ライフサイエンスコーパス: hydroxycholesterol

1 cid biosynthesis intermediates (27- and 7,27-hydroxycholesterol).

2 lipoprotein and sterols (cholesterol and 25-hydroxycholesterol).

3 terol 25-hydroxylase and the synthesis of 25-hydroxycholesterol.

4 f NPC1 and complexes with cholesterol and 25-hydroxycholesterol.

5 domain that can bind both cholesterol and 25-hydroxycholesterol.

6 of a closely eluting isomeric oxysterol, 25-hydroxycholesterol.

7 ostasis, we synthesized the enantiomer of 25-hydroxycholesterol.

8 required the conversion of cholesterol to 27-hydroxycholesterol.

9 nd to form two new products, one being 7beta-hydroxycholesterol.

10 election in high levels of the oxysterol, 25-hydroxycholesterol.

11 ergosterol, cholesterol, and 7-, 20- and 25-hydroxycholesterol.

12 ion of APP may be to produce low levels of 7-hydroxycholesterol.

13 approximately 1000-fold more potent than 27-hydroxycholesterol.

14 te block of the induction of apoptosis by 25-hydroxycholesterol.

15 talyzes the synthesis of the oxysterol 24(S)-hydroxycholesterol.

16 ion, than the widely used LXR agonist 22-(R)-hydroxycholesterol.

17 s, including 22(R)-hydroxycholesterol and 24-hydroxycholesterol.

18 ed for by the formation and excretion of 24S-hydroxycholesterol.

19 e very little affinity for cholesterol or 25-hydroxycholesterol.

20 -fold by 9CRA, and 37-fold by 9CRA and 22(R)-hydroxycholesterol.

21 sion of ABC8 following incubation with 22(R)-hydroxycholesterol.

22 no enhanced calcium uptake in response to 25-hydroxycholesterol.

23 of the estrogenic cholesterol metabolite 27-hydroxycholesterol.

24 droxycholesterol, and to a lesser extent, 25-hydroxycholesterol.

25 rs the protein resistant to inhibition by 25-hydroxycholesterol.

26 hen cells were grown in medium containing 25-hydroxycholesterol.

27 on with either low density lipoprotein or 25-hydroxycholesterol.

28 tivities of a typical, regulatory sterol: 25-hydroxycholesterol.

29 dium renders them resistant to killing by 25-hydroxycholesterol.

30 nd selection for resistance to killing by 25-hydroxycholesterol.

31 l synthesizing enzymes in the presence of 25-hydroxycholesterol.

32 the protein's ability to be inhibited by 25-hydroxycholesterol.

33 and renders it resistant to inhibition by 25-hydroxycholesterol.

34 gh-fat diet via its oxysterol metabolite, 27-hydroxycholesterol.

35 on tumour development were independent of 27-hydroxycholesterol.

36 ant cells, partly via the biosynthesis of 27-hydroxycholesterol.

37 ntly decreased by physiological levels of 25-hydroxycholesterol.

38 the brain, the predominant oxysterol was 24S-hydroxycholesterol.

39 oxycholesterol, 27-hydroxycholesterol, 22(R)-hydroxycholesterol, 20(S)-hydroxycholesterol, and 24(S),

40 22(R)-hydroxycholesterol (22(R)-OHC), 25-OHC, and 27-OHC each

41 c hydroxylations with formation first of 22R-hydroxycholesterol (22-HC) and then 20alpha,22R-dihydrox

42 We observed that the oxysterol 22-hydroxycholesterol (22-HC) in combination with its oblig

43 erivatives such as 25-hydroxycholesterol, 27-hydroxycholesterol, 22(R)-hydroxycholesterol, 20(S)-hydr

44 Other proposed LXR ligands, including 20(S)-hydroxycholesterol, 22(R)-hydroxycholesterol, and 24(S),

45 at involve the progressive production of 22R-hydroxycholesterol (22HC) and 20alpha,22R-dihydroxychole

