ライフサイエンスコーパス: methylglutaryl

1 Use of 3-hydroxyl-3-methylglutaryl-3 coenzyme A reductase (HMGCR) inhibitors

2 rom clinical trials suggest that 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors may help

3 nism for this putative effect of 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors, and whe

4 ed by compactin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA (HMG CoA) reductase that inhibits cho

5 c reticulum (ER)-resident enzyme 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase catalyzes the rat

6 Statins are inhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase used for the ther

7 Inhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, also known as st

8 ate degradation of the ER enzyme 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reductase), which

9 olesterol synthesis pathway with 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase) inhibit

10 MAD3 encodes 3-hydroxy-3-methylglutaryl CoA reductase (HMG1), which functions in

11 g fatty acid synthase (FASN) and 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR).

12 The enzymes 3-hydroxy-3-methylglutaryl CoA reductase (HMGR) and C24-sterol methy

13 ars to control the expression of 3-hydroxy-3-methylglutaryl CoA reductase (HMGR) and l-phenylalanine

14 -2 (COX-2) inhibitors and statins [hydroxy-3-methylglutaryl CoA reductase (HMGR) inhibitors] inhibit

15 Inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase (statins) reduce signs of d

16 ng the mevalonate (MVA) pathway, 3-Hydroxy-3-Methylglutaryl CoA Reductase 1 (HMGR1), interacts with D

17 n the two rate-limiting enzymes: 3-hydroxy-3-methylglutaryl CoA reductase and squalene monooxygenase.

18 reticulum (ER)-localized enzyme 3-hydroxy-3-methylglutaryl CoA reductase catalyzes a rate-limiting s

19 enase-2 inhibitor), and statins (3-hydroxy-3-methylglutaryl CoA reductase inhibitors) inhibit colon c

20 The statins, 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, have pleiotropi

21 abolic product of the acetyl CoA/3-hydroxy-3-methylglutaryl CoA reductase reaction.

22 y-3-methylglutaryl CoA synthase, 3-hydroxy-3-methylglutaryl CoA reductase), and fatty acid synthase.

23 nd pravastatin are inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase, and are used as antihyperc

24 acid, a downstream metabolite of 3-hydroxy-3-methylglutaryl CoA reductase, confirming that simvastati

25 t selectively inhibit the enzyme 3-hydroxy-3-methylglutaryl CoA reductase, leading to decreased chole

26 Inhibition of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme o

27 cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl CoA reductase, thus inducing the ubiquiti

28 sterol-stimulated degradation of 3-hydroxy-3-methylglutaryl CoA reductase.

29 cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl CoA reductase.

30 3-Hydroxy-3-methylglutaryl CoA synthase (HMGS) catalyzes the first c

31 Haloferax 3-hydroxy-3-methylglutaryl CoA synthase is sensitive to inactivation

32 uired for cholesterol synthesis (3-hydroxy-3-methylglutaryl CoA synthase, 3-hydroxy-3-methylglutaryl

33 tyl-CoA and acetoacetyl-CoA into 3-hydroxy-3-methylglutaryl CoA.

34 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase (HMGL) is involved in

35 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase catalyzes the divalen

36 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase is a key enzyme in th

37 PC1L1) inhibitor (ezetimibe) and 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors (stati

38 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or st

39 roceeds via an unprecedented (R)-3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) stereospecific route in nat

40 ays between the OleA homologues, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase and the fatty acid

41 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase catalyzes the firs

42 after they decrease the level of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA).

43 RAF V600E and a ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA lyase (HMGCL).

44 s expression of ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA lyase and promotes the formation of t

45 3-Hydroxy-3-methylglutaryl-CoA lyase-like protein (HMGCLL1) has been

46 normal yeast ER membrane protein 3-hydroxy-3-methylglutaryl-CoA reductase (Hmg2p) undergoes ERAD that

47 ines, SUGP1 knockdown stimulated 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) alternative splicin

48 creases the protein abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and ATP-citrate lya

49 ecognition protein (SRP) or anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibodies (Abs), a

50 combination with variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.

