ライフサイエンスコーパス: HMG-CoA reductase

1 erol uptake (LDL receptor) and biosynthesis (HMG-CoA reductase).

2 drophobic sterol-sensing domains in SCAP and HMG CoA reductase.

3 s closely mimicked by knockdown of zebrafish HMG-CoA reductase.

4 ndent degradation of the biosynthetic enzyme HMG-CoA reductase.

5 on of SREBPs and by enhancing degradation of HMG-CoA reductase.

6 in-induced upregulation of the statin target HMG-CoA reductase.

7 out the binding thermodynamics of statins to HMG-CoA reductase.

8 CC2, ATP-citrate lyase, glycerol kinase, and HMG-CoA reductase.

9 de of geranyl lipid production downstream of HMG-CoA reductase.

10 e was related to the degree of inhibition of HMG-CoA reductase.

11 d was dependent on inhibition of endothelial HMG-CoA reductase.

12 for regulation of the activity of a class I HMG-CoA reductase.

13 M, over 10(4) higher than that for a class I HMG-CoA reductase.

14 nally and structurally different from the ER HMG-CoA reductase.

15 pathway, including the rate-limiting enzyme HMG-CoA reductase.

16 the robust sterol-accelerated degradation of HMG-CoA reductase.

17 ole in the sterol-accelerated degradation of HMG-CoA reductase.

18 ERAD of the cholesterol biosynthetic enzyme HMG-CoA reductase.

19 rs blocks their sensitivity to inhibition of HMG-CoA reductase.

20 nzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase.

21 m (ER)-localized 3-hydroxy-3-methylglutaryl (HMG) CoA reductase.

22 hree lysines are conserved among all Class I HMG-CoA reductases.

23 d mechanism for catalysis is general for all HMG-CoA reductases.

24 e and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.

25 es of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase.

26 le or 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.

27 droxy-3-methylglutaryl-coenzime A reductase (HMG-CoA) reductase.

28 step in ER-associated degradation (ERAD) of HMG CoA reductase, a rate-limiting enzyme in cholesterol

29 Statins inhibit HMG-CoA reductase, a key enzyme in cholesterol synthesis

30 ls and thus shares properties with mammalian HMG-CoA reductase, a sterol-sensing domain protein whose

31 CSA13 inhibited colonic HMG-CoA reductase activity in an FPRL1-dependent manner.

32 hypolipidemic property of FVW-FO and reduced HMG-CoA reductase activity which is proportional to the

33 as treatment with mevalonate, the product of HMG-CoA reductase activity, abrogated these effects and

34 ovascular risk parameters via a reduction in HMG-CoA reductase activity, along with an increase in ar

35 th elevated 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase activity and mRNA levels.

36 latory element binding protein (SREBP-1) and HMG-CoA reductase also were enhanced with alcohol admini

37 nhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, also known as statins, are lipid-low

38 of two proteins with sterol-sensing domains, HMG CoA reductase and SCAP.

39 n vitro results with 24S-hydroxycholesterol, HMG CoA reductase and squalene synthase mRNA levels were

40 an inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zoledronic a

41 cated in the sterol-regulated degradation of HMG-CoA reductase and Insig-1 through ER-associated degr

42 ndeed essential for catalysis by the Class I HMG-CoA reductases and that the revised mechanism for ca

43 both 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and acetyl-CoA acetyltransferase acti

44 le of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and alphaPix.

45 f the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and subsequently the isoprenylation o

46 ethylglutaryl coenzyme A (HMG-CoA) synthase, HMG-CoA reductase, and low-density lipoprotein receptor.

47 Basal protein levels of SREBP2, HMG-CoA reductase, and steroidogenic acute regulatory pr

48 ate, an inhibitor of an enzyme downstream of HMG-CoA reductase, and to gliotoxin, an inhibitor acting

49 Antibodies against HMG-CoA reductase apparently provoke SINAM.

50 treatment and variants in the gene encoding HMG-CoA reductase are associated with reductions in both

51 olesterol metabolism proteins such as PCSK9, HMG-CoA reductase, ATP citrate lyase, and NPC1L1.

52 to assess the dependence of RSV's effects on HMG-CoA reductase blockade.

53 maging sensor, we confirm that inhibition of HMG-CoA reductase blocks MYC phosphorylation in vivo.

