ライフサイエンスコーパス: HSD

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

6 In both human and chimpanzee area 10, HSD was significantly higher in the postweaning specimen

7 hydroxysteroid dehydrogenase type 1 (11beta HSD-1).

8 Increased adipocyte 11beta HSD-1 activity may be a common molecular etiology for vi

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

11 11beta-HSD type 1 amplifies intracellular levels of active gluc

12 11beta-HSD-1(-/-) mice also have increased HDL cholesterol, wit

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

16 -hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) occurred.

17 Additionally, 11beta-HSD-1 mRNA was approximately ninefold higher (P < 0.01)

18 rning deficit was ameliorated in aged 11beta-HSD-1 knockout mice, implicating lower intraneuronal cor

19 Although 11beta-HSD-2 gene expression was very low in visceral fat, the

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

23 the prereceptor metabolism of GCS by 11beta-HSD is well documented in a variety of cells and tissues

24 intact hippocampal cells in culture, 11beta-HSD-1 acts as a functional 11beta-reductase reactivating

25 11beta-hydroxysteroid dehydrogenase (11beta-HSD) act at a prereceptor level to regulate the tissue-s

26 11beta-hydroxysteroid dehydrogenase (11beta-HSD) enzymes control the interconversion of active gluco

27 11beta-hydroxysteroid dehydrogenase (11beta-HSD) that interconvert active cortisol and inactive cort

28 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 pathway.

29 11-beta hydroxysteroid dehydrogenase (11beta-HSD) type 1, D3-cortisol production can be used as an in

30 11beta-hydroxysteroid dehydrogenases (11beta-HSD) perform prereceptor metabolism of glucocorticoids t

31 Ad lib fed 11beta-HSD-1(-/-) mice have markedly lower plasma triglyceride

32 Further, 11beta-HSD-1(-/-) mice have improved glucose tolerance.

33 ivated receptor-alpha mRNA is lost in 11beta-HSD-1(-/-) mice, consistent with attenuated glucocortico

34 ession of genes for fat catabolism in 11beta-HSD-1(-/-) mice, implying increased liver insulin sensit

35 e the rapid (within 3 h) induction of 11beta-HSD activity in cells elicited in the peritoneum by a si

36 re well documented, the expression of 11beta-HSD enzymes in immune cells is not well understood.

37 d D3 cortisol production (an index of 11beta-HSD type 1 activity) were measured using the combined he

38 production can be used as an index of 11beta-HSD type 1 activity.

39 ated, PPARgamma agonist inhibition of 11beta-HSD-1 and leptin gene expression was ablated, thereby su

40 tigates the metabolic consequences of 11beta-HSD-1 deficiency, focusing on the lipid and lipoprotein

41 in part, from the down-regulation of 11beta-HSD-1 expression in adipose tissue.

42 rosiglitazone inhibited expression of 11beta-HSD-1 in adipose tissue.

43 The importance of 11beta-HSD-1 in glucose homeostasis is suggested by the resista

44 amined the functional significance of 11beta-HSD-1 in the central nervous system by using knockout mi

45 Rgamma affects the down-regulation of 11beta-HSD-1 indirectly.

46 The half-maximal inhibition of 11beta-HSD-1 mRNA expression by the TZD, rosiglitazone, occurre

47 sis is suggested by the resistance of 11beta-HSD-1(-/-) mice to hyperglycemia upon stress or obesity,

48 D PPARgamma agonists markedly reduced 11beta-HSD-1 gene expression in 3T3-L1 adipocytes.

49 Selective 11beta-HSD-1 inhibitors may protect against hippocampal functio

50 implication, flux via the splanchnic 11beta-HSD type 1 pathway.

51 These data suggest that 11beta-HSD-1 deficiency produces an improved lipid profile, hep

52 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) catalyse the interconversion of active cortisol an

53 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) modulates cellular steroid action.

54 11beta-hydroxysteroid dehydrogenases (11beta-HSDs).

