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1 HSD caused a significantly greater decrease in intracran
2 HSD had a longer duration of effect than mannitol (p = .
3 HSD increased expression of COX-2 in WT mice and of COX-
4 HSD resuscitation results in transient inhibition of PMN
5 HSD-1 is orthologous to 3beta-hydroxysteroid dehydrogena
9 reated transgenic mice overexpressing 11beta HSD-1 selectively in adipose tissue to an extent similar
10 isol concentrations generated via the 11beta HSD type 1 pathway within the liver likely contribute to
13 -Hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) catalyzes conversion of circulating inert 11-dehy
14 -hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) converts inactive cortisone into the active gluco
15 -hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) intracellularly regenerates active corticosterone
18 rning deficit was ameliorated in aged 11beta-HSD-1 knockout mice, implicating lower intraneuronal cor
20 ted by 18beta-glycyrrhetinic acid, an 11beta-HSD inhibitor, and in cells transfected with cDNA encodi
21 -) macrophages, and carbenoxolone, an 11beta-HSD inhibitor, prevented the increase in phagocytosis el
22 A concise asymmetric synthesis of an 11beta-HSD-1 inhibitor has been achieved using inexpensive star
24 ptor, mineralocorticoid receptor, and 11beta-HSD types 1 and 2 were detected in nonpigmented ciliary
25 the prereceptor metabolism of GCS by 11beta-HSD is well documented in a variety of cells and tissues
26 intact hippocampal cells in culture, 11beta-HSD-1 acts as a functional 11beta-reductase reactivating
27 11beta-hydroxysteroid dehydrogenase (11beta-HSD) act at a prereceptor level to regulate the tissue-s
28 11beta-hydroxysteroid dehydrogenase (11beta-HSD) enzymes control the interconversion of active gluco
29 11beta-hydroxysteroid dehydrogenase (11beta-HSD) that interconvert active cortisol and inactive cort
31 11-beta hydroxysteroid dehydrogenase (11beta-HSD) type 1, D3-cortisol production can be used as an in
32 11beta-hydroxysteroid dehydrogenases (11beta-HSD) perform prereceptor metabolism of glucocorticoids t
34 n of the TZD was markedly greater for 11beta-HSD-1 gene expression than for leptin, suggesting that t
36 ivated receptor-alpha mRNA is lost in 11beta-HSD-1(-/-) mice, consistent with attenuated glucocortico
37 ession of genes for fat catabolism in 11beta-HSD-1(-/-) mice, implying increased liver insulin sensit
38 e the rapid (within 3 h) induction of 11beta-HSD activity in cells elicited in the peritoneum by a si
40 d D3 cortisol production (an index of 11beta-HSD type 1 activity) were measured using the combined he
42 ated, PPARgamma agonist inhibition of 11beta-HSD-1 and leptin gene expression was ablated, thereby su
43 tigates the metabolic consequences of 11beta-HSD-1 deficiency, focusing on the lipid and lipoprotein
47 amined the functional significance of 11beta-HSD-1 in the central nervous system by using knockout mi
50 sis is suggested by the resistance of 11beta-HSD-1(-/-) mice to hyperglycemia upon stress or obesity,
56 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) catalyse the interconversion of active cortisol an
60 was detected in transfected cells and 17beta-HSD type 2 transfection did not offer protection against
62 17beta-hydroxysteroid dehydrogenase (17beta-HSD), in the ZR-75-1 cells, which rapidly converts 2-MeO
63 time, that the high levels of type II 17beta-HSD present in ZR-75-1 cells were largely responsible fo
65 1 cells, which express high levels of 17beta-HSD type 2, and in MCF-7 cells transfected with 17beta-H
67 mRNA levels of three known oxidative 17beta-HSD isozymes (types II, IV, and VIII) revealed that only
69 hermore, MCF-7 cells transfected with 17beta-HSD type 2 were protected from the cytotoxic effects of
70 , and in MCF-7 cells transfected with 17beta-HSD type 2, high-performance liquid chromatography analy
71 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) catalyze the interconversion between the oxidized
73 T5b expression was up-regulated, and 20alpha-HSD mRNA was decreased, but in 15 d postcoitum pregnant
76 -alpha-hydroxysteroid dehydrogenase (20alpha-HSD; median, 2.5 arbitrary units [AU]; interquartile ran
77 0alpha-hydroxysteroid dehydrogenase [20alpha-HSD (EC 1.1.1.149)], and AKR1C2, which encodes a 3alpha-
82 diating the PGF(2alpha) induction of 20alpha-HSD, a steroidogenic enzyme involved in the catabolism o
84 increase in placental expression of 20alpha-HSD, which may be due to lower prolactin levels observed
87 the Delta(7)-DA biosynthetic enzyme DAF-36, HSD-1 is dispensable for proper gonadal migration and li
88 oxytibolone, AKR1C3 showed weak 3beta/3alpha-HSD activity, and AKR1C4 acted predominantly as a 3alpha
94 concentrations in vivo by activating 3alpha-HSD type III, we investigated whether these small molecu
96 demonstrate that 5alpha-R type I and 3alpha-HSD colocalize in cortical, hippocampal, and olfactory b
97 failed to detect 5alpha-R type I and 3alpha-HSD in cortical and hippocampal GABAergic interneurons.