54 Here, we show that inhibition of HMG-CoA reductase by atorvastatin (AT) blocks both MYC p

55 possibility in principle that inhibition of HMG-CoA reductase by statins in proximal tubule cells ma

56 droxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) by statins has shown potential effica

57 ds; TNF-alpha antagonists; and inhibitors of HMG-CoA reductase, calcineurin, IMPDH, PDE4, PI-3 kinase

58 HMG-CoA reductase catalyzes the four-electron reduction

59 ident enzyme 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase catalyzes the rate-limiting step in s

60 They inhibit HMG-CoA reductase competitively, reduce LDL levels more

61 In yeast, the membrane-bound HMG-CoA reductase degradation (HRD) ubiquitin-ligase com

62 The HMG-COA reductase degradation 1 (HRD1) and degradation o

63 The E3 ubiquitin ligase HMG-coA reductase degradation 1 homolog (Hrd1) and, cons

64 biquitylated by a protein complex termed the Hmg-CoA reductase degradation ligase (HRD-ligase), and d

65 The HRD (HMG-CoA reductase degradation) pathway is a conserved ro

66 these mutants cod mutants for the control of HMG-CoA reductase degradation.

67 edded ubiquitin ligases, in yeast Hrd1/Der3 (HMG-CoA reductase degradation/degradation of the ER) and

68 the identification of COD1/SPF1 (control of HMG-CoA reductase degradation/SPF1) through genetic stra

69 pulmonary disease alveolar macrophages in an HMG-CoA reductase-dependent manner.

70 n an 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase-dependent manner.

71 esulted from mutations in the genes encoding HMG-CoA reductase, downstream enzymes in the mevalonate

72 rank order of potency for inhibition of the HMG-CoA reductase enzyme.

73 f the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase enzyme (statins) are cholesterol-lowe

74 15(S)-HETE by inducing HMG-CoA reductase expression caused increased farnesylat

75 hepatic low-density lipoprotein receptor and HMG-CoA reductase expression in ApoE-p50-DKO but not in

76 nzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, facilitating its ubiquitination and

77 MG-CoA synthase and acetoacetyl-CoA thiolase/HMG-CoA reductase from E. faecalis.

78 We have isolated the gene encoding HMG-CoA reductase from Listeria monocytogenes and expres

79 istidine and lysine of Pseudomonas mevalonii HMG-CoA reductase, function in catalysis and that the ge

80 pplementation with the enzymatic products of HMG-CoA reductase functionally rescued lymphangiogenic s

81 e product represents the first example of an HMG-CoA reductase fused to another enzyme.

82 nsmembrane span ER-resident Hmg2p isozyme of HMG-CoA reductase fused to GFP, which undergoes regulate

83 enic to human chromosome 5q13.3, between the HMG-CoA reductase gene (HMGCR) and RAS p21 protein activ

84 ltiple tests on all 33 SNPs evaluated in the HMG-CoA reductase gene as well as for all 148 SNPs evalu

85 ls heterozygous for a genetic variant in the HMG-CoA reductase gene may experience significantly smal

86 ynthesis, apoptosis induced by inhibitors of HMG-CoA reductase, geranylgeranyltransferase, or RhoA ki

87 However, in L. monocytogenes HMG-CoA reductase histidine 143 and methionine 186 are p

88 valonate biosynthetic pathway and the enzyme HMG-CoA reductase (HMG-R) have been investigated.

89 d expression of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase (Hmg1) under iron starvation, reduced

90 ysiologically regulated degradation of yeast HMG-CoA reductase (Hmg2p) occurs by the HRD endoplasmic

91 ors during acute kidney injury that regulate HMG CoA reductase (HMGCR) activity, the rate-limiting st

92 accumulation, mediated in part by increased HMG CoA reductase (HMGCR) levels.

93 reased SR-B1, increased ABCA1, and increased HMG CoA reductase (HMGCR) protein and its mRNA.

94 rol synthesis, HMG CoA synthase (HMGCS1) and HMG CoA reductase (HMGCR), were also reduced in PGC1alph

95 arteriovenous angiogenesis by targeting the HMG-CoA reductase (HMGCR) pathway.

96 An autoantibody directed against HMG-CoA reductase (HMGCR), the pharmacologic target of s

97 Statins block HMG-CoA reductase (HMGCR), the rate-limiting enzyme of t

98 of the rate-limiting enzyme in the pathway, HMG-CoA reductase (HMGCR).