55 is thus similar to that expected of a 17beta-HSD substrate.

56 was detected in transfected cells and 17beta-HSD type 2 transfection did not offer protection against

57 17beta-hydroxysteroid dehydrogenase (17beta-HSD) type 2 in the metabolism of 2-MeOE2.

58 17beta-hydroxysteroid dehydrogenase (17beta-HSD), in the ZR-75-1 cells, which rapidly converts 2-MeO

59 time, that the high levels of type II 17beta-HSD present in ZR-75-1 cells were largely responsible fo

60 The type II 17beta-HSD-mediated conversion of 2-MeO-E2 to 2-methoxyestrone

61 1 cells, which express high levels of 17beta-HSD type 2, and in MCF-7 cells transfected with 17beta-H

62 tinal mucosa expresses high levels of 17beta-HSD type 2.

63 mRNA levels of three known oxidative 17beta-HSD isozymes (types II, IV, and VIII) revealed that only

64 The 17beta-HSD type 1 enzyme (17beta-HSD1) catalyzes the reduction

65 hermore, MCF-7 cells transfected with 17beta-HSD type 2 were protected from the cytotoxic effects of

66 , and in MCF-7 cells transfected with 17beta-HSD type 2, high-performance liquid chromatography analy

67 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) catalyze the interconversion between the oxidized

68 the progesterone-metabolizing enzyme 20alpha HSD and reduced nuclear progesterone levels.

69 T5b expression was up-regulated, and 20alpha-HSD mRNA was decreased, but in 15 d postcoitum pregnant

70 C2 to catalyze 3alpha-, 17beta-, and 20alpha-HSD reactions.

71 0alpha-hydroxysteroid dehydrogenase (20alpha-HSD).

72 -alpha-hydroxysteroid dehydrogenase (20alpha-HSD; median, 2.5 arbitrary units [AU]; interquartile ran

73 0alpha-hydroxysteroid dehydrogenase [20alpha-HSD (EC 1.1.1.149)], and AKR1C2, which encodes a 3alpha-

74 200a, decreased STAT5b, and enhanced 20alpha-HSD expression.

75 -HM) suppressed STAT5b and increased 20alpha-HSD mRNA levels.

76 In vitro inhibition of 20alpha-HSD activity in trophoblast cells reversed PI-based cART

77 crease in expression and activity of 20alpha-HSD in laboring myometrium from mouse and human.

78 diating the PGF(2alpha) induction of 20alpha-HSD, a steroidogenic enzyme involved in the catabolism o

79 Prolactin, a key regulator of 20alpha-HSD, was lower (P= .012) in HIV-infected pregnant women.

80 increase in placental expression of 20alpha-HSD, which may be due to lower prolactin levels observed

81 -positional-specific 3alpha-/17beta-/20alpha-HSDs.

82 Sixty-two patients (36 HSD, 26 LR) and 20 healthy volunteers were enrolled.

83 the Delta(7)-DA biosynthetic enzyme DAF-36, HSD-1 is dispensable for proper gonadal migration and li

84 oxytibolone, AKR1C3 showed weak 3beta/3alpha-HSD activity, and AKR1C4 acted predominantly as a 3alpha

85 Whereas AKR1C2 acted as a 3alpha-HSD toward 5alpha-DHT, it functioned exclusively as a 3b

86 inverted its stereospecificity from a 3alpha-HSD with 5alpha-DHT to a 3beta-HSD with tibolone.

87 , and AKR1C4 acted predominantly as a 3alpha-HSD.

88 to act as a 3beta-HSD as opposed to a 3alpha-HSD.

89 ous other small molecules to activate 3alpha-HSD type III catalyzed allopregnanolone formation.

