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1 NADPH-dependent reduction of ketosteroids to hydroxysteroids.
2 ransport, and sulfonylation of bile acids or hydroxysteroids.
3 abolism of androgenic and neuroactive 3alpha-hydroxysteroids.
4 ing pregnenolone and progesterone to 17alpha-hydroxysteroids.
5 atalyzes metabolism of retinoids and 3 alpha-hydroxysteroids.
6 characterized the functional effect of 3beta-hydroxysteroids.
7 ns of barbiturates was also reduced by 3beta-hydroxysteroids.
8 ation of synaptic currents induced by 3alpha-hydroxysteroids.
9 th a k(cat)/K(m) similar to that for 20alpha-hydroxysteroids.
10 ompetent kinetics) plus hydroxylated 17alpha-hydroxysteroids.
11 dipose tissue (WAT) genes but also represses hydroxysteroid 11-beta-dehydrogenase 1 (HSD11B1) indepen
12 On the other hand, LSD1 represses HSD11B1 (hydroxysteroid 11-beta-dehydrogenase isozyme 1), a key g
13 another deceased case (SF) with undetectable hydroxysteroid (17beta) dehydrogenase 10 (HSD10) activit
14 of the neurological handicap associated with hydroxysteroid (17beta) dehydrogenase 10 deficiency.
16 s reduced the potentiation induced by 3alpha-hydroxysteroids, 3beta-hydroxysteroids acted noncompetit
17 ion induced by 3alpha-hydroxysteroids, 3beta-hydroxysteroids acted noncompetitively with respect to p
18 encompassing 3-hydroxyacyl-CoA derivatives, hydroxysteroids, alcohols and beta-hydroxybutyrate, and
19 codes a sulfoconjugation enzyme that acts on hydroxysteroids and cholesterol-derived sterol bile acid
20 effect on GABAergic synaptic currents, 3beta-hydroxysteroids and low concentrations of sulfated stero
23 ne, indicating Delta4-ketosteroids to Delta5-hydroxysteroids conversion, provides strong evidence for
24 dology for the quantitative determination of hydroxysteroids dehydroepiandrosterone and pregnenolone
25 hat mediates sulfo-conjugation of endogenous hydroxysteroids (dehydroepiandrosterone, testosterone, b
27 target receptors and the isozymes of 11beta-hydroxysteroid dehydrogenase (11 beta-HSD) that regulate
30 ly of systemic levels, by isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) that interconv
31 verting cortisone to cortisol via the 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 pathway
32 ,12(2)H3] cortisol (D3-cortisol) via 11-beta hydroxysteroid dehydrogenase (11beta-HSD) type 1, D3-cor
33 ra with a luminal signaling sequence (11beta-hydroxysteroid dehydrogenase (11beta-HSD1)(1-41)/Rdh1(23
37 s study, we have examined the role of 17beta-hydroxysteroid dehydrogenase (17beta-HSD) type 2 in the
38 tive metabolizing enzyme, the type II 17beta-hydroxysteroid dehydrogenase (17beta-HSD), in the ZR-75-
39 ls in HEK293 cells expressing type 10 17beta-hydroxysteroid dehydrogenase (17beta-HSD10), but not its
41 ctivation of a steroidogenic enzyme, 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD), which in tur
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
52 converts cholesterol to pregnenolone), 3beta-hydroxysteroid dehydrogenase (3beta-HSD, converts pregne
56 mmonly requires enzymatic reactions by 3beta-hydroxysteroid dehydrogenase (3betaHSD), steroid-5alpha-
57 50, aldehyde dehydrogenase (ALDH3A2), and 21-hydroxysteroid dehydrogenase (AKR1C18) were found to be
61 e crystal structure of human type III 3alpha-hydroxysteroid dehydrogenase (HSD)/bile acid binding pro
62 rogenase 4 (RoDH4, SDR9C8), RoDH-like 3alpha-hydroxysteroid dehydrogenase (RL-HSD, SDR9C6), and RDH-l
66 e metabolism through its induction of 11beta-hydroxysteroid dehydrogenase 1 (HSD1) and glucocorticoid
69 8[TTTTA]n) or CYP17A1 (-34T/C) or the 17beta-hydroxysteroid dehydrogenase 1 gene HSD17B1 (Ser312Gly)
71 loid A3, stearoyl-CoA desaturase, and 11beta-hydroxysteroid dehydrogenase 1 were induced while actin
72 lucose elimination, and inhibitors of 11beta-hydroxysteroid dehydrogenase 1, which reduce the glucoco
73 hich was induced by both agents, and 11 beta-hydroxysteroid dehydrogenase 1, which was decreased by t
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