46 r brain-derived cholesterol metabolite 24(S)-hydroxycholesterol (24(S)-HC) is a very potent, direct,

47 In the central nervous system, 24(S)-hydroxycholesterol (24(S)-HC) is an oxysterol synthesize

48 (CYP46A1) increases the levels of both 24(S)-hydroxycholesterol (24-HC) and 24,25-EC in the developin

49 Serum and CSF 24(S)-hydroxycholesterol (24[S]-HC), which serves as a biomark

50 urally occurring oxysterols, including 22(R)-hydroxycholesterol, 24(S)-hydroxycholesterol, and 24(S),

51 24-(S)-hydroxycholesterol (24HC), a structural isomer of 25HC,

52 me Cyp46a1, which generates the oxysterol 24-hydroxycholesterol (24S-HC) in a pancreatic neuroendocri

53 tion of the brain cholesterol metabolite 24S-hydroxycholesterol (24S-OHC) found in B6.Mecp2-null mice

54 The levels of 24(S)-hydroxycholesterol (24S-OHC) were significantly reduced

55 ing enzyme for cholesterol conversion to 24S-hydroxycholesterol (24S-OHC).

56 age, A1- causes a 32% content increase in 24-hydroxycholesterol (24SOH), the major oxysterol in the b

57 Concentrations of circulating 24S-hydroxycholesterol (24SOHChol) are of interest as a prac

58 search for a membrane protein that binds 25-hydroxycholesterol (25-HC) and other oxysterols.

59 Here, we demonstrate that production of 25-hydroxycholesterol (25-HC) by macrophages is required to

60 25-Hydroxycholesterol (25-HC) is produced as an oxidation p

61 that are unable to produce the oxysterol 25-hydroxycholesterol (25-HC) overproduce inflammatory inte

62 We further showed that production of 25-hydroxycholesterol (25-HC) promotes macrophage foam cell

63 25-Hydroxycholesterol (25-HC), a known modulator of both in

64 shown that side-chain oxysterols, such as 25-hydroxycholesterol (25-HC), alter membrane structure in

65 that in vitro additions of the oxysterol 25-hydroxycholesterol (25-HC), exogenous cytosol, and ATP t

66 lesterol and its hydroxylated derivative, 25-hydroxycholesterol (25-HC), inhibit cholesterol synthesi

67 SREBP activation was also blocked by 25-hydroxycholesterol (25-HC).

68 (3)H]cholesterol (K(d), 130 nM) and [(3)H]25-hydroxycholesterol (25-HC, K(d), 10 nM) with one sterol

69 7beta-hydroxycholesterol (7beta-OH), and 25-hydroxycholesterol (25-OH).

70 evidence suggests that oxysterols such as 25-hydroxycholesterol (25HC) are biologically active and in

71 The oxysterol 25-hydroxycholesterol (25HC) plays multiple roles in lipid

72 Here we show that a lipid, oxysterol 25-hydroxycholesterol (25HC), directly binds to alpha5beta1

73 requires the production of the oxysterol 25-hydroxycholesterol (25HC), inhibition of cholesterol syn

74 infection and that its enzymatic product, 25-hydroxycholesterol (25HC), was a critical mediator of ho

75 iviral activity through the production of 25-hydroxycholesterol (25HC), which is believed to inhibit

76 hat converts cholesterol to the oxysterol 25-hydroxycholesterol (25HC).

77 veloped viruses through the production of 25-hydroxycholesterol (25HC).

78 holesterol to a soluble antiviral factor, 25-hydroxycholesterol (25HC).

