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1 NADPH-dependent reduction of ketosteroids to hydroxysteroids.
2 abolism of androgenic and neuroactive 3alpha-hydroxysteroids.
3 ing pregnenolone and progesterone to 17alpha-hydroxysteroids.
4 atalyzes metabolism of retinoids and 3 alpha-hydroxysteroids.
5 characterized the functional effect of 3beta-hydroxysteroids.
6 ns of barbiturates was also reduced by 3beta-hydroxysteroids.
7 ation of synaptic currents induced by 3alpha-hydroxysteroids.
8 ompetent kinetics) plus hydroxylated 17alpha-hydroxysteroids.
9 ransport, and sulfonylation of bile acids or hydroxysteroids.
10 dipose tissue (WAT) genes but also represses hydroxysteroid 11-beta-dehydrogenase 1 (HSD11B1) indepen
11 On the other hand, LSD1 represses HSD11B1 (hydroxysteroid 11-beta-dehydrogenase isozyme 1), a key g
13 , superfamily member 2 [TM6SF2] p.E167K; and hydroxysteroid 17-beta dehydrogenase 13 [HSD17B13] rs726
14 ain containing 7, glucokinase regulator, and hydroxysteroid 17-beta dehydrogenase 13) to NAFLD and ex
15 another deceased case (SF) with undetectable hydroxysteroid (17beta) dehydrogenase 10 (HSD10) activit
16 of the neurological handicap associated with hydroxysteroid (17beta) dehydrogenase 10 deficiency.
18 s reduced the potentiation induced by 3alpha-hydroxysteroids, 3beta-hydroxysteroids acted noncompetit
19 ion induced by 3alpha-hydroxysteroids, 3beta-hydroxysteroids acted noncompetitively with respect to p
20 encompassing 3-hydroxyacyl-CoA derivatives, hydroxysteroids, alcohols and beta-hydroxybutyrate, and
21 codes a sulfoconjugation enzyme that acts on hydroxysteroids and cholesterol-derived sterol bile acid
22 effect on GABAergic synaptic currents, 3beta-hydroxysteroids and low concentrations of sulfated stero
25 ne, indicating Delta4-ketosteroids to Delta5-hydroxysteroids conversion, provides strong evidence for
26 dology for the quantitative determination of hydroxysteroids dehydroepiandrosterone and pregnenolone
27 hat mediates sulfo-conjugation of endogenous hydroxysteroids (dehydroepiandrosterone, testosterone, b
31 ly of systemic levels, by isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) that interconv
32 verting cortisone to cortisol via the 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 pathway
33 ,12(2)H3] cortisol (D3-cortisol) via 11-beta hydroxysteroid dehydrogenase (11beta-HSD) type 1, D3-cor
34 ra with a luminal signaling sequence (11beta-hydroxysteroid dehydrogenase (11beta-HSD1)(1-41)/Rdh1(23
38 s study, we have examined the role of 17beta-hydroxysteroid dehydrogenase (17beta-HSD) type 2 in the
39 tive metabolizing enzyme, the type II 17beta-hydroxysteroid dehydrogenase (17beta-HSD), in the ZR-75-
40 ls in HEK293 cells expressing type 10 17beta-hydroxysteroid dehydrogenase (17beta-HSD10), but not its
43 he progesterone inactivating enzyme 20-alpha-hydroxysteroid dehydrogenase (20alpha-HSD; median, 2.5 a
46 DH-4 from a related enzyme, RoDH-like 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is 3-fo
49 these enzymes were analyzed using rat 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD, AKR1C9) as the
50 he source of NADPH-dependent cytosolic 3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity is unk
54 mmonly requires enzymatic reactions by 3beta-hydroxysteroid dehydrogenase (3betaHSD), steroid-5alpha-
55 50, aldehyde dehydrogenase (ALDH3A2), and 21-hydroxysteroid dehydrogenase (AKR1C18) were found to be
59 e crystal structure of human type III 3alpha-hydroxysteroid dehydrogenase (HSD)/bile acid binding pro
60 rogenase 4 (RoDH4, SDR9C8), RoDH-like 3alpha-hydroxysteroid dehydrogenase (RL-HSD, SDR9C6), and RDH-l
65 e metabolism through its induction of 11beta-hydroxysteroid dehydrogenase 1 (HSD1) and glucocorticoid
68 8[TTTTA]n) or CYP17A1 (-34T/C) or the 17beta-hydroxysteroid dehydrogenase 1 gene HSD17B1 (Ser312Gly)
70 loid A3, stearoyl-CoA desaturase, and 11beta-hydroxysteroid dehydrogenase 1 were induced while actin
71 lucose elimination, and inhibitors of 11beta-hydroxysteroid dehydrogenase 1, which reduce the glucoco
72 hich was induced by both agents, and 11 beta-hydroxysteroid dehydrogenase 1, which was decreased by t
75 died rs6834314 and its nearest gene, 17-beta hydroxysteroid dehydrogenase 13 (HSD17B13), to identify
78 e inner mitochondrial membrane protein 3beta-hydroxysteroid dehydrogenase 2 (3betaHSD2) synthesizes p
80 the glucocorticoid receptor and the 11-beta hydroxysteroid dehydrogenase 2 isozyme were significantl