51 udies report that utilization of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) inhibitors called s

52 3-Hydroxy-3-methylglutaryl-CoA reductase (HMGCR) is the target of th

53 ent-binding protein 1 (Srebp1c), 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr), and cytochrome P45

54 s a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the intended drug

55 nt binding factor 2 (Srebf2) and 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr).

56 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) catalyzes the format

57 The 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) enzyme catalyzes the

58 ticulum (ER) and the activity of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) imbedded therein res

59 mised proteasomal degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) or deficient in ubiq

60 Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) protein and mRNA are

61 eedback-regulated degradation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR).

62 s of isoprenoids is catalysed by 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR).

63 by 84% with empagliflozin, while 3-hydroxy-3-methylglutaryl-CoA reductase activity and total choleste

64 ximately 20-fold) decrease in ER 3-hydroxy-3-methylglutaryl-CoA reductase activity in vitro.

65 are associated with decreases in 3-hydroxy-3-methylglutaryl-CoA reductase and increases in ATP-bindin

66 Both 3-Hydroxy-3-Methylglutaryl-CoA Reductase and Proprotein Convertase S

67 k Trial trial, we found that the 3-Hydroxy-3-Methylglutaryl-CoA Reductase genetic score, known to be

68 dependent manner and whether the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor atorvastatin can

69 ed the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, on hippocampal A

70 2 in response to Ang II by using 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors and isoprenoid i

71 The use of statins, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors that block the s

72 cent reports suggest that statins (hydroxy-3-methylglutaryl-CoA reductase inhibitors) exhibit potenti

73 ition, our results indicate that 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, a class of chol

74 ase (squalene synthase), but not 3-hydroxy-3-methylglutaryl-CoA reductase or farnesyl diphosphate syn

75 The endoplasmic reticulum enzyme 3-hydroxy-3-methylglutaryl-CoA reductase produces mevalonate, which

76 ciated degradation of the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase represents one mechanism by

77 ase Subtilisin/Kexin type 9, and 3-Hydroxy-3-Methylglutaryl-CoA Reductase single nucleotide polymorph

78 pharmacologic inhibitors of the 3-hydroxy-3-methylglutaryl-CoA reductase that are potent regulators

79 farnesyl-pyrophosphate synthase, 3-hydroxy-3-methylglutaryl-CoA reductase, and low density lipoprotei

80 reatment reduced the activity of 3-hydroxy-3-methylglutaryl-CoA reductase, but it did not change acti

81 doplasmic reticulum (ER) enzyme, 3-hydroxy-3-methylglutaryl-CoA reductase, catalyzes the production o

82 nd -2 increased on promoters for 3-hydroxy-3-methylglutaryl-CoA reductase, fatty-acid synthase, and s

83 ized that statins, inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase, inhibit cardiac hypertroph

84 ect is through the inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase.

85 ive effect, indicating the role of hydroxy-3-methylglutaryl-CoA reductase.

86 in cholesterol synthesis beyond 3-hydroxy-3-methylglutaryl-CoA reductase.

87 ect repression of sterol enzymes 3-hydroxy-3-methylglutaryl-CoA synthase 1 and methylsterol monooxyge

88 Of these 10 genes, the 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2 (HMGCS2) was the highest u

89 etabolism pathway, mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), as a major down-

90 hain acyl-CoA dehydrogenase, and 3-hydroxy-3-methylglutaryl-CoA synthase 2, and enhances fat metaboli

91 of VMH ketone production with a 3-hydroxy-3-methylglutaryl-CoA synthase inhibitor reversed the 3- to

92 Replacement of 3-hydroxy-3-methylglutaryl-CoA synthase's glutamate 95 with alanine

93 te, comprising a ketosynthase, a 3-hydroxy-3-methylglutaryl-CoA synthase, a dehydratase, a decarboxyl

94 o the hydrophobic active site of 3-hydroxy-3-methylglutaryl-CoA synthase, site-directed mutagenesis w

95 synthases, polyketide synthases, 3-hydroxy-3-methylglutaryl-CoA synthases, and biosynthetic thiolases

96 stine, the expression of Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2), the gene encoding the

97 Furthermore, we show that the 3-hydroxy-3-methylglutaryl-CoA-reductase inhibitor mevastatin, which

98 Treatment with the 3-hydroxy-3-methylglutaryl coenyzme A reductase inhibitors (or stati

99 signal recognition particle and 3-hydroxy-3-methylglutaryl-coenzime A reductase (HMG-CoA) reductase.