90 with inhibitors of type 1- and type 2-17beta hydroxysteroid dehydrogenase did not affect the previous
93 ted levels of P4-metabolizing enzyme 20alpha-hydroxysteroid dehydrogenase in corpora lutea (CL) inact
94 he Rv1106c gene that is annotated as a 3beta-hydroxysteroid dehydrogenase in Mtb has been cloned and
96 te expression of 5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase mRNAs in the NTS, and this
97 GR and NF1 binding on the endogenous 11beta-hydroxysteroid dehydrogenase promoter, also regulated by
98 dihydrotestosterone (DHT) and/or its 3alpha-hydroxysteroid dehydrogenase reduced metabolite 3alpha-a
99 tion enzyme was identified as a novel 17beta-hydroxysteroid dehydrogenase responsible for the inactiv
100 r glucocorticoid reamplifying enzyme 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD-1) foun
102 tive 11-keto forms through the enzyme 11beta hydroxysteroid dehydrogenase type 1 (11beta HSD-1).
106 ion of D4 cortisol to D3 cortisol via 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) occur
108 The cortisol-regenerating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) amplif
112 heses of AMG 221 (2), an inhibitor of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) discov
113 novel, potent inhibitor against human 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme
115 urs through increased activity of the 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme
117 the glucocorticoid-generating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in adi
118 xpression of the GC-activating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in cul
119 tion of glucocorticoids by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in fat
120 neration of active glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in met
121 from a rapidly metabolized adamantane 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) inhibi
125 ve glucocorticoid by NADPH-dependent, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) oxored
126 glucocorticoids in vivo by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) plays
127 ification of glucocorticoids (GCs) by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) plays
130 a defect in the gene HSD11B1 encoding 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), a pri
131 cocorticoid (GC) regenerating enzyme, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), in ad
132 nd that tissue regeneration of GCs by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), rathe
133 glucocorticoid metabolism, including 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which
138 We investigated whether inhibition of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1, also k
139 ular glucocorticoid-amplifying enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1(-/-)) ha
140 CP2, glucocorticoid receptor (GR) and 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) and 2 (
141 culum by an enzyme complex containing 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) and hex
144 P2), glucocorticoid receptor (GR) and 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) mRNA in
149 on that leads to a gain-of-function in 3beta-hydroxysteroid dehydrogenase type 1 (3betaHSD1), which c
150 I-MS/MS) was used to observe in vitro 11beta-hydroxysteroid dehydrogenase type 1 (HSD1) enzyme-cataly
151 family 11, subfamily A1 (CYP11A1) and 3 beta-hydroxysteroid dehydrogenase type 1 (HSD3B1) also down-r
152 oid secretion and metabolism (notably 11beta-hydroxysteroid dehydrogenase type 1 and 5alpha-reductase
153 er reviews the functional role(s) of 11 beta-hydroxysteroid dehydrogenase type 1 and examines factors
154 polymorphisms in the genes encoding 11 beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phospha
155 trate that the reductase activity of 11 beta-hydroxysteroid dehydrogenase type 1 depends on reduced n
159 Hexose-6-phosphate dehydrogenase and 11 beta-hydroxysteroid dehydrogenase type 1 may play important r
160 d activity because global deletion of 11beta-hydroxysteroid dehydrogenase type 1 normalized Ca(2+) an