99 Mammalian 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR) undergoes sterol-dependent, en

100 3-Hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR), the rate-limiting enzymes of

101 lso causes a 65% protein content decrease in HMG-CoA reductase (HMGR) and a 28% decrease in sterol sy

102 SREBP cleavage-activating protein (SCAP) and HMG-CoA reductase (HMGR) both possess SSDs required for

103 HMG-CoA reductase (HMGR) catalyzes a rate-limiting step

104 The integral ER membrane protein HMG-CoA reductase (HMGR) is a key enzyme of the mevalona

105 HMG-CoA reductase (HMGR) is an enzyme critical for cellu

106 ingle ER-resident membrane proteins, such as HMG-CoA reductase (HMGR), can induce a dramatic restruct

107 SCAP (SREBP cleavage activating protein) and HMG-CoA reductase (HMGR).

108 red for the feedback inhibition of SREBP and HMG-CoA reductase (HMGR).

109 ) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) has been linked to cholestero

110 ucture of the class II Pseudomonas mevalonii HMG-CoA reductase in complex with the statin drug lovast

111 W-FO) on serum and liver lipids, activity of HMG-CoA reductase in liver microsomes and EPA+DHA incorp

112 The hypothesis that inhibition of HMG-CoA reductase in renal proximal tubule cells could r

113 3 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isopr

114 droxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase)) in mevalonate and cholesterol synthe

115 HMG-CoA reductase inhibition has a biphasic dose-depende

116 evalonate, implying a dependence on vascular HMG-CoA reductase inhibition.

117 tween 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition, coronary endothelial func

118 Depleting endogenous cholesterol with the HMG CoA reductase inhibitor lovastatin leads to a 2-fold

119 dominant-negative AKT, or treatment with the HMG CoA reductase inhibitor lovastatin suppressed AKT ph

120 The hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor lovastatin depletes cellula

121 Lovastatin, an HMG-CoA reductase inhibitor (statin), was immunomodulato

122 Clinically achievable levels of an HMG-CoA reductase inhibitor attenuate GAD in murine hear

123 and O2- in endothelium after exposure to the HMG-CoA reductase inhibitor cerivastatin were undertaken

124 patients were medicated with aspirin and an HMG-CoA reductase inhibitor for >/=6 weeks before enteri

125 mouse model of NF1 has been treated with the HMG-CoA reductase inhibitor lavastatin, which improves t

126 et al., in this issue, demonstrates that the HMG-CoA reductase inhibitor lovastatin can normalize pro

127 dermal tumors we evaluated the effect of the HMG-CoA reductase inhibitor lovastatin on the Ewing's sa

128 Treatment of pregnant mice with the HMG-CoA reductase inhibitor lovastatin reduced sterol sy

129 To test whether lipid lowering with an HMG-CoA reductase inhibitor retards macrophage accumulat

130 e effects of diabetes and treatment with the HMG-CoA reductase inhibitor rosuvastatin (RSV) were exam

131 These data indicate that the HMG-CoA reductase inhibitor rosuvastatin has a favorable

132 receive either vehicle or treatment with the HMG-CoA reductase inhibitor simvastatin (2 mg/kg per day

133 iposomes ([S]-LIP), that are loaded with the HMG-CoA reductase inhibitor simvastatin [S], were evalua

134 In vivo, the HMG-CoA reductase inhibitor simvastatin dose-dependently

135 In this study, we analyzed the effect of the HMG-CoA reductase inhibitor simvastatin on disease manif

136 hyl-beta-cyclodextrin, 2) treatment with the HMG-CoA reductase inhibitor simvastatin, and 3) shRNA-me

137 were partially rescued by treatment with the HMG-CoA reductase inhibitor simvastatin.

138 It is unclear whether the addition of an HMG-CoA reductase inhibitor to interferon or a more pote

139 f cholesterol biosynthesis using statins (an HMG-CoA reductase inhibitor) significantly increased the

140 ne monooxygenase inhibitor), or pravastatin (HMG-CoA reductase inhibitor).