79 25-Hydroxycholesterol (25OH) competitively inhibits this ex

80 ls, 22(R)-hydroxy-cholesterol (22ROH) and 25-hydroxycholesterol (25OH), and a nonsterol activator of

81 25-Hydroxycholesterol (25OHC) is an enzymatically derived o

82 27-Hydroxycholesterol (27-HC) is the most abundant oxystero

83 pc1-/- mice showed decreased synthesis of 27-hydroxycholesterol (27-HC), an endogenous LXR ligand; de

84 Here, we show that excess 27-hydroxycholesterol (27-OH), a cholesterol metabolite pas

85 ow that the cholesterol oxidation product 27-hydroxycholesterol (27-OHC) increases BACE1 and Abeta le

86 XRs include oxysterol derivatives such as 25-hydroxycholesterol, 27-hydroxycholesterol, 22(R)-hydroxy

87 tment with the alternative ERalpha ligand 27-hydroxycholesterol (27HC) induced ERalpha-dependent HSC

88 east cancer metastasis via its metabolite 27-hydroxycholesterol (27HC) that acts on immune myeloid ce

89 27-Hydroxycholesterol (27HC), a derivative of cholesterol f

90 Here, we show that 27-hydroxycholesterol (27HC), a primary metabolite of chole

91 Here we show that 27-hydroxycholesterol (27HC), an abundant cholesterol metab

92 t treatment of prostate cancer cells with 27-hydroxycholesterol (27HC), an enzymatic product of CYP27

93 studies have indicated that the oxysterol 27-hydroxycholesterol (27HC), and not cholesterol per se, m

94 The oxysterol 27-hydroxycholesterol (27HC), synthesized by the mitochondr

95 ong these, the most abundant oxysterol is 27-hydroxycholesterol (27HC), which can cross the blood-bra

96 e endogenous estrogen receptor antagonist 27-hydroxycholesterol (27OHC) is correlated with LDLC level

97 ntracellular domain (AICD) in response to 27-hydroxycholesterol (27OHC), an oxidized cholesterol meta

98 to 1, whereas the unnatural oxysterol 22(S)-hydroxycholesterol (4) was shown to be an antagonist of

99 ubstrates, whereas 7-ketocholesterol, 7 beta-hydroxycholesterol, 5 beta,6 beta-epoxycholesterol, and

100 inance of the 7-oxygenated products, 7 alpha-hydroxycholesterol (7 alpha HCh), 7 beta-hydroxycholeste

101 pha-hydroxycholesterol (7 alpha HCh), 7 beta-hydroxycholesterol (7 beta HCh), and 7-ketocholesterol (

102 velop cholestasis before up-regulation of 27-hydroxycholesterol 7alpha-hydroxylase activity.

103 One of the 7-oxygenated sterols, 7alpha-hydroxycholesterol (7alpha-OHC), serves as a key interme

104 varying concentrations of cholesterol, 7beta-hydroxycholesterol (7beta-OH), and 25-hydroxycholesterol

105 pstream promoter was induced 7-fold by 22(R)-hydroxycholesterol, 8-fold by 9CRA, and 37-fold by 9CRA

106 p to 2.5-fold) by LXR activation using 24(S)-hydroxycholesterol (a cerebral cholesterol metabolite) o

107 P450 enzyme that converts cholesterol to 24-hydroxycholesterol, a cholesterol elimination product an

108 A>G (P<0.01) and c.521T>C (P<0.05) and 4beta-hydroxycholesterol, a CYP3A activity marker (adjusted R(

109 while providing a complementary source of 25-hydroxycholesterol, a modulator of immune cell function

110 oxysterols, we assessed the effect of 22-(R)-hydroxycholesterol, a natural ligand of the liver X rece

111 25-hydroxycholesterol, a potent regulator of SCAP in vivo,

112 nd APP can oxidize cholesterol to form 7beta-hydroxycholesterol, a proapoptotic oxysterol that was ne

113 uction of cholesterol 25-hydroperoxide to 25-hydroxycholesterol, a role of potential significance for

114 ffects on serum levels of the oxysterol, 24S-hydroxycholesterol, a substrate of the encoded enzyme.

