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 lyase deficiency also results from mutations at

4 HMG-CoA lyase deficiency results from a human mutation t

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

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

7 HMG-CoA reductase catalyzes the four-electron reduction

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

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

10 HMG-CoA reductase inhibitors have been shown to upregula

11 HMG-CoA reductase inhibitors or statins are associated w

12 HMG-CoA reductase inhibitors such as statins are cholest

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

14 HMG-CoA synthase forms a homodimer.

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

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

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

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

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

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

21 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase catalyzes the divalent cation-dependent c

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

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

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

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

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

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

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

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

30 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) can exert benefi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a critical enzyme in the mevalonat

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

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

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

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

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

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

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

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

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

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

56 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase, a member of the family of acyl-conden

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

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

59 Antibodies against HMG-CoA reductase apparently provoke SINAM.

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

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

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

63 bination with tacrolimus, prednisone, and an HMG-CoA inhibitor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase inhibitors or statins are competitive

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

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

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

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

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

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

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

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

108 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase catalyzes the divalent cation-dependent c

109 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) lyase is a key enzyme in the ketogenic pathway

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

111 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, or statins, reduce the in

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

113 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase catalyzes the first physiologically ir

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 15(S)-HETE by inducing HMG-CoA reductase expression caused increased farnesylat

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

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

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

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

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

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

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

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

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

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

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

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

161 f key PPAR-alpha target (MCAD, mitochondrial HMG CoA synthase, ACO, CYP4A3) and other (CPT1, LCAD) ge

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 es the divalent cation-dependent cleavage of HMG-CoA to form acetyl-CoA and acetoacetate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 3 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isopr

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

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

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

200 rs blocks their sensitivity to 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 uccinyl-CoA after they decrease the level of HMG-CoA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.