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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 posure was genetically proxied inhibition of HMG-CoA reductase and secondary exposures were genetical

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

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

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

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

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

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

44 Antibodies against HMG-CoA reductase apparently provoke SINAM.

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

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

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

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

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

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

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

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

53 HMG-CoA reductase catalyzes the four-electron reduction

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

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

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

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

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

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

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

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

62 served ER-anchored ubiquitin ligases such as HMG-CoA reductase degradation1 (Hrd1).

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

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

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

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

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

68 15(S)-HETE by inducing HMG-CoA reductase expression caused increased farnesylat

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

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

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

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

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

74 risk reduction from medications that inhibit HMG-CoA reductase; further research is needed to underst

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

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

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

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

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

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

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

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

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

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

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

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

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

88 sociated degradation (ERAD) of ubiquitinated HMG CoA reductase (HMGCR), the rate-limiting enzyme of t

89 BIAD1 to the cholesterol biosynthetic enzyme HMG CoA reductase (HMGCR), thereby inhibiting its endopl

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

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

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

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

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

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

96 3-Hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR), the rate-limiting enzymes of

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

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

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

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

101 HMG-CoA reductase (HMGR) undergoes feedback-regulated de

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

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

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

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

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

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

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

109 3 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isopr

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

111 In the primary analysis, genetically proxied HMG-CoA reductase inhibition equivalent to a 1-mmol/L (3

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

113 CA1/2 mutation carriers, genetically proxied HMG-CoA reductase inhibition was associated with lower o

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

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

116 ed with the PKG activator sildenafil and the HMG CoA reductase inhibitor atorvastatin to further redu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 eptor (IGF1R) inhibitor, and fluvastatin, an HMG-CoA reductase inhibitor, as potential chemopreventiv

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 ular 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatment for dysl

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

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

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

152 PKG phosphorylates K-RAS and HMG CoA reductase inhibitors reduce K-RAS farnesylation

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

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

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

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

157 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors, e.g., simvastatin, have b

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

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

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

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

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

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

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

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

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

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

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

169 HMG-CoA reductase inhibitors (statins) improve cutaneous

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

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

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

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

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

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

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

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

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

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

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

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

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

183 HMG-CoA reductase inhibitors have been shown to upregula

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

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

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

187 HMG-CoA reductase inhibitors interfered with angiogenesi

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

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

190 HMG-CoA reductase inhibitors or statins are associated w

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

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

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

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

195 HMG-CoA reductase inhibitors such as statins are cholest

196 Statins are HMG-CoA reductase inhibitors that are known to inhibit c

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

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

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

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

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

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

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

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

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

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

207 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) can exert benefi

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

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

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

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

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

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

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

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

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

217 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins are competitive

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

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

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

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

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

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

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

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

226 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, reduce the in

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

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

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

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

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

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

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

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

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

236 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a critical enzyme in the mevalonat

237 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase is a rate-limiting enzyme in the meva

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

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

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

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

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

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

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

245 were used to proxy therapeutic inhibition of HMG-CoA reductase, Niemann-Pick C1-Like 1 (NPC1L1) and p

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

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

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

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

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

251 nate [3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase] pathway synthesizes lipids for G-pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 Understanding HMG-CoA reductase regulation has tremendous implications

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 Interestingly, HMG-CoA reductase, the rate-limiting enzyme in cholester

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

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

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

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

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

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 Genetically proxied inhibition of HMG-CoA reductase was significantly associated with lowe

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

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