ライフサイエンスコーパス: cholesterol biosynthesis

1 ls that promoted optimal GC polarization and cholesterol biosynthesis.

2 enzyme A that can be used for fatty acid and cholesterol biosynthesis.

3 4 methyl groups in one of the later steps of cholesterol biosynthesis.

4 EBP-2, a master transcriptional activator of cholesterol biosynthesis.

5 but can be modulated by agents that disrupt cholesterol biosynthesis.

6 including unexpected upregulation of retinal cholesterol biosynthesis.

7 l absorption, cholesterol precursors reflect cholesterol biosynthesis.

8 sion as well as the more commonly considered cholesterol biosynthesis.

9 olesterol to cholesterol in the last step of cholesterol biosynthesis.

10 P-1c and SREBP-2 and genes of fatty acid and cholesterol biosynthesis.

11 li-Opitz syndrome (SLOS) caused by defective cholesterol biosynthesis.

12 agonist and compactin, a statin inhibitor of cholesterol biosynthesis.

13 ns, are essential for feedback inhibition of cholesterol biosynthesis.

14 ed to lower cholesterol levels by inhibiting cholesterol biosynthesis.

15 plays an important role in the regulation of cholesterol biosynthesis.

16 E caused a pronounced inhibition of de novo cholesterol biosynthesis.

17 -CoA reductase that are potent regulators of cholesterol biosynthesis.

18 e CE but an approximately 3-fold decrease in cholesterol biosynthesis.

19 lesterol, indicative of a marked decrease in cholesterol biosynthesis.

20 glutaryl CoA reductase, leading to decreased cholesterol biosynthesis.

21 own-regulates lipid metabolism, particularly cholesterol biosynthesis.

22 cytoskeleton regulation, and fatty acid and cholesterol biosynthesis.

23 omplementing the statin drugs, which inhibit cholesterol biosynthesis.

24 e encodes a sterol dehydrogenase involved in cholesterol biosynthesis.

25 CR7), an enzyme catalyzing the final step of cholesterol biosynthesis.

26 assumed to stem from their ability to reduce cholesterol biosynthesis.

27 on of mevalonate, a rate-controlling step in cholesterol biosynthesis.

28 ase (HMGCoAR) is required for isoprenoid and cholesterol biosynthesis.

29 s having high cholesterol absorption and low cholesterol biosynthesis.

30 represents the first committed step in human cholesterol biosynthesis.

31 CoA) reductase, the rate-limiting enzyme for cholesterol biosynthesis.

32 osphatidylcholine that influences macrophage cholesterol biosynthesis.

33 ve inhibitors of the rate-limiting enzyme in cholesterol biosynthesis.

34 of cholesterol because of the inhibition of cholesterol biosynthesis.

35 rred with a similar potency as inhibition of cholesterol biosynthesis.

36 al of two C-4 methyl groups in post-squalene cholesterol biosynthesis.

37 mes caused by defects in the final stages of cholesterol biosynthesis.

38 , which catalyzes a rate-controlling step in cholesterol biosynthesis.

39 unable to suppress LDL receptor activity and cholesterol biosynthesis.

40 e reactions are the first committed steps in cholesterol biosynthesis.

41 ctase (HMGR) catalyzes the committed step in cholesterol biosynthesis.

42 ents, including peroxisomes, are involved in cholesterol biosynthesis.

43 plays an essential role in the regulation of cholesterol biosynthesis.

44 that functions in one of the later steps of cholesterol biosynthesis.

45 ffected Bpa mice support a role for Nsdhl in cholesterol biosynthesis.

46 described end-product feedback regulation of cholesterol biosynthesis.

47 ple malformation syndrome due to a defect in cholesterol biosynthesis.

48 olesterol could be slowed by inhibiting late cholesterol biosynthesis.

49 nonsteroidal inhibitors of MDR also inhibit cholesterol biosynthesis.

50 1.14.99.7) is a key rate-limiting enzyme in cholesterol biosynthesis.

51 ts novel components for modules, such as for cholesterol biosynthesis.