100 ically active Haloferax volcanii 3-hydroxy-3-methylglutaryl coenzyme A (CoA) synthase (EC 2.3.310).

101 3-Hydroxy-3-methylglutaryl coenzyme A (CoA) synthase (HMGCS) catalyz

102 alcohol dehydrogenase, elongation factor-TU, methylglutaryl coenzyme A (CoA), acyl CoA synthetase, ox

103 pting the H. capsulatum homolog of 3-hydroxy-methylglutaryl coenzyme A (HMG CoA) lyase (HCL1).

104 e possible by the development of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors

105 n-2 receptor blockers, and beta-hydroxy-beta-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors

106 ig-1 also binds to the ER enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, facilitat

107 erol biosynthetic pathway enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase.

108 rotein predicted to possess both 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and acetyl

109 o assess the association between 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition

110 the possible effects of a novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor,

111 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

112 Although 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

113 Three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

114 n randomized, controlled trials, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

115 iotropic activities reported for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

116 Statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

117 re, cholesterol-lowering agents, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

118 Statins, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

119 ical trials have shown that the 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

120 tensin-receptor blockers (ARBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors

121 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase is a rate-

122 the sterol biosynthetic enzyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase isozyme, H

123 2 cells) that expresses only one 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase protein wh

124 hich encodes a putative class II 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, is essent

125 atins, a class of inhibitors for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, significa

126 (NK-104) is a novel inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-

127 n is a specific inhibitor of three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, used comm

128 ed efferocytosis in vitro in an 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase-dependent

129 ysis has revealed two classes of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase.

130 There are two classes of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase: the class

131 ine 110 of Enterococcus faecalis 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase was mutated

132 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, a member o

133 promoters of the genes encoding 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, farnesyl d

134 ate pyrophosphate decarboxylase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, HMG-CoA re

135 olate the mvaS gene that encodes 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, the second

136 Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A HMG-CoA reductase (statins) ha

137 3-hydroxy-3-methylglutaryl coenzyme A inhibitors (statins) inhibit m

138 s of lipid modification with the 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, or statins.

139 tazone) as well as metformin and 3-hydroxy-3-methylglutaryl coenzyme A inhibitors.

140 at block the rate-limiting step (3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase))

141 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCoAr) provides a

142 ilisation of cholesterol, in the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) activity, an

143 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) inhibitors,

144 homocysteine (Hcy) revealed that 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) was upregula

145 mRNA leading to the formation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), a main regu

146 stimulates the ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), which catal

147 t histone deacetylase (HDAC) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) by having a h

148 The enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) has a key reg

149 have demonstrated that statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) inhibitors, a

150 Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) can modula

151 or expression) and biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase activity) are regula

152 Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase and effective lipid-

153 , not only statins targeting the 3-hydroxy-3-methylglutaryl coenzyme A reductase but also inhibitors

154 osynthesis through inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase but has no effect on

155 had the catalytic domain of the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene integrated into

156 e effect, confirming the role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition and sugge

157 poprotein (LDL) cholesterol with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor ("statin")

158 ge of long-term persistence with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) t

159 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) t

160 vational studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) u

161 Simvastatin, the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, effective

162 pleiotropic effects of statins, 3-hydroxy-3 methylglutaryl coenzyme A reductase inhibitor, have been

163 We studied the effect of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, simvastat

164 As 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

165 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

166 nce is available to suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

167 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

168 Although 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

169 py and when co-administered with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