141 All study subjects also received an HMG-CoA reductase inhibitor, and prophylaxis for cytomeg

142 demonstrated the potential of lovastatin, a HMG-CoA reductase inhibitor, for the restoration of impa

143 Simvastatin, an HMG-coA reductase inhibitor, is known to attenuate infla

144 LDLR SRE was observed in the presence of the HMG-CoA reductase inhibitor, lovastatin, when PP2A activ

145 imvastatin-treated animals in vivo, that the HMG-CoA reductase inhibitor, simvastatin, augments the c

146 ere treated with and without simvastatin, an HMG-CoA reductase inhibitor.

147 ssive 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) therapy on surroga

148 f the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor simvastatin to healthy subj

149 novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, rosuvastatin, on endotheli

150 ensin-converting enzyme (ACE) inhibitors and HMG CoA reductase inhibitors (statins) have more than do

151 that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductase inhibitors (statins) might slow aorti

152 beta-hydroxy-beta-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) within 60 days a

153 nt of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors--"statins." Initial studie

154 Hydroxymethylglutaryl (HMG) CoA reductase inhibitors (statins) may favorably af

155 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, e.g., simvastatin, have b

156 hen administered at a high dosage (including HMG-CoA reductase inhibitors >75 mg/day/adult).

157 of antiviral and proviral agents, including HMG-CoA reductase inhibitors (antiviral) and corticoster

158 Interactions between UCN-01 and HMG-CoA reductase inhibitors (ie, statins) have been exa

159 Orally administered cholesterol-lowering HMG-CoA reductase inhibitors (known as statins), which e

160 This study tested whether HMG-CoA reductase inhibitors (statins) alter interstitia

161 se cholesterol is a product of this pathway, HMG-CoA reductase inhibitors (statins) are used to treat

162 The HMG-CoA reductase inhibitors (statins) are widely prescr

163 plementary activity between these agents and HMG-CoA reductase inhibitors (statins) based on their ab

164 Recent evidence suggests that HMG-CoA reductase inhibitors (statins) can prevent the p

165 HMG-CoA reductase inhibitors (statins) have been shown t

166 Recent evidence suggests that HMG-CoA reductase inhibitors (statins) have beneficial e

167 There is experimental evidence to show that HMG-CoA reductase inhibitors (statins) may inhibit proli

168 HMG-CoA reductase inhibitors (statins) reduce GAD in hum

169 The ability of cholesterol lowering HMG-CoA reductase inhibitors (statins) to improve outcom

170 of low-density lipoprotein cholesterol with HMG-CoA reductase inhibitors (statins).

171 Collectively, these findings indicate that HMG-CoA reductase inhibitors act through a Ras farnesyla

172 ese results suggest that lipid lowering with HMG-CoA reductase inhibitors alters plaque biology by re

173 These data indicate that HMG-CoA reductase inhibitors ameliorate atherosclerosis

174 he design and synthesis of a novel series of HMG-CoA reductase inhibitors based upon a substituted py

175 These data suggest that HMG-CoA reductase inhibitors can both inhibit cell proli

176 ion, it has been shown in vitro that several HMG-CoA reductase inhibitors can decrease HCV RNA replic

177 synthesis of the delta-lactone moiety of the HMG-CoA reductase inhibitors compactin and mevinolin.

178 We hypothesized that HMG-CoA reductase inhibitors decrease exocytosis of Weib

179 study of fluvastatin, pravastatin, and other HMG-CoA reductase inhibitors for the prevention of GVD i

180 HMG-CoA reductase inhibitors have been shown to upregula

181 ng of antiviral activity associated with the HMG-CoA reductase inhibitors implies an important role f

182 ts explain some of the beneficial effects of HMG-CoA reductase inhibitors in cardiac transplantation.

183 Finally, HMG-CoA reductase inhibitors inhibited signaling by vasc

184 HMG-CoA reductase inhibitors interfered with angiogenesi

185 ial exocytosis is a novel mechanism by which HMG-CoA reductase inhibitors may reduce vascular inflamm

186 ive study designed to evaluate the effect of HMG-CoA reductase inhibitors on atherosclerosis.