115 iquid chromatography analysis showed that 27-hydroxycholesterol accumulated in the mitochondria of St

116 27-Hydroxycholesterol, an abundant oxysterol synthesized by

117 nzyme in humans converting cholesterol to 27-hydroxycholesterol, an oxysterol of multiple functions,

118 ia conversion of excess cholesterol into 24S-hydroxycholesterol, an oxysterol that is readily secrete

119 A library of 20(S)-hydroxycholesterol analogues with varying sterol side ch

120 acid and several oxysterols, including 22(R)-hydroxycholesterol and 24-hydroxycholesterol.

121 ibroblasts fail to appropriately generate 25-hydroxycholesterol and 27-hydroxycholesterol in response

122 rations, the efficiencies of oxidation of 27-hydroxycholesterol and 3beta-hydroxy-5-cholestenal to th

123 ophage-like cell line P388D1, oxysterols (25-hydroxycholesterol and 7-ketocholesterol) induced the de

124 Oxysterols (25-hydroxycholesterol and 7-ketocholesterol) reversed the i

125 by incubating cells with the oxysterols, 25-hydroxycholesterol and 7-ketocholesterol; these findings

126 was induced in an additive fashion by 22(R)-hydroxycholesterol and 9-cis-retinoic acid (9CRA), sugge

127 sh variant of amyloid precursor protein, 22R-hydroxycholesterol and 9-cis-retinoic acid induced ABCA1

128 without a double bond between C5-C6 (7alpha-hydroxycholesterol and cholestanol, respectively) and in

129 In addition, we show that formation of 27-hydroxycholesterol and cholestenoic acid, products of CY

130 es OSBP Golgi localization in response to 25-hydroxycholesterol and cholesterol depletion, impairs CE

131 s, we demonstrated that preincubations in 25-hydroxycholesterol and cholesterol lead to increased apo

132 ckstrin homology (PH) domain (ORP4S) bind 25-hydroxycholesterol and extract and transfer cholesterol

133 Here, we report that the oxysterol 25-hydroxycholesterol and geranylgeraniol combine to trigge

134 on of reductase were tightly regulated by 25-hydroxycholesterol and geranylgeraniol.

135 nued to process SREBPs in the presence of 25-hydroxycholesterol and hence they resisted killing by th

136 hrome P450 enzyme that has preference for 24-hydroxycholesterol and is expressed in the liver.

137 uclear hormone receptor LXR, including 22(R)-hydroxycholesterol and T0901317.

138 lpha-hydroxylase is to metabolize 25- and 27-hydroxycholesterol and that loss of this enzyme in the l

139 rystal structures of rat ATX bound to 7alpha-hydroxycholesterol and the bile salt tauroursodeoxychola

140 e two steroid substrates cholesterol and 24S-hydroxycholesterol and the protein redox partner adrenod

141 s, including 20(S)-hydroxycholesterol, 22(R)-hydroxycholesterol, and 24(S),25-epoxycholesterol, could

142 cholesterol, 22(R)-hydroxycholesterol, 20(S)-hydroxycholesterol, and 24(S),25-epoxycholesterol.

143 s, including 22(R)-hydroxycholesterol, 24(S)-hydroxycholesterol, and 24(S),25-epoxycholesterol.

144 in silico binding studies of lanosterol, 25-hydroxycholesterol, and ATP as a control to two wild typ

145 sterols that included 25-, 20(S)-, and 22(R)-hydroxycholesterol, and by a retinoid X receptor-specifi

146 ones in response to dibutyryl-cAMP and 22(R)-hydroxycholesterol, and displayed ultrastructural featur

147 eceptor pores by pregnenolone sulfate, 24(S)-hydroxycholesterol, and docosahexaenoic acid, three endo

148 roduces biologically active oxysterol, 24(S)-hydroxycholesterol, and is also the first step in enzyma

149 topically applying the LXR activator, 22(R)-hydroxycholesterol, and non-oxysterol activators of LXR,

150 l, lanosterol, ketosterone, 5-cholestene, 25-hydroxycholesterol, and testosterone), we can discuss ho

151 ation and inhibition of SREBP cleavage by 25-hydroxycholesterol, and they indicate that these two pro

152 activity that converts cholesterol into 24S-hydroxycholesterol, and to a lesser extent, 25-hydroxych

153 , such as cis-unsaturated fatty acids, 24(S)-hydroxycholesterol, and various neurosteroids.