161 , respectively, whereas mice lacking 11 beta-hydroxysteroid dehydrogenase type 1 resist diet-induced
162 ortisol by the reductase activity of 11 beta-hydroxysteroid dehydrogenase type 1, which can thus incr
163 d for the 11-oxoreductase activity of 11beta-hydroxysteroid dehydrogenase type 1, which converts inac
166 ion, and metabolic functions of human 17beta-hydroxysteroid dehydrogenase type 10/short chain L-3-hyd
167 cental glucocorticoid inactivation by 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays
169 centa) or inhibitors of fetoplacental 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the p
170 Expression of MR was similar, as was 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which
172 11b2(-/-) mice, which lack the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) and thu
174 nction mutations in the gene encoding 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), allowi
176 In the adrenals, testes, and ovaries, 3beta-hydroxysteroid dehydrogenase type 2 (3betaHSD2) catalyze
177 c acute regulatory protein (StAR), and 3beta-hydroxysteroid dehydrogenase type 2 (3betaHSD2) via its
178 zyme with sequence homology to CD13), 11beta-hydroxysteroid dehydrogenase type 2 (a steroid pathway e
179 These neurons express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) and are activ
180 terone-sensitive neurons that express 11beta-hydroxysteroid dehydrogenase type 2 (HSD2) in the nucleu
181 e glucocorticoid-inactivating enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), a signature
182 abel neurons in the NTS that express 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), an enzyme th
183 locorticoid receptors and the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes
184 n of neurons that express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes
191 mangiomas were identified, including 17-beta hydroxysteroid dehydrogenase type 2 and tissue factor pa
193 ptors, transgenic mice overexpressing 11beta-hydroxysteroid dehydrogenase type 2 in cardiomyocytes we
194 t the ability of the placental enzyme 11beta-hydroxysteroid dehydrogenase type 2 to inactivate cortis
195 izin (a potent inhibitor of placental 11beta-hydroxysteroid dehydrogenase type 2, the "barrier" to ma
196 ctus solitarius expresses the enzyme 11-beta-hydroxysteroid dehydrogenase type 2, which makes them se
199 onal variants: HSD17B4, which encodes 17beta-hydroxysteroid dehydrogenase type 4 (HSD17B4), also know
201 response element-luciferase reporter, 17beta-hydroxysteroid dehydrogenase type 6 (17betaHSD6) convert
203 lucocorticoid receptor (GR)-alpha and 11beta-hydroxysteroid dehydrogenase type I (11beta-HSD1)-mediat
207 to show that inhibition of the enzyme 11beta-hydroxysteroid dehydrogenase type II(11betaHSD2) reduces
208 to as the human bile acid binder and 3alpha-hydroxysteroid dehydrogenase type III, is a multifunctio
209 ffects of exogenous estradiol (E2) on 17beta-hydroxysteroid dehydrogenase type IV (HSD17B4) and the c
213 roteins including cytochrome b(5) and 11beta-hydroxysteroid dehydrogenase were degraded slowly or not
214 l type of microsomal NAD(+)-dependent 3alpha-hydroxysteroid dehydrogenase with unique catalytic prope
215 aldo-keto reductase AKR1C1 (20alpha(3alpha)-hydroxysteroid dehydrogenase) is induced by electrophili
216 do-keto reductase 1C3 (AKR1C3; type 5 17beta-hydroxysteroid dehydrogenase) is overexpressed in castra
218 esizing enzymes (5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase) was increased in the hypot
219 oteins involved in steroid biogenesis (e.g., hydroxysteroid dehydrogenase), antioxidant functions (e.
221 teroidogenic acute regulatory protein, 3beta-hydroxysteroid dehydrogenase, and P450c17) was impaired.
222 a-reductase, 6alpha-hydroxylase, 3alpha/beta-hydroxysteroid dehydrogenase, and reverse Delta4minus si
223 The enzyme is most efficient as a 3alpha-hydroxysteroid dehydrogenase, converting 3alpha-tetrahyd
224 in expression of 5alpha-reductase and 3alpha-hydroxysteroid dehydrogenase, especially in cerebellum.
