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

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

2 y secondary to inappropriate derepression of cholesterol biosynthesis.

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

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

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

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

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

8 glutaryl CoA reductase, leading to decreased cholesterol biosynthesis.

9 own-regulates lipid metabolism, particularly cholesterol biosynthesis.

10 cytoskeleton regulation, and fatty acid and cholesterol biosynthesis.

11 omplementing the statin drugs, which inhibit cholesterol biosynthesis.

12 e encodes a sterol dehydrogenase involved in cholesterol biosynthesis.

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

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

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

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

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

18 s having high cholesterol absorption and low cholesterol biosynthesis.

19 represents the first committed step in human cholesterol biosynthesis.

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

21 osphatidylcholine that influences macrophage cholesterol biosynthesis.

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

23 of cholesterol because of the inhibition of cholesterol biosynthesis.

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

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

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

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

28 unable to suppress LDL receptor activity and cholesterol biosynthesis.

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

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

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

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

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

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

35 described end-product feedback regulation of cholesterol biosynthesis.

36 l proliferation, leukocyte extravasation and cholesterol biosynthesis.

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

38 olesterol could be slowed by inhibiting late cholesterol biosynthesis.

39 rol efflux, but also simultaneously inhibits cholesterol biosynthesis.

40 nonsteroidal inhibitors of MDR also inhibit cholesterol biosynthesis.

41 y regulated by sterol molecules derived from cholesterol biosynthesis.

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

43 4 methyl groups in one of the later steps of cholesterol biosynthesis.

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

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

46 including unexpected upregulation of retinal cholesterol biosynthesis.

47 l absorption, cholesterol precursors reflect cholesterol biosynthesis.

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

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

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

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

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

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

54 ed to lower cholesterol levels by inhibiting cholesterol biosynthesis.

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

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

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

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

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

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

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

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

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

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

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

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

67 nation chemotherapeutic strategies targeting cholesterol biosynthesis and PARP inhibition.

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

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

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

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

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

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

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

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

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

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

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

79 Proper coordination of cholesterol biosynthesis and trafficking is essential to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 27-hydroxycholesterol, known suppressors of cholesterol biosynthesis, enhance SF-1-dependent transcr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 Cholesterol biosynthesis in somatic cells is controlled

151 Cholesterol biosynthesis in the endoplasmic reticulum (E

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

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

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

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

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

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

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

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

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

161 Cholesterol biosynthesis inhibitors caused growth inhibi

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

163 Cholesterol biosynthesis is an integral part of HCV RNA

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

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

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

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

168 Cholesterol biosynthesis is regulated by end product neg

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

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

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

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

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

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

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

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

177 These bacteria lack genes for cholesterol biosynthesis or modification.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 Host cholesterol biosynthesis remains unchanged after infecti

200 Genetic disorders of cholesterol biosynthesis result in accumulation of chole

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 Cholesterol biosynthesis was depressed in hyperplastic l

220 Third, cholesterol biosynthesis was moderately decreased in TT1

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

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

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

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

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

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

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

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

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

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

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