187 HMG-CoA reductase inhibitors or statins are associated w

188 Recent studies suggest that HMG-CoA reductase inhibitors promote vascular endothelia

189 ay represent an important mechanism by which HMG-CoA reductase inhibitors protect against the develop

190 Lipid lowering with HMG-CoA reductase inhibitors reduces acute coronary even

191 transplant recipients should be treated with HMG-CoA reductase inhibitors starting early posttranspla

192 HMG-CoA reductase inhibitors such as statins are cholest

193 angiogenesis and an antiangiogenic effect of HMG-CoA reductase inhibitors with possible important the

194 Statins (HMG-CoA reductase inhibitors) are the most prescribed cl

195 tDNA transcription; second, that a subset of HMG-CoA reductase inhibitors, combined with propranolol,

196 HMG-coA reductase inhibitors, commonly known as statins,

197 l components of red mold fermented products, HMG-CoA reductase inhibitors, did not exacerbate pre-exi

198 Statins, a class of HMG-CoA reductase inhibitors, display pleiotropic immuno

199 In conclusion, atorvastatin, and likely all HMG-CoA reductase inhibitors, does not inhibit HCV RNA r

200 idemia in mild to moderate CKD patients with HMG-CoA reductase inhibitors.

201 ing pathway constitutes a novel function for HMG-CoA reductase inhibitors.

202 d for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are related to r

203 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) can exert benefi

204 hough 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) can restore endo

205 ntly, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been the ma

206 rative effects of hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins) on oxidative str

207 etimibe) and 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins) provides a power

208 Three-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) reduce coronary

209 RBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins), and selective s

210 The 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are widely prescribed for

211 the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors atorvastatin and simvastat

212 the 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors known as statins have anti

213 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins are competitive

214 Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are well tolera

215 ugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins, are used in th

216 Three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors protect the vasculature fr

217 ents, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are shown to interfere wi

218 ether 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, described as inhibitors o

219 s, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, have anti-inflammatory ef

220 ials, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, in the form of statins, h

221 ch as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, may prevent the developme

222 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, reduce the in

223 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, target liver

224 tins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, which are approved for ch

225 th 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase) inhibitors (statins).

226 In addition, inhibitors of HMG-CoA reductase interfere with insulin release and thi

227 Here, we show that degradation of HMG CoA reductase is accelerated by the sterol-induced b

228 for a statin drug confirmed that E. faecalis HMG-CoA reductase is a class II enzyme.

229 Therefore, HMG-CoA reductase is a critical regulator of MYC phospho

230 Degradation of HMG-CoA reductase is also stimulated by various forms of

231 at the overall structure of L. monocytogenes HMG-CoA reductase is likely similar to the known structu

232 The activity of the class I Syrian hamster HMG-CoA reductase is regulated by phosphorylation-dephos

233 Furthermore, the peroxisomal HMG-CoA reductase is significantly more resistant to inh

234 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a critical enzyme in the mevalonat

235 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase is a rate-limiting enzyme in the meva

236 Hydroxymethylglutaryl-CoA (HMG-CoA) reductase is the primary target in the current

237 ss II 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, is essential for in vitro growth of

238 The yeast HMG-CoA reductase isozyme Hmg2, like its mammalian count

239 zyme, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase isozyme, Hmg1p, induce assembly of nu

240 AP leads to ER retention, insig-1 binding to HMG CoA reductase leads to accelerated degradation that

241 HMG-CoA reductase levels are regulated in response to st

242 The inhibition of HMG-CoA reductase may be a useful target for the treatme

243 oteins 1c and 2, acetyl-CoA carboxylase, and HMG-CoA reductase mRNAs/proteins and inactive non-phosph

244 The HMG-CoA reductase of the thermophilic archaeon Sulfolobu

245 In the absence of HMG-CoA reductase, only the atorvastatin active o-hydrox

246 h mevalonolactone, the downstream product of HMG-CoA reductase, or by ectopic expression of myristoyl

247 with mevalonate, an immediate metabolite of HMG-CoA reductase, partially inhibited vasodilation to s

248 The up-regulation of the HMG-CoA reductase pathway in the endothelium is the majo

249 l fibrosis via FPRL1-dependent modulation of HMG-CoA reductase pathway.

250 findings demonstrate for the first time that HMG-CoA reductase plays a determinant role in 12/15-Lox-

251 -associated myopathy, statin-associated anti-HMG-CoA reductase-positive autoimmune myopathy, and stat

252 e autoimmune myopathy, and statin-naive anti-HMG-CoA reductase-positive myopathy.