82 dipose tissue compared to SC, whereas 17beta-hydroxysteroid dehydrogenase 5 (AKR1C3) showed predomina
83 ainly with mRNA and protein levels of 17beta-hydroxysteroid dehydrogenase 6 (17beta-HSD6), one of sev
84 tive loss of AKR1C1, which encodes a 20alpha-hydroxysteroid dehydrogenase [20alpha-HSD (EC 1.1.1.149)
85 .1.149)], and AKR1C2, which encodes a 3alpha-hydroxysteroid dehydrogenase [3alpha-HSD (EC 1.1.1.52)],
86 %), but does not have the retinol and 3alpha-hydroxysteroid dehydrogenase activity of either, nor is
87 ens with high positional selectivity (17beta-hydroxysteroid dehydrogenase activity) as well as 3-keto
88 oblasts express significant oxidative 3alpha-hydroxysteroid dehydrogenase activity, which can convert
91 with inhibitors of type 1- and type 2-17beta hydroxysteroid dehydrogenase did not affect the previous
94 ted levels of P4-metabolizing enzyme 20alpha-hydroxysteroid dehydrogenase in corpora lutea (CL) inact
95 he Rv1106c gene that is annotated as a 3beta-hydroxysteroid dehydrogenase in Mtb has been cloned and
97 te expression of 5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase mRNAs in the NTS, and this
98 CE) by depositing NADH and the enzyme 3alpha-hydroxysteroid dehydrogenase onto the MB-SPCE surface; s
99 GR and NF1 binding on the endogenous 11beta-hydroxysteroid dehydrogenase promoter, also regulated by
100 dihydrotestosterone (DHT) and/or its 3alpha-hydroxysteroid dehydrogenase reduced metabolite 3alpha-a
101 romentin, the proposed inhibition of 17-beta-hydroxysteroid dehydrogenase should be considered as a s
102 r glucocorticoid reamplifying enzyme 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD-1) foun
104 tive 11-keto forms through the enzyme 11beta hydroxysteroid dehydrogenase type 1 (11beta HSD-1).
108 ion of D4 cortisol to D3 cortisol via 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) occur
110 The cortisol-regenerating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) amplif
114 heses of AMG 221 (2), an inhibitor of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) discov
117 novel, potent inhibitor against human 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme
118 urs through increased activity of the 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme
120 the glucocorticoid-generating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in adi
121 xpression of the GC-activating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in cul
122 tion of glucocorticoids by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in fat
123 neration of active glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in met
124 from a rapidly metabolized adamantane 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) inhibi
128 ve glucocorticoid by NADPH-dependent, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) oxored
129 ification of glucocorticoids (GCs) by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) plays
130 glucocorticoids in vivo by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) plays
133 a defect in the gene HSD11B1 encoding 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), a pri
134 cocorticoid (GC) regenerating enzyme, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), in ad
135 nd that tissue regeneration of GCs by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), rathe
136 glucocorticoid metabolism, including 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which
137 acid (CA) is a selective inhibitor of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which
138 ) in Src-1/-2 dKO fetal lungs encodes 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which
143 We investigated whether inhibition of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1, also k
144 ular glucocorticoid-amplifying enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1(-/-)) ha
145 CP2, glucocorticoid receptor (GR) and 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) and 2 (
146 culum by an enzyme complex containing 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) and hex
149 P2), glucocorticoid receptor (GR) and 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) mRNA in
154 on that leads to a gain-of-function in 3beta-hydroxysteroid dehydrogenase type 1 (3betaHSD1), which c
155 I-MS/MS) was used to observe in vitro 11beta-hydroxysteroid dehydrogenase type 1 (HSD1) enzyme-cataly
156 family 11, subfamily A1 (CYP11A1) and 3 beta-hydroxysteroid dehydrogenase type 1 (HSD3B1) also down-r
157 oid secretion and metabolism (notably 11beta-hydroxysteroid dehydrogenase type 1 and 5alpha-reductase