52 n of PD-L1, and enrichment for signatures of cholesterol biosynthesis.

53 alene to 2,3(S)-oxidosqualene, a key step in cholesterol biosynthesis.

54 p < 0.05 for each), which suggests increased cholesterol biosynthesis.

55 tumor suppressor gene through inhibition of cholesterol biosynthesis.

56 ion (but not lipofuscin) via upregulation of cholesterol biosynthesis.

57 y secondary to inappropriate derepression of cholesterol biosynthesis.

58 l proliferation, leukocyte extravasation and cholesterol biosynthesis.

59 nol; and (iii) weak cerebellar regulation of cholesterol biosynthesis.

60 rol efflux, but also simultaneously inhibits cholesterol biosynthesis.

61 y regulated by sterol molecules derived from cholesterol biosynthesis.

62 hway in WD-fed rats was the 'Superpathway of cholesterol biosynthesis' (10/29 genes regulated, p = 1.

63 ing region of the rate controlling enzyme of cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coe

64 Statins, the widely used inhibitors of cholesterol biosynthesis, also have immunomodulatory pro

65 egulated genes, 19 genes are associated with cholesterol biosynthesis and 5 genes specify aspects of

66 signatures of cholesterol suggest increased cholesterol biosynthesis and accumulation in the materna

67 affects the expression of genes involved in cholesterol biosynthesis and alters the cholesterol leve

68 nhibitors that are known to inhibit cellular cholesterol biosynthesis and are clinically prescribed t

69 lular cholesterol accumulation by inhibiting cholesterol biosynthesis and by promoting cholesterol ex

70 causes both repression of genes controlling cholesterol biosynthesis and cellular uptake and inducti

71 esults demonstrate that MDV hijacks cellular cholesterol biosynthesis and cholesterol trafficking to

72 pression of many genes involved in lipid and cholesterol biosynthesis and decreased levels of cholest

73 pension derivatives highlighted switching in cholesterol biosynthesis and expression of five key gene

74 c mechanism of EBP-mediated isomerization in cholesterol biosynthesis and how this protein may act as

75 The mechanism by which genes involved in cholesterol biosynthesis and import are preferentially u

76 PR-Cas9-based genetic screens and identified cholesterol biosynthesis and iron uptake as essential me

77 e (SM) is the second rate-limiting enzyme in cholesterol biosynthesis and is regulated both transcrip

78 atins) are related to reductions in cellular cholesterol biosynthesis and isoprenoid levels.

79 with wild-type) include lipid, steroid, and cholesterol biosynthesis and metabolism; nucleosome and

80 nation chemotherapeutic strategies targeting cholesterol biosynthesis and PARP inhibition.

81 argeting HMGCR activity primarily influences cholesterol biosynthesis and prenylation of signaling pr

82 ieved in humans by simultaneously inhibiting cholesterol biosynthesis and promoting ABCG5/ABCG8-media

83 rization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor ac

84 inhibits the expression of genes involved in cholesterol biosynthesis and reduces plasma cholesterol

85 t StARD3 overexpression results in increased cholesterol biosynthesis and Src kinase activity in brea

86 and dampens the activity of a key enzyme in cholesterol biosynthesis and that a receptor deficiency

87 esterification does not cause inhibition of cholesterol biosynthesis and that inhibition of choleste

88 ce of environmental compounds that interrupt cholesterol biosynthesis and that methodologically hiPSC

89 ctase domain of LBR plays a critical role in cholesterol biosynthesis and that this process is essent

90 ata reveal a reciprocal relationship between cholesterol biosynthesis and the clearance of mutant neu

91 mevalonate (MEV) cascade is responsible for cholesterol biosynthesis and the formation of the interm

92 terone-sensitive pathway is involved in both cholesterol biosynthesis and the processing of LDL-deriv

93 enzymatic function in steroid biosynthesis, cholesterol biosynthesis and thyroid hormone metabolic p

94 Proper coordination of cholesterol biosynthesis and trafficking is essential to

95 replication and mevalonic acid, sterol, and cholesterol biosynthesis and trafficking/redistribution.