154 f new cholesterol and the secretion of 24(S)-hydroxycholesterol are closely coupled and that at least

155 5 alpha,6 alpha-epoxycholesterol and 7 alpha-hydroxycholesterol are comparable with cholesterol as th

156 wever, levels of another major oxysterol, 24-hydroxycholesterol, are not increased in these mice, sug

157 aved SREBP-1, consistent with the role of 24-hydroxycholesterol as an LXR agonist.

158 defined spectral changes while generating 25-hydroxycholesterol as the major product.

159 or 7-ketocholesterol to 101+/-12% for 7alpha-hydroxycholesterol at 200ngg(-1) and from 82+/-2% for 7-

160 ated by 24(S), 25-epoxycholesterol and 24(S)-hydroxycholesterol at physiologic concentrations.

161 25-Hydroxycholesterol, at concentrations higher than 1 micr

162 rol cholesterol binding without affecting 25-hydroxycholesterol binding.

163 E) had increased in vitro cholesterol and 25-hydroxycholesterol-binding capacity, and cholesterol ext

164 responsible for the rate-limiting step in 27-hydroxycholesterol biosynthesis, significantly reduces m

165 ng cells, sterols such as cholesterol and 25-hydroxycholesterol block the lateral movement of sterol

166 n even in the presence of cholesterol and 25-hydroxycholesterol both of which are known suppressors o

167 -164, and 351-361) and eight peptides in 24S-hydroxycholesterol-bound enzyme (50-64, 65-80, 109-116,

168 ina and RPE, the authors could not detect 27-hydroxycholesterol but unexpectedly found that its oxida

169 The rate of production of 7beta-hydroxycholesterol by APP was approximately 200 times lo

170 APP/PS1-Tg mice at a dose lowering brain 24S-hydroxycholesterol by approximately 50%.

171 Conversion of cholesterol to 25-hydroxycholesterol by cholesterol 25-hydroxylase (CH25H)

172 ) with subsequent 7alpha-hydroxylation of 27-hydroxycholesterol by oxysterol 7alpha-hydroxylase (CYP7

173 This is important because 25-hydroxycholesterol can be present in significant amounts

174 ts that oxysterols such as lanosterol and 25-hydroxycholesterol can restore vision by binding to alph

175 The conversion of cholesterol to 7alpha-hydroxycholesterol catalyzed by cytochrome P450 7A1 (CYP

176 ty by less than 2-fold and addition of 22(R)-hydroxycholesterol caused a small but significant stimul

177 oblastoma cells with retinoic acid and 22(R)-hydroxycholesterol caused significant increases in secre

178 tiviral role for macrophage production of 25-hydroxycholesterol (cholest-5-en-3beta,25-diol, 25HC) as

179 Second, 24-, 25-, and 27-hydroxycholesterol concentrations were moderately increa

180 By converting cholesterol to 24S-hydroxycholesterol, cytochrome P450 46A1 (CYP46A1) initi

181 In contrast, 24S-hydroxycholesterol decreased levels of LXR-independent S

182 In neuroblastoma cells, 24S-hydroxycholesterol decreased mRNA levels of the choleste

183 22(R)-Hydroxycholesterol decreased NO (*NO) and increased supe

184 sterol 7alpha-hydroxylase, which degrades 25-hydroxycholesterol, decreased serum IgA.

185 d an NADP+-dependent liver microsomal 7alpha-hydroxycholesterol dehydrogenase (7alpha-HCD) activity t

186 nhibitor of 11beta-HSD, was 75 nM for 7alpha-hydroxycholesterol dehydrogenation and 210 nM for cortic

187 The regulation of LC by U18666A or 25-hydroxycholesterol did not affect total cellular sphingo

188 pathway, such as mevalonate, squalene, or 25-hydroxycholesterol, did not alter barrier development.