170 ors, proton-pump inhibitors, and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

171 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

172 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

173 Cardiovascular risk reduction by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

174 Hepatic 3-methylglutaryl coenzyme A reductase inhibitors (statins)

175 evention benefit of therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

176 trospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

177 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

178 cholesterol-lowering properties, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

179 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins)

180 The hepatotoxic potential of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in patien

181 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors or "stati

182 We found that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors rapidly a

183 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are an i

184 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are asso

185 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are curr

186 t beneficial effects of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) on renal

187 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) promote

188 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors), commonl

189 he debate whether statins, 3-hydroxymethyl-3-methylglutaryl coenzyme A reductase inhibitors, are safe

190 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, statins,

191 results indicate that 'statins', 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, which ar

192 synthase kinase-3 inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.

193 on upon Insig-1 binding, whereas 3-hydroxy-3-methylglutaryl coenzyme A reductase is ubiquitinated and

194 ciated with a marked increase in 3-hydroxy-3-methylglutaryl coenzyme A reductase protein.

195 3-hydroxy-3-methylglutaryl coenzyme A reductase regulates the produc

196 the first step of this pathway (3-hydroxy-3-methylglutaryl coenzyme A reductase) reduces the growth

197 HMGCR(3-Hydroxy-3-methylglutaryl coenzyme A reductase), the direct target

198 y acid synthase, squalene epoxidase, hydroxy-methylglutaryl coenzyme A reductase), while genes involv

199 l-regulated ubiquitination marks 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-determining

200 n and proteasomal degradation of 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-limiting enz

201 rol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the cholesterol

202 -1 (SREBP-1), fatty acid synthase, hydroxy-3-methylglutaryl coenzyme A reductase, farnesyl pyrophosph

203 Statins, inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase, have been used succ

204 By inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, statins not only re

205 ER) allows for ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting e

206 tatins as dependent on inhibition of hydroxy-methylglutaryl coenzyme A reductase, we treated C57Bl/6

207 body by specifically inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which is a rate-lim

208 or the continued proteolysis of 3-hydroxyl-3-methylglutaryl coenzyme A reductase, which may undermine

209 cleavage-activating protein) and 3-hydroxy-3-methylglutaryl coenzyme A reductase.

210 phogen receptor, Patched, and to 3-hydroxy-3-methylglutaryl coenzyme A reductase.

211 The 3-hydroxy-3-methylglutaryl coenzyme A synthases (HCSs) are responsib

212 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMGR) inhibitors, m

213 duction, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity, and cell w

214 yofiber cascades downstream from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG Co-A) reductase inhibitio

215 deposition, we hypothesised that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductase inhibitors

216 The enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase catalyzes the

217 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase catalyzes the

218 rly, apolipoprotein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) ha

219 ogenesis, we studied the role of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and alphaP

220 as mediated by inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and subseq

221 Inhibitors of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase enzyme (st

222 t systemic administration of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor

223 termine the effect of aggressive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor

224 This study evaluated whether 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors

225 Until recently, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors

226 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors

227 and smooth muscle cells, such as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors

228 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a criti

229 Mevastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-

230 SNPs were in the gene coding for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the targe

231 toacetyl-coenzyme A thiolase and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.

232 e signal recognition particle or 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.

233 The mevalonate [3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase] pathway s

234 Ceestatin binds to 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase and irrever

235 ,2-(13)C]acetyl-CoA to wild-type 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase is characte

236 re a class of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMGcoA) reductase, a critical

237 Inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase)

238 sterol-sensing domains (SSD) of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-R) and sterol r

239 Autoantibodies recognizing 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are found in

240 3-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMGCR) encodes the

241 mevalonate pathway, such as the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) gene.

242 r alone or in combination with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) inhibitor (s

243 ipitation of in vitro-translated 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) protein.

244 biosynthesis pathway upstream of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the target

245 al recognition particle (SRP) or 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).

246 e those to genetic inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).