96 Our data also demonstrate that changes in cholesterol biosynthesis and uptake are only observed in

97 vestigated the effects of HIV-1 infection on cholesterol biosynthesis and uptake using microarrays.

98 ence that MDV replication depends on de novo cholesterol biosynthesis and uptake.

99 ranscription regulators of genes involved in cholesterol biosynthesis and uptake.

100 ojection neurons in vivo essentially require cholesterol biosynthesis and which cell types support ne

101 ering fatty acid composition and restricting cholesterol biosynthesis and, thus, ligand availability

102 e growth, protein transport, RNA processing, cholesterol biosynthesis, and apoptosis via death domain

103 that genes associated with lipid metabolism, cholesterol biosynthesis, and circadian rhythm were most

104 relationships between membrane microdomains, cholesterol biosynthesis, and endothelial function will

105 Statins are potent inhibitors of cholesterol biosynthesis, and in clinical trials, statin

106 tion at early times, and lipid biosynthesis, cholesterol biosynthesis, and mediators of immune respon

107 ) inhibits cellular proliferation, decreases cholesterol biosynthesis, and triggers apoptosis, at lea

108 parable to those previously shown to inhibit cholesterol biosynthesis, and, can be derived from chole

109 ges in terms related to P450s, transporters, cholesterol biosynthesis, and, unexpectedly, antigen pre

110 Adult neurons that lack cholesterol biosynthesis are mainly supported by astrocy

111 vel 3-substituted quinuclidine inhibitors of cholesterol biosynthesis are reported.

112 We also define SYK/PI3K-dependent cholesterol biosynthesis as a feed-forward mechanism of

113 because they have a compensatory increase in cholesterol biosynthesis as a result of increased choles

114 ene epoxidase, an oxygen-requiring enzyme in cholesterol biosynthesis, as a driver of dysregulated me

115 ns and was concomitant with reduced UPR- and cholesterol biosynthesis-associated gene expression.

116 l enhanced expression of the GTPase RAC1 and cholesterol-biosynthesis-associated genes together with

117 nuclidine series previously known to inhibit cholesterol biosynthesis at the squalene synthase step,

118 asmic reticulum membrane protein involved in cholesterol biosynthesis, autophagy, oligodendrocyte for

119 cell metabolism, particularly glycolysis and cholesterol biosynthesis before the preovulatory surge o

120 oenzyme A reductase, statins not only reduce cholesterol biosynthesis but also decrease the formation

121 known for catalysing a rate-limiting step in cholesterol biosynthesis, but it also participates in th

122 he enzymatic role of DHCR7 as a reductase in cholesterol biosynthesis, but may also involve defects i

123 vivo) and a pathway for direct regulation of cholesterol biosynthesis by bile acids.

124 Disruption of distal cholesterol biosynthesis by conditional inactivation of

125 liver X receptor alpha (LXRalpha), regulates cholesterol biosynthesis by directly silencing the expre

126 r, we demonstrate that progesterone inhibits cholesterol biosynthesis by interfering with MDR activit

127 At 20 micromol/l, troglitazone inhibited cholesterol biosynthesis by more than 80%, resulting in

128 port prevents cholesterol esterification and cholesterol biosynthesis by preventing sterol substrates

129 indicates that oocytes regulate cumulus cell cholesterol biosynthesis by promoting the expression of

130 r supports the conclusion that inhibition of cholesterol biosynthesis by troglitazone is unlikely to

131 r, which encodes the rate-limiting enzyme of cholesterol biosynthesis called 3-hydroxy-3-methyl-gluta

132 ent-binding protein 2, a master regulator in cholesterol biosynthesis, can be activated in a noncanon

133 reductase), which catalyzes the last step in cholesterol biosynthesis, cause the disease.