158 er reviews the functional role(s) of 11 beta-hydroxysteroid dehydrogenase type 1 and examines factors
159 polymorphisms in the genes encoding 11 beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phospha
160 trate that the reductase activity of 11 beta-hydroxysteroid dehydrogenase type 1 depends on reduced n
164 Hexose-6-phosphate dehydrogenase and 11 beta-hydroxysteroid dehydrogenase type 1 may play important r
165 d activity because global deletion of 11beta-hydroxysteroid dehydrogenase type 1 normalized Ca(2+) an
166 , respectively, whereas mice lacking 11 beta-hydroxysteroid dehydrogenase type 1 resist diet-induced
167 ortisol by the reductase activity of 11 beta-hydroxysteroid dehydrogenase type 1, which can thus incr
168 d for the 11-oxoreductase activity of 11beta-hydroxysteroid dehydrogenase type 1, which converts inac
171 ion, and metabolic functions of human 17beta-hydroxysteroid dehydrogenase type 10/short chain L-3-hyd
172 e HCV interactome, we identified the 17-beta-hydroxysteroid dehydrogenase type 12 (HSD17B12) as a hum
173 cental glucocorticoid inactivation by 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays
175 centa) or inhibitors of fetoplacental 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the p
176 Expression of MR was similar, as was 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which
178 11b2(-/-) mice, which lack the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) and thu
180 nction mutations in the gene encoding 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), allowi
182 ribe the design of a nanomolar potent 17beta-hydroxysteroid dehydrogenase type 2 (17beta-HSD2) inhibi
183 on, such as potentially inhibitors of 17beta-hydroxysteroid dehydrogenase type 2 (17beta-HSD2), may b
184 In the adrenals, testes, and ovaries, 3beta-hydroxysteroid dehydrogenase type 2 (3betaHSD2) catalyze
185 c acute regulatory protein (StAR), and 3beta-hydroxysteroid dehydrogenase type 2 (3betaHSD2) via its
186 zyme with sequence homology to CD13), 11beta-hydroxysteroid dehydrogenase type 2 (a steroid pathway e
187 These neurons express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) and are activ
188 terone-sensitive neurons that express 11beta-hydroxysteroid dehydrogenase type 2 (HSD2) in the nucleu
189 e glucocorticoid-inactivating enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), a signature
190 abel neurons in the NTS that express 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), an enzyme th
191 locorticoid receptors and the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes
192 n of neurons that express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes
199 mangiomas were identified, including 17-beta hydroxysteroid dehydrogenase type 2 and tissue factor pa
201 ptors, transgenic mice overexpressing 11beta-hydroxysteroid dehydrogenase type 2 in cardiomyocytes we
202 t the ability of the placental enzyme 11beta-hydroxysteroid dehydrogenase type 2 to inactivate cortis
203 izin (a potent inhibitor of placental 11beta-hydroxysteroid dehydrogenase type 2, the "barrier" to ma
204 ctus solitarius expresses the enzyme 11-beta-hydroxysteroid dehydrogenase type 2, which makes them se
207 biosynthesis by using an inhibitor of 17beta-hydroxysteroid dehydrogenase type 3 (17beta-HSD3) is a s
208 onal variants: HSD17B4, which encodes 17beta-hydroxysteroid dehydrogenase type 4 (HSD17B4), also know
209 response element-luciferase reporter, 17beta-hydroxysteroid dehydrogenase type 6 (17betaHSD6) convert
211 lucocorticoid receptor (GR)-alpha and 11beta-hydroxysteroid dehydrogenase type I (11beta-HSD1)-mediat
215 to show that inhibition of the enzyme 11beta-hydroxysteroid dehydrogenase type II(11betaHSD2) reduces
216 to as the human bile acid binder and 3alpha-hydroxysteroid dehydrogenase type III, is a multifunctio
217 ffects of exogenous estradiol (E2) on 17beta-hydroxysteroid dehydrogenase type IV (HSD17B4) and the c
221 roteins including cytochrome b(5) and 11beta-hydroxysteroid dehydrogenase were degraded slowly or not
222 l type of microsomal NAD(+)-dependent 3alpha-hydroxysteroid dehydrogenase with unique catalytic prope
223 do-keto reductase 1C3 (AKR1C3; type 5 17beta-hydroxysteroid dehydrogenase) is overexpressed in castra
225 esizing enzymes (5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase) was increased in the hypot
227 teroidogenic acute regulatory protein, 3beta-hydroxysteroid dehydrogenase, and P450c17) was impaired.