90 concentrations in vivo by activating 3alpha-HSD type III, we investigated whether these small molecu

91 However, 5alpha-R type I and 3alpha-HSD are significantly expressed in principal GABAergic o

92 demonstrate that 5alpha-R type I and 3alpha-HSD colocalize in cortical, hippocampal, and olfactory b

93 failed to detect 5alpha-R type I and 3alpha-HSD in cortical and hippocampal GABAergic interneurons.

94 on, this study compares 5alpha-RI and 3alpha-HSD mRNA brain expression levels in group housed and in

95 s study evaluates 5alpha-R type I and 3alpha-HSD mRNA expression level in mouse brain by using in sit

96 Two other proteins (RODH-4 and 3alpha-HSD) are significantly less conserved.

97 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD), which is 3-fold more active with free retinol than

98 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD).

99 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD).

100 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD, AKR1C9) as the protein model.

101 3alpha-hydroxysteroid dehydrogenase [3alpha-HSD (EC 1.1.1.52)], was found in 24 paired breast cancer

102 Orthologs for 3alpha-HSD are present in all mammals analyzed, whereas ortholo

103 acterization of the kinetics of human 3alpha-HSD catalyzed allopregnanolone formation.

104 ity that is observed in all the human 3alpha-HSD isoforms but not in the rat isoform.

105 lpha-DHP reduction catalyzed by human 3alpha-HSD type III by using steady-state kinetics studies and

106 molecules were able to activate human 3alpha-HSD type III.

107 Importantly, 3alpha-HSD mRNA expression was unchanged by protracted social i

108 nt and that, in contrast to RoDH-like 3alpha-HSD, RoDH-4 can access the bound form of retinol for ret

109 gically important reaction, rat liver 3alpha-HSD (AKR1C9) was used as the protein model for the human

110 Neither 5alpha-R type I nor 3alpha-HSD mRNAs are expressed in S100beta- or glial fibrillary

111 hese results characterize the role of 3alpha-HSD type III in allopregnanolone formation and suggest t

112 echanism of a mammalian HSD using rat 3alpha-HSD of the aldo-keto reductase superfamily (AKR1C9) with

113 ing pocket of AKR1C2 with that of rat 3alpha-HSD reveals significant differences in the positions of

114 d for testosterone in the related rat 3alpha-HSD.NADP(+).testosterone ternary complex, where testoste

115 pregnanolone oxidation indicated that 3alpha-HSD type III utilized a ternary complex (sequential) kin

116 fined by the crystal structure of the 3alpha-HSD.NADP(+).testosterone ternary complex.

117 3Alpha-hydroxysteroid dehydrogenases (3alpha-HSDs) catalyze the interconversion between 5alpha-dihydr

118 3alpha-hydroxysteroid dehydrogenases (3alpha-HSDs).

119 beta-HSD compared with the wild-type 1 3beta-HSD activity.

120 primary structure of the human type 1 3beta-HSD/isomerase.

121 at)) is 2-fold greater for wild-type 2 3beta-HSD compared with the wild-type 1 3beta-HSD activity.

122 tion kinetics of the wild-type 1 and 2 3beta-HSD, plus a catalytic role for the Tyr(154) and Lys(158)

123 ructure/function of human type 1 and 2 3beta-HSD/isomerase may lead to the design of selective inhibi

124 1C1 and AKR1C2 demonstrated how 3alpha/3beta-HSD activities are achieved.

125 the in vivo significance of the 3alpha/3beta-HSD activities of the AKR1C enzymes.

126 stereochemical preference to act as a 3beta-HSD as opposed to a 3alpha-HSD.

127 so synthesizes steroid hormones with a 3beta-HSD enzyme (v3beta-HSD) encoded by gene A44L.

128 ha-DHT, it functioned exclusively as a 3beta-HSD on tibolone.

129 from a 3alpha-HSD with 5alpha-DHT to a 3beta-HSD with tibolone.

130 , suggesting that HSD-1 functions as a 3beta-HSD.

131 n the Delta(4)-double bond and confers 3beta-HSD activity on the 5beta-reductase.