134 RSH/SLOS is due to an inborn error of cholesterol biosynthesis caused by mutation of the 3 bet

135 t, we demonstrate that progesterone inhibits cholesterol biosynthesis, causing the accumulation of a

136 AI-resistant cells activate endogenous cholesterol biosynthesis (CB) through stable epigenetic

137 -Opitz syndrome (SLOS) is an inborn error of cholesterol biosynthesis characterized by diminished cho

138 arch that demonstrate chemical inhibition of cholesterol biosynthesis compromises neurodevelopment.

139 oupled with oral and selective inhibition of cholesterol biosynthesis derived from OSC inhibition (ra

140 lesterol biosynthesis and that inhibition of cholesterol biosynthesis does not cause inhibition of ch

141 ive reactions such as fatty acid elongation, cholesterol biosynthesis, drug metabolism, and methemogl

142 sociated with CDP, including peroxisomal and cholesterol biosynthesis dysfunction and other inborn er

143 ologically or genetically induced defects in cholesterol biosynthesis, embryonic cholesterol transpor

144 27-hydroxycholesterol, known suppressors of cholesterol biosynthesis, enhance SF-1-dependent transcr

145 ions involved in de novo lipogenesis, TG and cholesterol biosynthesis, FA elongation and oxidation, l

146 ly unrecognized role of Tcf7l2 in control of cholesterol biosynthesis for CNS myelinogenesis.

147 e best inhibition (following oral dosing) of cholesterol biosynthesis from mevalonate (ED50 = 2.7 mg/

148 Finally, we show that cholesterol biosynthesis from mevalonate can occur in se

149 SREBP2 and reduces chromatin acetylation at cholesterol-biosynthesis gene loci.

150 In that context, Tcf7l2 directly activates cholesterol biosynthesis genes and cholesterol supplemen

151 not rapamycin, significantly down-regulates cholesterol biosynthesis genes in a 4E-BP1-dependent man

152 ing revealed a coordinated downregulation of cholesterol biosynthesis genes in LG2KO mice that was as

153 tis is associated with altered expression of cholesterol biosynthesis genes in synovial biopsies of p

154 We also found that many cholesterol biosynthesis genes were decreased in cells o

155 Additionally, 45,X NCCs increase cholesterol biosynthesis genes while reducing transcript

156 nregulated genes specifically predicted that cholesterol biosynthesis genes would be affected by miR-

157 ctivation of SREBP2, the master regulator of cholesterol biosynthesis genes.

158 rogram, dominating SREBP2 via its binding to cholesterol-biosynthesis genes and its facilitation of t

159 d stress responses, as well as downregulated cholesterol biosynthesis, glycolysis, and interleukin IL

160 n of cholesterol precursors due to defective cholesterol biosynthesis has been reported to result in

161 rs involving enzyme defects in post-squalene cholesterol biosynthesis have been identified-desmostero

162 Veratrum alkaloids and distal inhibitors of cholesterol biosynthesis have been studied for more than

163 C. burnetii lacks enzymes for de novo cholesterol biosynthesis; however, the organism encodes

164 showed a much stronger inhibition of overall cholesterol biosynthesis (IC(50) 2.3 nM) than BM 15.766

165 ng vesicle trafficking, DNA modification and cholesterol biosynthesis, identifying these as potential

166 The rate of cholesterol biosynthesis in 7- to 9-day-old PEX2(-/-) mi

167 erol levels through increased fatty acid and cholesterol biosynthesis in adipose and liver.

168 n of the unfolded protein response (UPR) and cholesterol biosynthesis in adult rat sensory neurons.

169 ue to CHO cells; progesterone also inhibited cholesterol biosynthesis in all human cell lines tested.

170 This conversion is not required in cholesterol biosynthesis in animals but is a key step in

171 y, we examined the effect of troglitazone on cholesterol biosynthesis in cultured Chinese hamster ova

172 ctors, particularly, BMP15 and GDF9, promote cholesterol biosynthesis in cumulus cells, probably as c

173 chemical effects was conducted by assessing cholesterol biosynthesis in human induced pluripotent st

174 l uptake can be regulated independently from cholesterol biosynthesis in mammalian cells.

175 ces cerevisiae ergosterol biosynthesis, like cholesterol biosynthesis in mammals, is regulated at the

176 tions of action on the inhibition of hepatic cholesterol biosynthesis in rats.

