)-based metabolomics data sets. Features of biological interest were first of all annotated using the ESI-MS database of the laboratory. They were also grouped, thanks to software tools, and annotated using public databases. Metabolite identification was achieved using two complementary approaches: (i) formal identification by matching chromatographic retention times, mass spectra, and also product ion spectra (if required) of metabolites to be characterized in biological data sets to those of reference compounds and (ii) putative identification from biological data thanks to MS/MS experiments for metabolites not available in our chemical library. By these means, 384 metabolites corresponding to 1484 annotated features (659 in negative ion mode and 825 in positive ion mode) were characterized in human urine samples. Of these metabolites, 192 and 66 were formally and putatively identified, respectively, and 54 are reported in human urine for the first time. These lists of features could be used by other laboratories to annotate their ESI-MS metabolomics data sets. | Leonardi R, Zhang YM, Yun MK, Zhou R, Zeng FY, Lin W, Cui J, Chen T, Rock CO, White SW, Jackowski S (2010) Modulation of pantothenate kinase 3 activity by small molecules that interact with the substrate/allosteric regulatory domain. Chemistry & biology 17, 892-902 [PubMed:20797618] [show Abstract] Pantothenate kinase (PanK) catalyzes the rate-controlling step in coenzyme A (CoA) biosynthesis. PanK3 is stringently regulated by acetyl-CoA and uses an ordered kinetic mechanism with ATP as the leading substrate. Biochemical analysis of site-directed mutants indicates that pantothenate binds in a tunnel adjacent to the active site that is occupied by the pantothenate moiety of the acetyl-CoA regulator in the PanK3acetyl-CoA binary complex. A high-throughput screen for PanK3 inhibitors and activators was applied to a bioactive compound library. Thiazolidinediones, sulfonylureas and steroids were inhibitors, and fatty acyl-amides and tamoxifen were activators. The PanK3 activators and inhibitors either stimulated or repressed CoA biosynthesis in HepG2/C3A cells. The flexible allosteric acetyl-CoA regulatory domain of PanK3 also binds the substrates, pantothenate and pantetheine, and small molecule inhibitors and activators to modulate PanK3 activity. | Sato H, Macchiarulo A, Thomas C, Gioiello A, Une M, Hofmann AF, Saladin R, Schoonjans K, Pellicciari R, Auwerx J (2008) Novel potent and selective bile acid derivatives as TGR5 agonists: biological screening, structure-activity relationships, and molecular modeling studies. Journal of medicinal chemistry 51, 1831-1841 [PubMed:18307294] [show Abstract] TGR5, a metabotropic receptor that is G-protein-coupled to the induction of adenylate cyclase, has been recognized as the molecular link connecting bile acids to the control of energy and glucose homeostasis. With the aim of disclosing novel selective modulators of this receptor and at the same time clarifying the molecular basis of TGR5 activation, we report herein the biological screening of a collection of natural occurring bile acids, bile acid derivatives, and some steroid hormones, which has resulted in the discovery of new potent and selective TGR5 ligands. Biological results of the tested collection of compounds were used to extend the structure-activity relationships of TGR5 agonists and to develop a binary classification model of TGR5 activity. This model in particular could unveil some hidden properties shared by the molecular shape of bile acids and steroid hormones that are relevant to TGR5 activation and may hence be used to address the design of novel selective and potent TGR5 agonists. | Hemminki A, Niemi S, Hautoniemi L, Söderlund H, Takkinen K (1998) Fine tuning of an anti-testosterone antibody binding site by stepwise optimisation of the CDRs. Immunotechnology : an international journal of immunological engineering 4, 59-69 [PubMed:9661815] [show Abstract]
BackgroundWe have previously reported specificity improvement of an anti-testosterone monoclonal antibody (3-C4F5) by random mutagenesis of the third complementarity determining regions (CDR3s) and by phage display selection.ObjectivesHere we extend the mutagenesis strategy to the other CDRs and select the mutant libraries using two different approaches in order to further fine-tune the binding properties of this recombinant Fab fragment.Study designTo improve the affinity the new mutant libraries were selected by using limiting, decreasing concentrations of biotinylated testosterone (TES) in solution and capturing the binders on streptavidin-coated microtiter plate. The specificity was improved by preincubating the mutant libraries in solution with a high concentration of the most problematic cross-reacting steroid, dehydroepiandrosterone sulfate (DHEAS).ResultsIn two different light chain CDR1 mutant clones isolated from the affinity pannings, the relative TES affinity was increased over 10-fold while the cross-reactivities to related steroids were preserved at the same level as in the parental combined CDR3 mutant clone. New heavy chain CDR1 and light chain CDR2 mutants showing slightly decreased cross-reactivities were isolated from specificity selections. By combining compatible mutant CDRs together we were able to create a Fab fragment with over 12-fold higher relative TES affinity and significantly lower cross-reactivity to DHEAS when compared to the original monoclonal antibody 3-C4F5.ConclusionsOur results demonstrate that a high-affinity and selective recombinant Fab fragment working over a wide TES concentration range with clinical samples could be generated by CDR mutagenesis and phage display selection. | Barrou Z, Charru P, Lidy C (1997) Dehydroepiandrosterone (DHEA) and aging. Archives of gerontology and geriatrics 24, 233-241 [PubMed:15374110] [show Abstract] Dehydroepiandrosterone sulfate (DHEAS) is the most abundant circulating steroid hormone in humans and can readily be converted to its parent steroid DHEA by tissue sulfatases. Yet, a biologic function for these steroids has not been defined. The link between DHEA and aging has been raised by: (1) its well documented age-related decline, and (2) a preventive effect of DHEA on numerous age-related illnesses: ischemic heart-disease, cognitive impairment, immunodeficiency, malignancies, osteoporosis. These effects have been suggested by epidemiological studies in humans. Animal studies support a protective effect of DHEA on these age-related diseases. However, it remains unknown whether these results in animals can be transposed in humans, because adrenal secretion of DHEA seems to be particular to primates. In humans, only a few studies have been performed. The effects of oral supplementation with DHEA have, so far, focused on the possible metabolic effects of DHEA. A few studies have shown: the absence of any side-effects; no change in body-weight; conflicting results on body-composition and lipids and no effect on insulin-tolerance. The latest study showed a beneficial effect on well-being but these results need to be confirmed. |
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