132 ic 3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity is unknown to date.

133 he 3beta-hydroxysteroid dehydrogenase (3beta-HSD) isoenzymes play a key role in cellular steroid horm

134 d K273Q mutants have low, pH-dependent 3beta-HSD activity, exhibit only 5% of the maximal isomerase a

135 se regions contained the gene encoding 3beta-HSD (HSD3B7).

136 The catalytic efficiency achieved for 3beta-HSD activity is higher than that observed for any AKR to

137 me has substrate kinetic constants for 3beta-HSD activity that are very similar to those of the wild-

138 the Michaelis-Menten constant (Km) for 3beta-HSD substrate and inhibition constants (Ki) for epostane

139 not affect an SF-1 dependent LC gene (3beta-HSD) without overlapping sites.

140 Our structural model of human 3beta-HSD localizes His156 or Tyr156 in the subunit interface

141 riation in expressivity that occurs in 3beta-HSD deficiency and underscores the need to consider a bi

142 ydroxysteroid dehydrogenase/isomerase (3beta-HSD/isomerase) in humans.

143 man hepatoma (HepG2) cells (which lack 3beta-HSD/Delta(5-4) ketosteroid isomerase mRNA expression, bu

144 The Y154F and K158Q mutants exhibit no 3beta-HSD activity, have substantial isomerase activity, and u

145 The diagnosis of 3beta-HSD deficiency was confirmed by documenting high levels

146 Delta(5)-C(27)-steroid oxidoreductase (3beta-HSD) deficiency, a disorder that usually presents in ear

147 lysis shows that epostane inhibits the 3beta-HSD activity of the wild-type 1 enzyme with 14-17-fold g

148 er downstream of or in parallel to the 3beta-HSD function in the dafachronic acid biosynthetic pathwa

149 Tyr(154) and Lys(158) residues in the 3beta-HSD reaction have been identified.

150 rogenase/Delta(5)-Delta(4) isomerases (3beta-HSDs), which are key steroidogenic enzymes in vertebrate

151 ial target of salt in immune cells, we fed a HSD to CD4(Cre)SGK1(fl/fl) B6-transplanted recipients an

152 Feeding a HSD to C57BL/6 wild-type recipients of bm12 allografts l

153 (+) T cells to Tregs in mice recipients of a HSD compared with mice recipients of a NSD.

154 ed abrogation of the deleterious effect of a HSD in the absence of SGK1 on CD4(+) cells.

155 lla undermines the homeostatic response to a HSD.

156 Whether a HSD affects the immune response in transplantation is un

157 In adults, HSD-1 was required for full lifespan extension in IIS mu

158 ochemical features of AK and bifunctional AK-HSD enzymes have been characterized, but the molecular p

159 This is in contrast to the two AK-HSD isoforms in soybean that are sensitive to threonine

160 D) type II and has PGFS activity and 3 alpha-HSD activity.

161 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) type II and has PGFS activity and 3 alpha-HSD activ

162 ning with a K+ channel blocker did not alter HSD.

163 Similar to the IL-10-deficient model, an HSD also enhanced cytokine expression during infection b

164 dium accumulated in the colons of mice on an HSD, suggesting a direct effect of salt within the colon

165 We demonstrate that an HSD exacerbates inflammatory pathology in the IL-10-defi

166 e first 3 d of infection, suggesting that an HSD potentiates an innate immune response.

167 m Hg, 95% confidence interval, 5.8-11.8) and HSD (median decrease, 13 mm Hg; 95% confidence interval,

168 methanogenesis rates between ULSD, LSD, and HSD.

169 1 beta-hydroxysteroid dehydrogenase (11 beta-HSD) interconvert cortisol (F) and inactive cortisone (E

170 first in vivo evidence that adipose 11 beta-HSD-1 deficiency beneficially alters adipose tissue dist

171 e report novel protective effects of 11 beta-HSD-1 deficiency on adipose function, distribution, and

172 metabolic syndrome in mice, whereas 11 beta-HSD-1 deficiency or inhibition has beneficial metabolic

173 ting the reported effects of hepatic 11 beta-HSD-1 deficiency or inhibition.

