ライフサイエンスコーパス: HMG-CoA

1 HMG-CoA (3-hydroxy-3-methylglutarylcoenzyme A) reductase

2 HMG-CoA lyase (HMGCL) is crucial to ketogenesis, and inh

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

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

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

6 HMG-CoA reductase catalyzes the four-electron reduction

7 HMG-CoA reductase inhibitors (statins) improve cutaneous

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

9 HMG-CoA reductase inhibitors or statins are associated w

10 HMG-CoA reductase inhibitors such as statins are cholest

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

12 HMG-CoA synthase forms a homodimer.

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

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

15 cells increased expression of KLF2 through a HMG-CoA/prenylation-dependent pathway.

16 olog of 3-hydroxy-methylglutaryl coenzyme A (HMG CoA) lyase (HCL1).

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

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

19 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase catalyzes the divalent cation-dependent c

20 nzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase catalyzes the terminal steps in ketone bo

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

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

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

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

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

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

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

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

29 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) can exert benefi

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

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

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

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

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

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

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

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

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

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

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

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

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

43 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a critical enzyme in the mevalonat

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

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

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

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

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

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

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

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

52 ds to 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase and irreversibly inhibits HMG-CoA synt

53 calis 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase was mutated to a glycine.

54 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, a member of the family of acyl-conden

55 lase, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, HMG-CoA reductase, and low-density li

56 levels of hydroxymethylglutaryl-coenzyme A (HMG-CoA) synthase, squalene epoxidase, and acyl-CoA:chol

57 Antibodies against HMG-CoA reductase apparently provoke SINAM.

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

59 Treatment with small interfering RNA against HMG-CoA synthase led to a substantial reduction in HCV r

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

61 omogeneity, and shown biochemically to be an HMG-CoA synthase.

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

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

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

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

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

67 tion, representing the first structure of an HMG-CoA synthase from any organism.

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

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

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

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

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

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

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

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

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

77 cetyl-CoA, acetoacetyl-CoA, malonyl-CoA, and HMG-CoA in their cytosol.

78 ylglycerol, diacylglycerol, malonyl-CoA, and HMG-CoA.

79 edback response, which upregulates HMGCR and HMG-CoA synthase 1 (HMGCS1) following statin treatment.

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

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

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

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

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

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

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

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

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

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

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

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

92 rast, the effects of hymeglusin on bacterial HMG-CoA synthase, mvaS, have been minimally characterize

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

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

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

96 Using NAD(P)(H), the enzyme catalyzes HMG-CoA reduction approximately 200-fold more efficientl

97 was characterized and demonstrated to cleave HMG-CoA to acetoacetate and acetyl-CoA with catalytic an

98 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins are competitive

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

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

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

102 CoA, malonyl-CoA, hydroxymethylglutaryl-CoA (HMG-CoA), and acetyl-CoA in INS-1 832/13 cells as judged

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

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

105 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase (HMGL) is involved in branched-chain amin

106 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase is a key enzyme in the ketogenic pathway

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

108 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, reduce the in

109 cedented (R)-3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) stereospecific route in nature.

110 homologues, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase and the fatty acid biosynthesis enzyme

111 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase catalyzes the first physiologically ir

112 erivatives, such as acetyl-CoA, butyryl-CoA, HMG-CoA, and malonyl-CoA, as well as NADPH but not NADP(

113 All 12 CoA's (CoASH, HMG CoA, methylmalonyl CoA, succinyl CoA, methylcrotonyl

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

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

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

117 sumoylation state of Caenorhabditis elegans HMG-CoA synthase (HMGS-1).

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

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

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

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

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

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

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

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

126 yl-CoA into HMG-CoA, catalyzed by the enzyme HMG-CoA synthase.

127 ible wavelength spectrophotometric assay for HMG-CoA synthase has been developed.

128 ue is also supported by a homology model for HMG-CoA lyase based on the structure of 4-hydroxy-2-keto

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

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

131 e-41, R41Q and R41M recombinant mutant human HMG-CoA lyase proteins have been constructed, expressed,

132 nducted using the crystal structure of human HMG-CoA lyase.

133 ollection as a previously unidentified human HMG-CoA lyase (HMGCL).

134 of this residue (R41Q) correlates with human HMG-CoA lyase deficiency.

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

136 diminution of sterol synthesis, identifying HMG-CoA synthase as a potential drug target and suggesti

137 addition, both fungi and humans deficient in HMG CoA lyase accumulate acidic intermediates as a conse

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

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

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

141 Arginine-41 is an invariant residue in HMG-CoA lyases.

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

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

144 ore rapidly after mTOR inhibition, including HMG-CoA synthase, whose enhanced degradation probably li

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

146 15(S)-HETE by inducing HMG-CoA reductase expression caused increased farnesylat

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

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

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

150 (HMG-CoA) synthase and irreversibly inhibits HMG-CoA synthase in a dose-dependent manner.