98 on, this study compares 5alpha-RI and 3alpha-HSD mRNA brain expression levels in group housed and in
99 s study evaluates 5alpha-R type I and 3alpha-HSD mRNA expression level in mouse brain by using in sit
101 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is 3-fold more active with free retinol than
105 3alpha-hydroxysteroid dehydrogenase [3alpha-HSD (EC 1.1.1.52)], was found in 24 paired breast cancer
109 lpha-DHP reduction catalyzed by human 3alpha-HSD type III by using steady-state kinetics studies and
112 nt and that, in contrast to RoDH-like 3alpha-HSD, RoDH-4 can access the bound form of retinol for ret
113 gically important reaction, rat liver 3alpha-HSD (AKR1C9) was used as the protein model for the human
115 hese results characterize the role of 3alpha-HSD type III in allopregnanolone formation and suggest t
116 echanism of a mammalian HSD using rat 3alpha-HSD of the aldo-keto reductase superfamily (AKR1C9) with
117 ing pocket of AKR1C2 with that of rat 3alpha-HSD reveals significant differences in the positions of
118 d for testosterone in the related rat 3alpha-HSD.NADP(+).testosterone ternary complex, where testoste
119 pregnanolone oxidation indicated that 3alpha-HSD type III utilized a ternary complex (sequential) kin
121 3Alpha-hydroxysteroid dehydrogenases (3alpha-HSDs) catalyze the interconversion between 5alpha-dihydr
125 at)) is 2-fold greater for wild-type 2 3beta-HSD compared with the wild-type 1 3beta-HSD activity.
126 tion kinetics of the wild-type 1 and 2 3beta-HSD, plus a catalytic role for the Tyr(154) and Lys(158)
127 ructure/function of human type 1 and 2 3beta-HSD/isomerase may lead to the design of selective inhibi
135 The mRNA for cytochrome P450scc and 3beta-HSD were detected only in actively myelinating coculture
138 he 3beta-hydroxysteroid dehydrogenase (3beta-HSD) isoenzymes play a key role in cellular steroid horm
139 d K273Q mutants have low, pH-dependent 3beta-HSD activity, exhibit only 5% of the maximal isomerase a
141 The catalytic efficiency achieved for 3beta-HSD activity is higher than that observed for any AKR to
142 me has substrate kinetic constants for 3beta-HSD activity that are very similar to those of the wild-
143 the Michaelis-Menten constant (Km) for 3beta-HSD substrate and inhibition constants (Ki) for epostane
146 riation in expressivity that occurs in 3beta-HSD deficiency and underscores the need to consider a bi
148 man hepatoma (HepG2) cells (which lack 3beta-HSD/Delta(5-4) ketosteroid isomerase mRNA expression, bu
149 The Y154F and K158Q mutants exhibit no 3beta-HSD activity, have substantial isomerase activity, and u
151 Delta(5)-C(27)-steroid oxidoreductase (3beta-HSD) deficiency, a disorder that usually presents in ear
152 lysis shows that epostane inhibits the 3beta-HSD activity of the wild-type 1 enzyme with 14-17-fold g
153 er downstream of or in parallel to the 3beta-HSD function in the dafachronic acid biosynthetic pathwa
155 rogenase/Delta(5)-Delta(4) isomerases (3beta-HSDs), which are key steroidogenic enzymes in vertebrate
156 ial target of salt in immune cells, we fed a HSD to CD4(Cre)SGK1(fl/fl) B6-transplanted recipients an
163 ochemical features of AK and bifunctional AK-HSD enzymes have been characterized, but the molecular p
166 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) type II and has PGFS activity and 3 alpha-HSD activ
168 Similar to the IL-10-deficient model, an HSD also enhanced cytokine expression during infection b
169 dium accumulated in the colons of mice on an HSD, suggesting a direct effect of salt within the colon
172 m Hg, 95% confidence interval, 5.8-11.8) and HSD (median decrease, 13 mm Hg; 95% confidence interval,
174 1 beta-hydroxysteroid dehydrogenase (11 beta-HSD) interconvert cortisol (F) and inactive cortisone (E
175 first in vivo evidence that adipose 11 beta-HSD-1 deficiency beneficially alters adipose tissue dist
176 e report novel protective effects of 11 beta-HSD-1 deficiency on adipose function, distribution, and
177 metabolic syndrome in mice, whereas 11 beta-HSD-1 deficiency or inhibition has beneficial metabolic
186 hydroxysteroid dehydrogenase type 1 (11 beta-HSD-1) found in adipose tissue of obese humans and roden
187 An efficient asymmetric synthesis of 11-beta-HSD inhibitor 1 has been accomplished in five linear ste