174 Transgenic overexpression of 11 beta-HSD-1 in adipose tissue reproduces a metabolic syndrome

175 tion, and gene expression in vivo in 11 beta-HSD-1 nullizygous (11 beta-HSD-1(-/-)) mice.

176 Isolated 11 beta-HSD-1(-/-) adipocytes exhibited higher basal and insulin

177 11 beta-HSD-1(-/-) mice also exhibited reduced visceral fat accu

178 11 beta-HSD-1(-/-) mice expressed lower resistin and tumor necro

179 High-fat-fed 11 beta-HSD-1(-/-) mice rederived onto the C57BL/6J strain resis

180 n vivo in 11 beta-HSD-1 nullizygous (11 beta-HSD-1(-/-)) mice.

181 hydroxysteroid dehydrogenase type 1 (11 beta-HSD-1) found in adipose tissue of obese humans and roden

182 An efficient asymmetric synthesis of 11-beta-HSD inhibitor 1 has been accomplished in five linear ste

183 ficance to the high levels of GR and 11-beta-HSD Type 1 expression in cerebellum.

184 by the coenzyme product, NADH, of the 3 beta-HSD activity.

185 study tested the hypothesis that the 3 beta-HSD and isomerase activities shared a common coenzyme do

186 hifts the cofactor preference of both 3 beta-HSD and isomerase from NAD(H) to NADP(H), which shows th

187 Human 3 beta-HSD I in placenta is essential for placental progesteron

188 ocated between -2896 and -2831 of the 3 beta-HSD VI promoter.

189 The murine ortholog, 3 beta-HSD VI, is the only isoform expressed in giant trophobla

190 or trophoblast-specific expression of 3 beta-HSD VI.

191 or trophoblast-specific expression of 3 beta-HSD VI.

192 droxysteroid dehydrogenase/isomerase (3 beta-HSD) is essential for the biosynthesis of all active ste

193 cture/function relationships of human 3 beta-HSD/isomerase and bring us closer to the goal of selecti

194 e for the NAD(H) specificity of human 3 beta-HSD/isomerase and identifies the Rossmann-fold coenzyme

195 droxysteroid dehydrogenase/isomerase (3 beta-HSD/isomerase) catalyzes the two sequential enzyme react

196 not for other prostanoids, was depressed by HSD in WT and even more so in both mutant strains.

197 tive (CDs) rats fed a diabetogenic-diet (CDs-HSD).

198 ucose tolerance and insulin secretion in CDs-HSD rats.

199 ed CDs-HSD rats compared with nontreated CDs-HSD rats.

200 GSIS (P < 0.05) compared with nontreated CDs-HSD rats.

201 xocrine parenchyma of IL-1betaAb-treated CDs-HSD rats compared with nontreated CDs-HSD rats.

202 ucose tolerance test, IL-1betaAb-treated CDs-HSD rats showed lower blood glucose concentrations (P <

203 te kinase (AK) and homoserine dehydrogenase (HSD) function as key regulatory enzymes at branch points

204 enzyme 11beta-hydroxysteroid dehydrogenase (HSD) type 1 converts inactive cortisone into active cort

205 ugh the 11beta hydroxysteroid dehydrogenase (HSD) type 1 pathway can be measured by determining the r

206 ype III 3alpha-hydroxysteroid dehydrogenase (HSD)/bile acid binding protein (AKR1C2) complexed with N

207 Hydroxysteroid dehydrogenases (HSDs) are essential for the biosynthesis and mechanism o

208 lls for human hydroxysteroid dehydrogenases (HSDs) of the aldo-keto reductase (AKR) superfamily.

209 3alpha/3beta-hydroxysteroid dehydrogenases (HSDs) on 5alpha-dihydrotestosterone (5alpha-DHT).