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

152 ation of acetyl-CoA and acetoacetyl-CoA into HMG-CoA, catalyzed by the enzyme HMG-CoA synthase.

153 requirement for mitochondrial OPA3 to limit HMG-CoA-derived MGC and protect the electron transport c

154 ductase inhibitors, or statins, target liver HMG-CoA and are of proven benefit in the prevention of c

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

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

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

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

159 During standard diet, mitochondrial HMG CoA synthase mRNA was selectively reduced in L-FABP

160 pa3 mutants derives from extra-mitochondrial HMG-CoA through a non-canonical pathway.

161 ution of the recombinant human mitochondrial HMG-CoA lyase containing a bound activator cation and th

162 d protein analysis identified, mitochondrial HMG-CoA synthase, aldehyde dehydrogenase, and catalase a

163 and hepatic mRNA expression of mitochondrial HMG-CoA synthase.

164 articularly high levels of the mitochondrial HMG-CoA synthase 2 (Hmgcs2) compared with all other tiss

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

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

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

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

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

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

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

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

173 anti-HCV effects are reversed by addition of HMG-CoA, mevalonic acid, or geranylgeraniol.

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

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

176 es the divalent cation-dependent cleavage of HMG-CoA to produce acetyl-CoA and acetoacetate.

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

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

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

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

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

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

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

184 tes in the cholesterol pathway downstream of HMG-CoA.

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

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

187 ngly, renal as well as hepatic expression of HMG-CoA synthase 2 increased with prolonged starvation.

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

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

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

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

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

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

194 3 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isopr

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

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

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

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

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

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

201 s its anti-HCV effects through inhibition of HMG-CoA synthase.

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

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

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

205 odel for the catalytic reaction mechanism of HMG-CoA lyase based on the examination of previously rep

206 sis for an understanding of the mechanism of HMG-CoA synthase.

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

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

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

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

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

212 ase catalyzes the four-electron reduction of HMG-CoA to mevalonate and is an enzyme of considerable b

213 atalyzing the NAD(P)H-dependent reduction of HMG-CoA to mevalonate.

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

215 ylated enzyme, and the hydrolytic release of HMG-CoA from the enzyme.

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

217 a non-cell wall antibiotic, the structure of HMG-CoA synthase from Enterococcus faecalis (MVAS) was d

218 In addition, a crystal structure of HMG-CoA synthase with acetoacetyl-CoA was determined at

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

220 reased capture of ZOL and by upregulation of HMG-CoA synthase and reductase transcription.

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

222 Statins, or HMG CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductas

223 In other organisms, HMG CoA lyase catalyzes the last step in the leucine cat

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

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

226 n from leucine into these three SC-CoAs plus HMG-CoA in their mitochondria and enzymes that can form

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

228 ack-reaction with its physiological product (HMG-CoA).

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

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

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

232 and, while similar to the recently published HMG-CoA synthase structures from Staphylococcus aureus,

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

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

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

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

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

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

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

240 etoacetate synthesis when incubated with (S)-HMG-CoA.

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

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

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

244 y deficient HMGCL R41M mutant with substrate HMG-CoA have been determined to 2.4 and 2.2 A, respectiv

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

246 -limiting enzymes for cholesterol synthesis, HMG CoA synthase (HMGCS1) and HMG CoA reductase (HMGCR),

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

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

249 vere growth defect in BMDMs, indicating that HMG CoA lyase gene function is critical for macrophage c

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

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

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

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

254 These structures show that HMG-CoA synthase from Enterococcus is a member of the fa

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

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

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

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

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

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

261 ondensation with acetoacetyl-CoA to form the HMG-CoA product.

262 dithio-CoA and implicate this residue in the HMG-CoA cleavage reaction chemistry that leads to acetyl

263 lyase Asp-42 and Glu-72 are conserved in the HMG-CoA lyase protein family, which includes proteins th

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

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

266 Here we present crystal structures of the HMG-CoA lyases from Bacillus subtilis and Brucella melit

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

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

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

270 Recent structural studies of the HMG-CoA synthase members of the thiolase superfamily hav

271 Induction of the HMG-CoA synthase promoter required a binding site for st

272 Activity of the HMG-CoA synthase promoter was induced by autocrine PDGF

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

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

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

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

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

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

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

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

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

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

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

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

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

286 Acidic residues corresponding to HMG-CoA lyase Asp-42 and Glu-72 are conserved in the HMG

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

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

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

290 Understanding HMG-CoA reductase regulation has tremendous implications

291 ction in HCV replication, further validating HMG-CoA synthase as an enzyme essential for HCV replicat

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

293 the "backwards" reaction in solution, where HMG-CoA is cleaved to form acetoacetyl-CoA (AcAc-CoA) an

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

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

296 In comparison with HMG-CoA (CoA) synthase, the homologous enzyme from prima

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

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

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

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