177 confirming a novel and fundamental role for cholesterol biosynthesis in regulating LCD.

178 d correlates with suppression of cSREBP1 and cholesterol biosynthesis in sensitive cell lines.

179 Cholesterol biosynthesis in somatic cells is controlled

180 Cholesterol biosynthesis in the endoplasmic reticulum (E

181 back upregulation of genes in the pathway of cholesterol biosynthesis in the lovastatin-treated G5G8(

182 these oxysterols to inhibit isoprenoid-based cholesterol biosynthesis in these cells.

183 t neurons, we have conditionally ablated the cholesterol biosynthesis in these neurons in mice either

184 cific effects of aging, uncovering increased cholesterol biosynthesis in type-2 pneumocytes and lipof

185 eductase is not the rate-limiting enzyme for cholesterol biosynthesis in UT2 cells.

186 innate immunity, fatty acid biosynthesis and cholesterol biosynthesis) in separate modules identified

187 tions identified several pathways related to cholesterol biosynthesis, including cholesterol metaboli

188 in cell proliferation, immune responses, and cholesterol biosynthesis, increased infiltration of neut

189 Squalestatin (1 micromol/L), an inhibitor of cholesterol biosynthesis, increased mdr2 mRNA levels by

190 of a skin-specific regulatory mechanism for cholesterol biosynthesis, independent of cholesterol reg

191 for the most part the direct consequence of cholesterol biosynthesis inhibition and the subsequent c

192 of MG63 cells with mevinolin, a statin-type cholesterol biosynthesis inhibitor that depletes the con

193 tamoxifen and the other in complex with the cholesterol biosynthesis inhibitor U18666A.

194 Cholesterol biosynthesis inhibitors caused growth inhibi

195 cancer recurrence, while the use of statins, cholesterol biosynthesis inhibitors widely used for trea

196 Cholesterol biosynthesis is an integral part of HCV RNA

197 that a steroid hormone's ability to inhibit cholesterol biosynthesis is correlated with: 1) its gene

198 In this study, we provide new evidence that cholesterol biosynthesis is important to myeloid cell gr

199 wth and maximal cholesterol demand, neuronal cholesterol biosynthesis is indispensable.

200 Feedback regulation of cholesterol biosynthesis is mediated by membrane-bound t

201 Cholesterol biosynthesis is regulated by end product neg

202 cate that PSDP, a recognized intermediate of cholesterol biosynthesis, is present in immune effector

203 p regulated pathways are involved in steroid/cholesterol biosynthesis, liver cirrhosis, and connectiv

204 to interferon or a more potent inhibitor of cholesterol biosynthesis may be required to inhibit HCV

205 We hypothesize that inhibition of cholesterol biosynthesis may result from the disruption

206 ently activated T cells is necessary for the cholesterol biosynthesis metabolic gene expression progr

207 coordinated repression of genes involved in cholesterol biosynthesis, namely, HMGCR, FDFT1, SQLE, an

208 the majority, including enzymes involved in cholesterol biosynthesis, of changes were regulated in m

209 account for some of the effects of perturbed cholesterol biosynthesis on animal development.

210 all three of these enzymes are required for cholesterol biosynthesis, only inhibition of the most up

211 EBPs, important regulators of fatty acid and cholesterol biosynthesis, operate via a post-transcripti

212 s should be considered as two key factors in cholesterol biosynthesis or metabolism disorders, where

213 These bacteria lack genes for cholesterol biosynthesis or modification.

214 ivated receptor activity, and the isoprenoid/cholesterol biosynthesis pathway additionally suggest a

215 FBXW7 knockdown induced activation of the cholesterol biosynthesis pathway and changed the prenyla

216 GCR) encodes the rate-limiting enzyme in the cholesterol biosynthesis pathway and is inhibited by sta

217 odulates RhoB activity via alteration of the cholesterol biosynthesis pathway and, consequently, of t

218 Here, we identify the cholesterol biosynthesis pathway as a key regulator of t

219 ranked the DNA replication pathway above the cholesterol biosynthesis pathway as a R273H mtp53 activa

220 results point to Th PRMT5 and its downstream cholesterol biosynthesis pathway as promising therapeuti

221 l to cholesterol is the last reaction in the cholesterol biosynthesis pathway catalyzed by the micros

222 d only intermediates, not the end product of cholesterol biosynthesis pathway for these functions.