189 biosynthesis pathway with atorvastatin or 25-hydroxycholesterol during switching from IFNgamma(+) to

190 romoter" sterols cholesterol, ergosterol, 25-hydroxycholesterol, epicholesterol, or dihydrocholestero

191 year-old human lenses in 0.25 and 0.50 mM 25-hydroxycholesterol failed to increase the levels of solu

192 The IC(50) of 24(S)-hydroxycholesterol for inhibiting Abeta secretion was ap

193 rvastatin, but not placebo, reduced serum 27-hydroxycholesterol from 853 ng/ml [interquartile range (

194 urons of the brain and that secretion of 24S-hydroxycholesterol from this tissue in the mouse is deve

195 nd 4) in a coactivator association assay, 27-hydroxycholesterol functionally activated LXR.

196 cells and polymorphonuclear-neutrophils, 27-hydroxycholesterol functions as a biochemical mediator o

197 n P450c27 is also able to further oxidize 27-hydroxycholesterol giving first an aldehyde and then 3be

198 that P450 46A1 can further metabolize 24(S)-hydroxycholesterol, giving 24,25- and 24,27-dihydroxycho

199 25-Hydroxycholesterol had virtually no effect in cells expr

200 of cells with an alkynyl derivative of 20(S)-hydroxycholesterol has allowed us to directly visualize

201 ed to provide evidence that lanosterol or 25-hydroxycholesterol have either anti-cataractogenic activ

202 lso similar to the in vitro results with 24S-hydroxycholesterol, HMG CoA reductase and squalene synth

203 vated plasma and tissue levels of 25- and 27-hydroxycholesterol; however, levels of another major oxy

204 Soticlestat lowered brain 24S-hydroxycholesterol in a dose-dependent manner and substa

205 eptors seem to mediate adverse effects of 27-hydroxycholesterol in breast cancer when the levels of t

206 ytes incubated in the presence of 25- or 22R-hydroxycholesterol in low calcium.

207 Here we describe a central role for 25-hydroxycholesterol in regulating the immune system.

208 iately generate 25-hydroxycholesterol and 27-hydroxycholesterol in response to LDL cholesterol.

209 ore, epithelial cells released additional 25-hydroxycholesterol in response to pyolysin.

210 The concentrations of 24S-hydroxycholesterol in serum are low in newborn mice, rea

211 450 7A1 oxidation product (dansylated 7alpha-hydroxycholesterol) in human liver extracts using an LC-

212 model to identify its known product, 7alpha-hydroxycholesterol, in liver extracts.

213 Sterols such as 25-hydroxycholesterol inactivate SCAP, suppressing SREBP pr

214 LC extraction by 25-hydroxycholesterol increased APAP-mediated mitophagy and

215 24S-hydroxycholesterol increased levels of SREBP-1 mRNA and

216 22R-hydroxycholesterol increased transglutaminase 1 and invo

217 Furthermore, addition of hydroxycholesterols increased pregnenolone synthesis, su

218 the hydrosoluble cholesterol derivative, 22R-hydroxycholesterol, increased steroid production by the

219 ciency of hydroxylation of cholesterol to 27-hydroxycholesterol indicating that the first hydroxylati

220 o restore inhibition of SREBP cleavage by 25-hydroxycholesterol, indicating that the ACAT deficiency

221 c acid, or eicosapentaenoic acid, but not 25-hydroxycholesterol, induced ACAT1 mRNA levels 1.5--2-fol

222 cium channel blocker nifedipine prevented 25-hydroxycholesterol induction of apoptosis.