247 in the genes encoding PCSK9 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR; the target o

248 Induction of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR; EC 1.1.1.34)

249 we identified a mutation in the 3-hydroxy-3-methylglutaryl-Coenzyme A reductase 1b (hmgcr1b) gene th

250 Inhibitors of 3-hydroxy-3-methylglutaryl-Coenzyme A reductase and isoprenylation a

251 cleation was also induced by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin

252 hosphate binding activity by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor simvastati

253 hown in mice that pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, prevents

254 The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors ("statins

255 The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins)

256 Due to the efficacy of 3-hydroxy 3-methylglutaryl-coenzyme A reductase inhibitors (statins)

257 The use of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins)

258 The advent of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins)

259 Purpose The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins)

260 The role of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins)

261 The 3-hydroxyl-3-methylglutaryl-coenzyme A reductase inhibitors, or stati

262 els were noticeably resistant to 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors.

263 erated degradation of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase is one of several me

264 rs were associated with elevated 3-hydroxy-3-methylglutaryl-coenzyme A reductase mRNA levels and anti

265 its severity, inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway to protect a

266 e main synthetic products in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway.

267 cholesterol biosynthetic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase results from its ste

268 ontinuation or non-initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase therapy in patients

269 n (SREBP)-1a, SREBP-1c, SREBP-2, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylg

270 ns: 1) sterol-induced binding to 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an action that lead

271 element-binding protein 2, human 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and human low-densi

272 iosynthesis rate-limiting enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and increased plasm

273 Inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, angiotensin-convert

274 LDL-cholesterol by inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are among the most

275 ypercholesterolemia, inhibit the 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting e

276 ge-activating protein (SCAP) and 3-hydroxy-3-methylglutaryl-coenzyme A reductase.

277 transactivate the genes encoding 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE1 (HMGR1) and MAKIBIS

278 ylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylglutaryl-coenzyme A synthase, and LDL receptor mRN

279 ation of lipogenic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty acid synthase,

280 HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase (HMGR) catalyzes th

281 Statins, or HMG CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors, are dru

282 in kinase (SnRK1) phosphorylates 3-hydroxy-3-methylglutaryl-Coenzyme A, nitrate reductase and sucrose

283 several new autoantibodies (e.g. 3-hydroxy-3 methylglutaryl-coenzyme-A reductase and melanoma differe

284 The 3-hydroxy-3-methylglutaryl-coenzyme-A reductase inhibitors, or stati

285 ignaling pathways, inhibition of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase may also result in p

286 mponents include a halogenase, a 3-hydroxy-3-methylglutaryl enzyme cassette for polyketide beta-branc

287 uercetin-3-O-hexoside, quercetin 3-hydroxy-3-methylglutaryl-glycoside), an O-triglycosyl flavanone (n

288 4'-methyl ether and scoparin), a 3-hydroxy-3-methylglutaryl glycosyl flavonol (3-hydroxy-3-methylglut

289 ethylglutaryl glycosyl flavonol (3-hydroxy-3-methylglutaryl glycosyl quercetin) and a flavone O-glyco

290 plasmic reticulum (ER)-localized 3-hydroxy-3-methylglutaryl (HMG) CoA reductase.

291 etermine whether atorvastatin, a 3-hydroxy-3-methylglutaryl (HMG)-co-enzyme A (CoA) reductase inhibit

292 Mammalian 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR) undergoes ster

293 3-Hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR), the rate-limi

294 The hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor lovastatin

295 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, e.g., sim

296 reased expression of SREBP-2 and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, which results in inc

297 iquely among condensing enzymes, 3-hydroxy-3-methylglutaryl (HMG)-CoA synthase (HMGS) catalyzes the f

298 posure to beta-cyclodextrins and 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A reductase inhibitors (st

299 a gamma-chlorination step on (S)-3-hydroxy-3-methylglutaryl mediated by Cur halogenase, a non-haem Fe

300 The branching enzyme, 3-hydroxy-3-methylglutaryl synthase (HMGS), catalyzes the aldol addi