223 risingly revealed that downregulation of the cholesterol biosynthesis pathway improves neurological p

224 n is available on the peroxisomal isoprenoid/cholesterol biosynthesis pathway in normal brain tissue

225 iets, yellow perch juveniles up-regulate the cholesterol biosynthesis pathway in order to maintain ho

226 e for one or more products of the mevalonate/cholesterol biosynthesis pathway in the progression of p

227 ndogenous role for AhR as a regulator of the cholesterol biosynthesis pathway independent of its DRE-

228 sitivity to SQLE inhibition results not from cholesterol biosynthesis pathway inhibition, but rather

229 sterol lowering but via effects dependent on cholesterol biosynthesis pathway inhibition.

230 indings suggest that the upregulation of the cholesterol biosynthesis pathway may negatively impact f

231 in vivo and highlight EBP, an enzyme in the cholesterol biosynthesis pathway that could potentially

232 Inhibition of the cholesterol biosynthesis pathway with atorvastatin or 25

233 clasts, inhibits a rate-limiting step in the cholesterol biosynthesis pathway, essential for osteocla

234 elta8,Delta7-isomerase), a key enzyme in the cholesterol biosynthesis pathway, which was previously i

235 ike)), an essential enzyme in the ergosterol/cholesterol biosynthesis pathway.

236 the majority of which were intrinsic to the cholesterol biosynthesis pathway.

237 of the Dhcr7 enzyme, the last enzyme in the cholesterol biosynthesis pathway.

238 triggering factor for down regulation of the cholesterol biosynthesis pathway.

239 factor (TGF)-beta gene and the genes of the cholesterol biosynthesis pathway.

240 crease in the expression of 4 enzymes of the cholesterol biosynthesis pathway.

241 excess cholesterol generated by an activated cholesterol biosynthesis pathway.

242 nd linked to specific transformations in the cholesterol biosynthesis pathway.

243 assess the effects of small molecules on the cholesterol biosynthesis pathway.

244 encoding the majority of enzymes forming the cholesterol biosynthesis pathway.

245 ATP citrate lyase is an enzyme in the cholesterol-biosynthesis pathway upstream of 3-hydroxy-3

246 g analysis showed the Complement Cascade and Cholesterol Biosynthesis Pathways as the most enriched a

247 that nuclear factor kappa B (NF-kappaB) and cholesterol biosynthesis pathways were activated, and sp

248 pregulation of genes involved in the Wnt and cholesterol biosynthesis pathways.

249 variant detected significant upregulation of cholesterol biosynthesis pathways.

250 predicted an increase in cancer, immune, and cholesterol biosynthesis pathways.

251 se proper CNS development depends on de novo cholesterol biosynthesis, peroxisomes must play a critic

252 However, of the ~20 enzymes in cholesterol biosynthesis, post-translational regulation

253 ich mutations in enzymes catalyzing steps in cholesterol biosynthesis produce a buildup of sterol int

254 Inhibiting the last step in cholesterol biosynthesis profoundly reduced tissue and p

255 our study uncovers a master regulator of the cholesterol-biosynthesis program and an attractive targe

256 ast cancer (TNBC) exhibits a hyper-activated cholesterol-biosynthesis program that is strongly linked

257 ions as an essential activator of the entire cholesterol-biosynthesis program, dominating SREBP2 via

258 as evidenced by elevated mRNA levels of the cholesterol biosynthesis rate-limiting enzyme 3-hydroxy-

259 Host cholesterol biosynthesis remains unchanged after infecti

260 Genetic disorders of cholesterol biosynthesis result in accumulation of chole

261 t, we demonstrate that progesterone inhibits cholesterol biosynthesis resulting in the accumulation o

262 ly genome lacks several enzymes required for cholesterol biosynthesis, ruling out cholesterol and cho

263 pression of the critical master regulator of cholesterol biosynthesis, SREBP1.