223 7beta-Hydroxycholesterol inhibited secretion of soluble APP fr

224 potent suppressor of SREBP-2 activation, 25-hydroxycholesterol, inhibits CYP4F2 mRNA induction by lo

225 25-Hydroxycholesterol is a natural ligand of LXRs that is p

226 ate that in a reconstituted system, after 27-hydroxycholesterol is formed from cholesterol, it is rel

227 by promoters bearing SRE-1 element(s) by 25-hydroxycholesterol is increased by C18 fatty acid supple

228 ummary, neither SREBP-regulated genes nor 27-hydroxycholesterol is involved in setting the ER cholest

229 25-Hydroxycholesterol is produced in mammalian tissues.

230 Oxygenated sterols such as 25-hydroxycholesterol kill Chinese hamster ovary cells beca

231 Here, we show that 25-, 26-, or 27-hydroxycholesterol, known suppressors of cholesterol bio

232 sterol, and desmosterol), and six do not (25-hydroxycholesterol, lanosterol, androstenolone, coprosta

233 /day for 9 weeks in 14 SPG5 patients with 27-hydroxycholesterol levels in serum as the primary outcom

234 Moreover, 27-hydroxycholesterol levels in serum correlated with disea

235 rvastatin treatment can effectively lower 27-hydroxycholesterol levels in serum of SPG5 patients.

236 Similarly, 25-hydroxycholesterol levels in serum were reduced.

237 Mouse 27-hydroxycholesterol levels in the plasma, brain, and live

238 Mouse plasma and hepatic 27-hydroxycholesterol levels were decreased 2.6- and 1.6-fo

239 These effects of 22R-hydroxycholesterol may provide a novel strategy to decre

240 f mature SREBP1, known to be decreased by 25-hydroxycholesterol, mediates the changes in the lipoprot

241 l (CHOL), 7-ketocholesterol (KETO), or 7beta-hydroxycholesterol (OHCHOL).

242 the differing effects of cholesterol and 25-hydroxycholesterol on bilayer properties.

243 of exogenous low density lipoprotein and 25-hydroxycholesterol on HMG-CoA reductase activity from sk

244 The robust effects of 27-hydroxycholesterol on metastasis requires myeloid immune

245 ds also increase the inhibitory effect of 25-hydroxycholesterol on proteolytic maturation and nuclear

246 tion can enhance the inhibitory effect of 25-hydroxycholesterol on sterol and fatty acid biosynthesis

247 AD, we compared the effects of 24(S)- and 27-hydroxycholesterol on the processing of APP and analyzed

248 fects of the enzymatic product of Cyp46, 24S-hydroxycholesterol, on the cholesterol regulatory genes,

249 treatment of normal hairless mice with 22(R)-hydroxycholesterol or 24(S),25-epoxycholesterol resulted

250 genes associated with the formation of 24(S)-hydroxycholesterol or neurosteroids such as CYP46A1, 3al

251 e to the ER after treatment of cells with 25-hydroxycholesterol or sphingomyelinase.

252 Treatment of cells with 25-hydroxycholesterol or statins, which respectively inhibi

253 Conversely, activation of LXRs by either 25-hydroxycholesterol or synthetic TO901317 stimulates myel

254 ells or human placental explants with 22-(R)-hydroxycholesterol or T0901317 resulted in a clear incre

255 rol preferentially activating SF-1 and 22(R)-hydroxycholesterol preferentially activating LXR.

256 der potency for these two receptors, with 25-hydroxycholesterol preferentially activating SF-1 and 22

257 , dihydrocholesterol, epicholesterol, and 25-hydroxycholesterol) promote formation of DPPC-enriched d

258 On the other hand, 27-hydroxycholesterol, rather than cholesterol itself or bi

259 The pro-metastatic actions of 27-hydroxycholesterol requires both polymorphonuclear-neutr

260 These effects were not seen in a 25-hydroxycholesterol-resistant CHO/CD36 mutant (OX(R)), wh

261 CH25H and its product, 25-hydroxycholesterol, restrict replication of diverse viru

262 tive SREBP cleavage-activating protein or 25-hydroxycholesterol significantly suppressed the effect o

263 25-Hydroxycholesterol stimulated calcium uptake by CHO-K1 c

264 the basal, angiotensin-II-stimulated, and 25-hydroxycholesterol-stimulated syntheses of these steroid

265 of apoB100 were concomitantly reversed by 25-hydroxycholesterol, suggesting that the content of matur

266 bition of APP processing in neurons by 24(S)-hydroxycholesterol suggests that CYP46A1 affects the pat

267 t the hCG-induced cAMP synthesis and the 22R-hydroxycholesterol-supported steroidogenesis.