190 study tested the hypothesis that the 3 beta-HSD and isomerase activities shared a common coenzyme do
191 hifts the cofactor preference of both 3 beta-HSD and isomerase from NAD(H) to NADP(H), which shows th
197 droxysteroid dehydrogenase/isomerase (3 beta-HSD) is essential for the biosynthesis of all active ste
198 cture/function relationships of human 3 beta-HSD/isomerase and bring us closer to the goal of selecti
199 e for the NAD(H) specificity of human 3 beta-HSD/isomerase and identifies the Rossmann-fold coenzyme
200 droxysteroid dehydrogenase/isomerase (3 beta-HSD/isomerase) catalyzes the two sequential enzyme react
207 ucose tolerance test, IL-1betaAb-treated CDs-HSD rats showed lower blood glucose concentrations (P <
208 te kinase (AK) and homoserine dehydrogenase (HSD) function as key regulatory enzymes at branch points
209 enzyme 11beta-hydroxysteroid dehydrogenase (HSD) type 1 converts inactive cortisone into active cort
210 ugh the 11beta hydroxysteroid dehydrogenase (HSD) type 1 pathway can be measured by determining the r
211 ype III 3alpha-hydroxysteroid dehydrogenase (HSD)/bile acid binding protein (AKR1C2) complexed with N
213 lls for human hydroxysteroid dehydrogenases (HSDs) of the aldo-keto reductase (AKR) superfamily.
217 quency stimulation [homosynaptic depression (HSD)] of the sensory neuron were expressed in both contr
218 nic potentiation or homosynaptic depression (HSD)], or short-term heterosynaptic plasticity [serotoni
224 ive to wild types (WTs) on a high-salt diet (HSD); this was attenuated by a PGI(2) receptor agonist.
226 d in the soleus muscle of high sucrose diet (HSD) induced insulin resistant rats and TNF-alpha expose
234 ly greater in AC than in OA and normal eyes (HSD test, P </= 0.05), but there was no significant diff
236 he cytoplasmic sequestration of DAF-16/FoxO, HSD-1 inhibits nuclear DAF-16/FoxO activity without affe
240 rest, contrary to what would be expected if HSD represented an exhaustion of the exocytosis mechanis
242 t switching off of release sites resulted in HSD that was independent of initial synaptic strength.
244 n an equimolar, rapid, intravenous infusion, HSD reduces intracranial pressure more effectively than
246 ingle point mutation in AKR1D1 can introduce HSD activity with unexpected configurational and stereoc
248 he complete kinetic mechanism of a mammalian HSD using rat 3alpha-HSD of the aldo-keto reductase supe
249 eroid dehydrogenase (3betaHSD) family member HSD-1, which participates in Delta(4)-DA biosynthesis, a
254 Both PA-LTF and the attenuated kinetics of HSD were reversed by either a transient blockade of PKC
255 dels, we evaluated alternative mechanisms of HSD, including vesicle depletion, to determine which mec
258 tructures indicate that stereospecificity of HSD activity is achieved because the steroid flips over
260 for 30 min to PC2(-/-) mice after 1 week of HSD lowered MAP from hypertensive levels to normal; infu
261 lpipe razin-1-ylsulfonyl)phenyl)propan-2-ol (HSD-016) was discovered to be a potent, selective, and e
262 ast, P-LTF was unaffected when either PTP or HSD was evoked in the presence of either rapamycin or an
265 in two phases, an initial movement of PPXD, HSD, and HWD as a unit, followed by a movement of PPXD a
269 like 3alpha-hydroxysteroid dehydrogenase (RL-HSD, SDR9C6), and RDH-like SDR (RDHL, SDR9C4) do not aff
270 f threonine-resistant to threonine-sensitive HSD activity in soybean tissues varies and likely reflec
271 -blind trial of traumatic hypovolemic shock, HSD (250 mL) versus lactated Ringer's solution (LR) as t
273 s of hypertonic saline and dextran solution (HSD, Rescueflow) with 20% mannitol solution for reductio
278 consistent with our earlier observation that HSD is accompanied by only a modest decrease in release
280 e NCR-1 and/or -2 functions, suggesting that HSD-1-mediated steroid hormone production is an importan
284 th targeted disruption of the Mc3r gene, the HSD also led to marked hypertension accompanied by eleva
295 g in their probabilities of release, undergo HSD at the same rate; this suggests that the major mecha
296 suggests that the major mechanism underlying HSD in these SNs may not be depletion of the releasable
297 ta suggest that steroid production by v3beta-HSD contributes to virus virulence by inhibiting an effe
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