210 C enzymes are hydroxysteroid dehydrogenases (HSDs).

211 s) undergo dramatic homosynaptic depression (HSD) with only a few low-frequency stimuli.

212 quency stimulation [homosynaptic depression (HSD)] of the sensory neuron were expressed in both contr

213 nic potentiation or homosynaptic depression (HSD)], or short-term heterosynaptic plasticity [serotoni

214 Hyperthermic spreading depression (HSD) in immature rat hippocampal slices is mediated by N

215 of ULSD, low- (LSD), and high sulfur diesel (HSD) and monitored for sulfate depletion.

216 tabolic alkalosis (MAlk) and high-salt diet (HSD) also increase expression of NBCn1 and NBCn2 (effect

217 ents the VEGFC response to a high-salt diet (HSD) and increases blood pressure.

218 A high-salt diet (HSD) in humans is linked to a number of complications, i

219 odels of colitis on either a high salt diet (HSD) or a low salt diet.

220 ive to wild types (WTs) on a high-salt diet (HSD); this was attenuated by a PGI(2) receptor agonist.

221 18% Na(+) and a moderately high sodium diet (HSD) containing 1.25% Na(+) .

222 d in the soleus muscle of high sucrose diet (HSD) induced insulin resistant rats and TNF-alpha expose

223 hypothesis, we fed rats a high-sucrose diet (HSD).

224 e use a Drosophila model of high-sugar diet (HSD)-enhanced tumourigenesis to uncover a systemic host-

225 ing the Tukey honest significant difference (HSD) test for multiple comparisons.

226 t-hoc Tukey honestly significant difference (HSD) test.

227 ukey-Kramer honestly significant difference [HSD], P < 0.001).

228 Horizontal spacing distance (HSD) and gray level ratio (GLR) of layer III neurons wer

229 ng domain (PPXD), a helical scaffold domain (HSD), and a helical wing domain (HWD).

230 net NaCl backflux into the mTAL cell during HSD.

231 cruited and received two treatments of each, HSD and 20% mannitol, in a randomized order.

232 ly greater in AC than in OA and normal eyes (HSD test, P </= 0.05), but there was no significant diff

233 lular ATP serves as a possible mechanism for HSD genesis.

234 he cytoplasmic sequestration of DAF-16/FoxO, HSD-1 inhibits nuclear DAF-16/FoxO activity without affe

235 Patients give HSD showed a trend toward higher levels of IL-1beta and

236 ion of NBCn1 and NBCn2 (effect of NaHCO(3) > HSD).

237 On the other hand, HSD did not alter measured GFR but decreased the abundan

238 al structure has now been solved for a human HSD member of the aldo-keto reductase superfamily.

239 rest, contrary to what would be expected if HSD represented an exhaustion of the exocytosis mechanis

240 e similar mean BP and serum sodium levels in HSD and normal salt diet (NSD) groups.

241 t switching off of release sites resulted in HSD that was independent of initial synaptic strength.

242 Once induced, HSD persisted during 40 min of rest with no detectable r

243 n an equimolar, rapid, intravenous infusion, HSD reduces intracranial pressure more effectively than

244 ion of a monofunctional feedback-insensitive HSD from any plant.

245 ingle point mutation in AKR1D1 can introduce HSD activity with unexpected configurational and stereoc

246 shes 5beta-reductase activity and introduces HSD activity.

247 he complete kinetic mechanism of a mammalian HSD using rat 3alpha-HSD of the aldo-keto reductase supe

248 eroid dehydrogenase (3betaHSD) family member HSD-1, which participates in Delta(4)-DA biosynthesis, a

249 In wild-type mice, HSD for 1 week did not alter MAP versus LSD mice, but pl

250 he cDNA and gene encoding the monofunctional HSD (GmHSD) from soybean.

251 e molecular properties of the monofunctional HSD remain unexamined.