264 mice through repression of genes involved in cholesterol biosynthesis, such as Hmgcr, which encodes t

265 tradiol, which is a more potent inhibitor of cholesterol biosynthesis than expected based solely on h

266 or-activated receptor-alpha by precursors of cholesterol biosynthesis, that underlie common changes (

267 reases in mRNAs encoding multiple enzymes of cholesterol biosynthesis, the LDL receptor, and fatty ac

268 that SREBP-2 regulates all genes involved in cholesterol biosynthesis, the LDL receptor, and PCSK9; a

269 ucial role that lanosterol synthase plays in cholesterol biosynthesis, there is great interest in the

270 serum cholesterol through inhibiting hepatic cholesterol biosynthesis thereby upregulating the hepati

271 heterodimer partner also directly regulates cholesterol biosynthesis through inhibition of 3-hydroxy

272 d chemical probe (SH42), we inhibited distal cholesterol biosynthesis through selective inhibition of

273 ion of scavenger receptor BI, and to inhibit cholesterol biosynthesis through the direct repression o

274 d function of the PM lipid rafts: they bring cholesterol biosynthesis to completion by participating

275 novel pathway by which UV radiation acts on cholesterol biosynthesis to control Ca(2+) influx by Ora

276 cholesterol, or mevastatin, an inhibitor of cholesterol biosynthesis, to deplete cholesterol.

277 a suggest that targeting beta-catenin and/or cholesterol biosynthesis, together with AKT, could have

278 xidized oxysterols are strong suppressors of cholesterol biosynthesis under specific pathological con

279 qualene epoxidase, a rate-limiting enzyme in cholesterol biosynthesis, underlies suppression in one l

280 , whose enhanced degradation probably limits cholesterol biosynthesis upon insulin deficiency.

281 e identify shared transcriptional changes in cholesterol biosynthesis upon loss of top-ranked genes.

282 I also found that the inhibition of cholesterol biosynthesis using statins (an HMG-CoA reduc

283 esterol uptake, using Ldlr(-/-) cells, or of cholesterol biosynthesis, using mevastatin-treated WT ce

284 del, representing dioxin-mediated effects on cholesterol biosynthesis via the mevalonate pathway, had

285 Cholesterol biosynthesis was depressed in hyperplastic l

286 Third, cholesterol biosynthesis was moderately decreased in TT1

287 h, triglyceride synthesis was unchanged, but cholesterol biosynthesis was reduced by 20%, and acetate

288 th defective efflux and sterol accumulation, cholesterol biosynthesis was reduced in Abcg1(-/-)/Abcg4

289 g hormone (TSH) exerts an inductor effect on cholesterol biosynthesis, we aimed to investigate the re

290 Because lathosterol is an intermediate in cholesterol biosynthesis, we conclude it is unlikely tha

291 commonly found for enzymes of post-squalene cholesterol biosynthesis, we have identified a novel ass

292 Transcripts encoding enzymes for cholesterol biosynthesis were downregulated in both Bmp1

293 alyses revealed that the effects of ROCK2 on cholesterol biosynthesis were instead mediated via a nov

294 he variability, genes encoding regulators of cholesterol biosynthesis were reproducibly down-regulate

295 d biosynthesis of which 17 of 18 involved in cholesterol biosynthesis were significantly up regulated

296 In mammals, SREBP-2 controls cholesterol biosynthesis, whereas SREBP-1 controls triac

297 Srebp2, the master transcription factor for cholesterol biosynthesis, which in turn transactivates N

298 disorders and mouse models of post-squalene cholesterol biosynthesis will then be discussed.

299 ammatory circuit that links perturbations in cholesterol biosynthesis with activation of innate immun

300 hare the same Delta-14 reductase activity in cholesterol biosynthesis, yet little is known about thei