225 chain cleavage enzyme, P450 aromatase, 3beta-hydroxysteroid dehydrogenase, luteinization hormone rece
228 ocorticoid binding by the absence of 11-beta hydroxysteroid dehydrogenase, salt-mineralocorticoid-ind
229 enveloped virus host range protein, dUTPase, hydroxysteroid dehydrogenase, superoxide dismutase, serp
230 than reported for 3alpha-reduction by 3alpha-hydroxysteroid dehydrogenase, the major enzyme known to
232 cocorticoid (GC) metabolising enzyme, 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1) converts in
233 d compounds, acting by inhibition of 11-beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1), gave rise
235 in E3-ligase, AMFR, mediating loss of 11beta-hydroxysteroid dehydrogenase-2 (11beta-HSD2), which othe
236 Human ECs also express the enzyme 11-beta-hydroxysteroid dehydrogenase-2 (11betaHSD2), and inhibit
237 for the O-GlcNAc mark identified the 17 beta hydroxysteroid dehydrogenase-3 (Hsd17b3) locus in male E
245 or P450 side chain cleavage and Delta5-3beta-hydroxysteroid dehydrogenase/Delta5-Delta4- isomerase en
248 tissues) and type 2 (adrenals, gonads) 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD/isomer
249 pe 2 (adrenals and gonads) isoforms of 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD1 and 3
251 opment of a fluorogenic substrate for 17beta-hydroxysteroid-dehydrogenase type 10 (17beta-HSD10), whi
254 renal axis, and the activities of the 11beta-hydroxysteroid dehydrogenases (11-HSDs) that interconver
257 ptor metabolism of glucocorticoids by 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) modulates ce
264 s high selectivity in living cells for human hydroxysteroid dehydrogenases (HSDs) of the aldo-keto re
265 forms have been shown to act as 3alpha/3beta-hydroxysteroid dehydrogenases (HSDs) on 5alpha-dihydrote
267 GR), mineralocorticoid receptor (MR), 11beta-hydroxysteroid dehydrogenases 1 and 2 (11beta-HSD1 and 1
268 zymes are closely related to the short-chain hydroxysteroid dehydrogenases and differ substantially f
270 and encodes a protein with homology to 3beta-hydroxysteroid dehydrogenases that functions in one of t
271 ature distinguishes it from all known 17beta-hydroxysteroid dehydrogenases, and endows mitochondria w
274 ntermediates suggested a deficiency of 3beta-hydroxysteroid-delta8,delta7-isomerase (sterol-delta8-is
275 ensitive to both the direct effects of 3beta-hydroxysteroids on GABA(A) responses and the reduction o
276 oid reductase activity of the enzymes, their hydroxysteroid oxidase activity was potently inhibited b
277 Cs also expressed substantial 3alpha[17beta]-hydroxysteroid oxidase activity with 3alpha-Diol as the
278 progesterone (P4)'s 5 alpha-reduced, 3 alpha-hydroxysteroid oxidoreduced product, facilitates lordosi
279 uctase inhibitor, or indomethacin, a 3 alpha-hydroxysteroid oxidoreductase inhibitor, either systemic
280 wer than in group-housed mice whereas 3alpha-hydroxysteroid oxidoreductase mRNA expression was equal
281 lic reduction by 5alpha-reductase and 3alpha-hydroxysteroid oxidoreductase to form 5alpha-dihydrodeox
284 near (typical R2 is superior to 0.98 for all hydroxysteroids studied) over the concentration range of
285 ol (E2) but insignificant ability to sulfate hydroxysteroids such as dehydroepiandrosterone (DHEA).
286 oepiandrosterone sulfotransferase (STD) is a hydroxysteroid sulfo-conjugating enzyme with preferentia
288 te from a previously determined structure of hydroxysteroid sulfotransferase (SULT2A1) binding dehydr
290 of an alternative exon 1, the gene for human hydroxysteroid sulfotransferase (SULTB1) encodes for two
291 ite-selected mutagenesis of this 3alpha/beta-hydroxysteroid sulfotransferase chimera involving the 12
292 -glucuronosyltransferase 1A1, 1A3, 1A4, 1A6, hydroxysteroid sulfotransferase enzyme 2A1, multidrug re
294 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
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