252 The kinetics of HSD was attenuated at synapses expressing PA-LTF, which

253 Both PA-LTF and the attenuated kinetics of HSD were reversed by either a transient blockade of PKC

254 dels, we evaluated alternative mechanisms of HSD, including vesicle depletion, to determine which mec

255 is route ensured multikilogram quantities of HSD-016 necessary for clinical studies.

256 To investigate the role of HSD, we have cloned the cDNA and gene encoding the monof

257 tructures indicate that stereospecificity of HSD activity is achieved because the steroid flips over

258 Herein, a reliable and scalable synthesis of HSD-016 is described.

259 for 30 min to PC2(-/-) mice after 1 week of HSD lowered MAP from hypertensive levels to normal; infu

260 lpipe razin-1-ylsulfonyl)phenyl)propan-2-ol (HSD-016) was discovered to be a potent, selective, and e

261 ast, P-LTF was unaffected when either PTP or HSD was evoked in the presence of either rapamycin or an

262 d HSDs, and six of them did not affect other HSDs.

263 PPXD, HSD, and NBD2 form a clamp that positions the polypeptid

264 in two phases, an initial movement of PPXD, HSD, and HWD as a unit, followed by a movement of PPXD a

265 Compared to chow-fed, control rats, HSD impaired myocardial insulin responsiveness and induc

266 ed acceptable selectivity over other related HSDs, and six of them did not affect other HSDs.

267 Threonine-resistant HSD offers a useful biotechnology tool for manipulating

268 like 3alpha-hydroxysteroid dehydrogenase (RL-HSD, SDR9C6), and RDH-like SDR (RDHL, SDR9C4) do not aff

269 nalyzed by one-way ANOVA followed by Tukey's HSD test.

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

272 L of 7.5% saline and 6% dextran-70 solution (HSD) over 5 mins.

273 s of hypertonic saline and dextran solution (HSD, Rescueflow) with 20% mannitol solution for reductio

274 The hypothesis that short-term HSD involves primarily a stepwise silencing of release s

275 This conclusion that HSD is a release-independent phenomenon was supported by

276 Further, we found that HSD elevated skin osmolality above plasma levels.

277 an extension in IIS mutants, indicating that HSD-1 interactions with IIS are context-dependent.

278 consistent with our earlier observation that HSD is accompanied by only a modest decrease in release

279 c acid biosynthetic pathway, suggesting that HSD-1 functions as a 3beta-HSD.

280 e NCR-1 and/or -2 functions, suggesting that HSD-1-mediated steroid hormone production is an importan

281 This study suggests that HSD is not be mediated by depletion of intracellular ATP

282 The HSD augmented in all strains urinary prostanoid metaboli

283 pressed on regular chow and unaltered by the HSD in both mutants.

284 th targeted disruption of the Mc3r gene, the HSD also led to marked hypertension accompanied by eleva

285 velopment of hypertension when ingesting the HSD.

286 We tested the effect of the HSD (8% NaCl) compared with LSD (0.07%) on mean arterial

287 nto the channel by a two-helix finger of the HSD.

288 On the HSD, MAP rose to a markedly hypertensive level while pla

289 gamma-MSH resistance and hypertension on the HSD.

290 Finally, we found that the HSD-1-mediated signal activates insulin/IGF-I signaling

291 is necessary for the normal response to the HSD.

292 Thus, HSD-1 and IIS inhibit DAF-16/FoxO activity via distinct

293 Thus, HSDs in the aldo-keto reductase superfamily thermodynami

294 , p = 0.043, one-way ANOVA; p = 0.035, Tukey HSD).

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

298 oid hormones with a 3beta-HSD enzyme (v3beta-HSD) encoded by gene A44L.

299 Here we examined the effects of v3beta-HSD in VV disease using wild-type (vA44L), deletion (vDe

300 Those resuscitated with HSD had a significant reduction in CD11b expression 12 h