228 a-reductase, 6alpha-hydroxylase, 3alpha/beta-hydroxysteroid dehydrogenase, and reverse Delta4minus si
229 The enzyme is most efficient as a 3alpha-hydroxysteroid dehydrogenase, converting 3alpha-tetrahyd
230 in expression of 5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase, especially in cerebellum.
231 chain cleavage enzyme, P450 aromatase, 3beta-hydroxysteroid dehydrogenase, luteinization hormone rece
234 ocorticoid binding by the absence of 11-beta hydroxysteroid dehydrogenase, salt-mineralocorticoid-ind
235 enveloped virus host range protein, dUTPase, hydroxysteroid dehydrogenase, superoxide dismutase, serp
236 than reported for 3alpha-reduction by 3alpha-hydroxysteroid dehydrogenase, the major enzyme known to
238 cocorticoid (GC) metabolising enzyme, 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1) converts in
239 d compounds, acting by inhibition of 11-beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1), gave rise
242 in E3-ligase, AMFR, mediating loss of 11beta-hydroxysteroid dehydrogenase-2 (11beta-HSD2), which othe
243 Human ECs also express the enzyme 11-beta-hydroxysteroid dehydrogenase-2 (11betaHSD2), and inhibit
244 for the O-GlcNAc mark identified the 17 beta hydroxysteroid dehydrogenase-3 (Hsd17b3) locus in male E
251 or P450 side chain cleavage and Delta5-3beta-hydroxysteroid dehydrogenase/Delta5-Delta4- isomerase en
254 tissues) and type 2 (adrenals, gonads) 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD/isomer
255 pe 2 (adrenals and gonads) isoforms of 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD1 and 3
257 opment of a fluorogenic substrate for 17beta-hydroxysteroid-dehydrogenase type 10 (17beta-HSD10), whi
263 ptor metabolism of glucocorticoids by 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) modulates ce
270 s high selectivity in living cells for human hydroxysteroid dehydrogenases (HSDs) of the aldo-keto re
271 forms have been shown to act as 3alpha/3beta-hydroxysteroid dehydrogenases (HSDs) on 5alpha-dihydrote
273 GR), mineralocorticoid receptor (MR), 11beta-hydroxysteroid dehydrogenases 1 and 2 (11beta-HSD1 and 1
274 ature distinguishes it from all known 17beta-hydroxysteroid dehydrogenases, and endows mitochondria w
278 ar interest, we identify EBP (encoding 3beta-hydroxysteroid-Delta8,Delta7-isomerase), a key enzyme in
279 ensitive to both the direct effects of 3beta-hydroxysteroids on GABA(A) responses and the reduction o
280 oid reductase activity of the enzymes, their hydroxysteroid oxidase activity was potently inhibited b
281 Cs also expressed substantial 3alpha[17beta]-hydroxysteroid oxidase activity with 3alpha-Diol as the
282 progesterone (P4)'s 5 alpha-reduced, 3 alpha-hydroxysteroid oxidoreduced product, facilitates lordosi
283 uctase inhibitor, or indomethacin, a 3 alpha-hydroxysteroid oxidoreductase inhibitor, either systemic
284 wer than in group-housed mice whereas 3alpha-hydroxysteroid oxidoreductase mRNA expression was equal
285 lic reduction by 5alpha-reductase and 3alpha-hydroxysteroid oxidoreductase to form 5alpha-dihydrodeox
288 near (typical R2 is superior to 0.98 for all hydroxysteroids studied) over the concentration range of
289 oepiandrosterone sulfotransferase (STD) is a hydroxysteroid sulfo-conjugating enzyme with preferentia
290 te from a previously determined structure of hydroxysteroid sulfotransferase (SULT2A1) binding dehydr
292 of an alternative exon 1, the gene for human hydroxysteroid sulfotransferase (SULTB1) encodes for two
293 -glucuronosyltransferase 1A1, 1A3, 1A4, 1A6, hydroxysteroid sulfotransferase enzyme 2A1, multidrug re
295 e 5'-phosphosulfate, and either rat or human hydroxysteroid sulfotransferase, the formation of DNA ad
297 This direct, noncompetitive effect of 3beta-hydroxysteroids was sufficient to account for the appare
299 d external neurosteroid antagonist site, and hydroxysteroids, which bind an independent site, are eff
300 e exhibits an oxidoreductase activity toward hydroxysteroids with NAD(+) and NADH as the preferred co