253 Anti-HMG-CoA reductase-positive patients can be further subdi

254 ts of AT are blocked by cotreatment with the HMG-CoA reductase product mevalonate.

255 oteins for SREBP-dependent activation of the HMG-CoA reductase promoter.

256 influx protein), ABCA1 (a FC exporter), and HMG CoA reductase protein/mRNA levels were also assessed

257 tionation and immunoelectron microscopy that HMG-CoA reductase protein and activity are localized bot

258 ly, deletion of SET1 leads to a reduction in HMG-CoA reductase protein and total cellular ergosterol.

259 The amount of HMG-CoA reductase protein was elevated out of proportion

260 er increase in SREBP2 and down-regulation of HMG-CoA reductase protein.

261 y one 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase protein which is localized exclusivel

262 e restored by mevalonate, the product of the HMG CoA reductase reaction, and by ligands for the nucle

263 hen be reduced by NADPH to mevalonate in the HMG-CoA reductase reaction and/or cleaved to acetoacetat

264 histidine during the first redox step of the HMG-CoA, reductase reaction was suggested by the ability

265 alyzed both the acetoacetyl-CoA thiolase and HMG-CoA reductase reactions.

266 Understanding HMG-CoA reductase regulation has tremendous implications

267 A comparative analysis of SREBP and HMG-CoA reductase regulation in mammals, yeast, and flie

268 atin are weak inhibitors of L. monocytogenes HMG-CoA reductase, requiring micromolar concentrations f

269 l-Mevalonate, the product of HMG-CoA reductase, reversed atorvastatin's effects on an

270 s for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, significantly suppress de novo chole

271 NA levels of the cholesterol synthesis genes HMG CoA reductase, squalene synthase, and FPP synthase b

272 ors of 3-hydroxy-3-methylglutaryl coenzyme A HMG-CoA reductase (statins) have emerged as promising to

273 Sequence comparisons with other HMG-CoA reductases suggest that the essential active-sit

274 Simvastatin, a potent inhibitor of HMG-CoA reductase, suppressed 15(S)-HETE-induced Rac1 ac

275 Finally, we show that inhibition of HMG-CoA reductase suppresses MYC phosphorylation through

276 inhibitor of 3-hydroxy-3-methylglutaryl CoA (HMG CoA) reductase that inhibits cholesterol synthesis.

277 Inhibitors of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase (the statins) reduce levels of choles

278 genetic variant known to mimic inhibition of HMG-CoA reductase (the intended drug target) with the sa

279 roxy-3-methyl glutaryl coenzyme A reductase (HMG-CoA reductase), the key enzyme in the cholesterol bi

280 t homogeneity and was shown to be a class II HMG-CoA reductase, the first class II eubacterial biosyn

281 Statins lower cholesterol by inhibiting HMG-CoA reductase, the rate-limiting enzyme of the metab

282 Unlike most other HMG-CoA reductases, the S. aureus enzyme exhibits dual c

283 or of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme for cholest

284 hat inhibit 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase, the rate-limiting enzyme in the synt

285 or of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-limiting step for cholester

286 g for 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the target enzyme that is inhibited

287 es of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase: the class I enzymes of eukaryotes an

288 ns are cholesterol-lowering drugs, targeting HMG-CoA reductase, thereby reducing the risk of coronary

289 Statins inhibit HMG-CoA reductase to reduce the synthesis of cholesterol

290 Statins inhibit HMG-CoA reductase to reduce the synthesis of cholesterol

291 ay inhibitors targeting downstream enzyme to HMG-CoA reductase (upstream enzyme) and farnesyl-pyropho

292 nhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase used for the therapeutic reduction of

293 f three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, used commonly for the treatment of h

294 asma cholesterol levels, liver expression of HMG-CoA reductase was found to be approximately 2-fold l

295 The activity of HMG-CoA reductase was reduced (p<0.05) in the FVW-FO fed

296 nt in rat liver nuclei, and its target gene, HMG-CoA reductase, was expressed above adult levels prio

297 he three conserved lysines of Syrian hamster HMG-CoA reductase were mutated to alanine.

298 me 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reductase), which catalyzes a rate-controlling s

299 BIAD1 to the cholesterol biosynthetic enzyme HMG CoA reductase, which is subject to sterol-accelerate

300 n of SREBP-2 and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, which results in increased cholester