268 B cells with nanomolar concentrations of 25-hydroxycholesterol suppressed IL-2-mediated stimulation

269 Coincubation of cultured hepatocytes with 25-hydroxycholesterol suppressed squalestatin 1-mediated CY

270 n levels, whereas conversely, addition of 25-hydroxycholesterol suppressed SR-BI levels by approximat

271 ic enzyme that converts cholesterol into 24S-hydroxycholesterol, the primary mechanism of cholesterol

272 ith the binding of NAD(+) followed by 7alpha-hydroxycholesterol to form a central complex.

273 undefined, that abolishes the ability of 25-hydroxycholesterol to inhibit the cleavage of both stero

274 We show that addition of cholesterol or 25-hydroxycholesterol to microsomal membranes in vitro bloc

275 After TBI, as after 24S-hydroxycholesterol treatment in vitro, SREBP-1 mRNA leve

276 r-neutrophils and gammadelta-T cells, and 27-hydroxycholesterol treatment results in a decreased numb

277 Plasma and tissue levels of 25- and 27-hydroxycholesterol, two oxysterol substrates of this enz

278 ncreased by certain oxysterols such as 22(R)-hydroxycholesterol via activation of the nuclear hormone

279 7beta-Hydroxycholesterol was also a potent inhibitor of alpha-

280 ed production of Abeta in neurons, but 24(S)-hydroxycholesterol was approximately 1000-fold more pote

281 cumulation of CYP7B1 substrates including 27-hydroxycholesterol was confirmed in serum (n = 19) and c

282 ecific 24-hydroxylase, and its product 24(S)-hydroxycholesterol was not a useful indicator in mouse p

283 In cerebrospinal fluid 27-hydroxycholesterol was reduced by 8.4% but this did not

284 27-Hydroxycholesterol was thought to be the only product fo

285 Levels of 27-hydroxycholesterol were > 4,500 times normal.

286 The Km values for corticosterone and 7alpha-hydroxycholesterol were 1.2 and 1.9 microM, respectively

287 ells, and repression of HMGR synthesis by 25-hydroxycholesterol were confirmed.

288 otent sterol repressor of HMGR synthesis (25-hydroxycholesterol), were assayed on two cell lines: Hep

289 enile hormone III), or liver X receptor (22R-hydroxycholesterol), were injected into the amniotic flu

290 cholanoate together with their precursor, 27-hydroxycholesterol, were identified in liver homogenates

291 e of molecular orientations accessible to 25-hydroxycholesterol when compared to cholesterol.

292 he central cavity of Insig-2 accommodates 25-hydroxycholesterol, whereas TM3 and TM4 engage in Scap b

293 CH25H produces 25-hydroxycholesterol, which inhibited TEV uptake.

294 that SGE-301, a synthetic analogue of 24(S)-hydroxycholesterol, which is a potent and selective posi

295 7beta-Hydroxycholesterol, which is the most cytotoxic of the e

296 phosphatidylcholine monolayers containing 25-hydroxycholesterol, which produce both an upper and a lo

297 e most potent of regulatory oxysterols is 25-hydroxycholesterol, whose biosynthetic enzyme has not ye

298 Even though 25-hydroxycholesterol will compete for cholesterol binding

299 ar endothelial cells were treated with 22(R)-hydroxycholesterol with and without L-4F.

300 a useful method to image intracellular 20(S)-hydroxycholesterol with both high sensitivity and spatia